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What is the specific role of the cerebellum when it comes to 'coordinating movement'?

What is the specific role of the cerebellum when it comes to 'coordinating movement'?


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In elementary biology (high school level in the UK - A levels), we are told that the cerebellum is the part of the brain that 'coordinates movement'. Literally nobody takes the time to explain what the word 'coordinates' encompasses. Hence, I do not know the specific role of the cerebellum in coordinating movement.

For example, one very daunting thing that we are told is that the frontal lobe contains the 'primary motor cortex', which supposedly contains motor neurons that connect to the spinal cord and brain stem and can send nerve impulses that enable movement in the body. Where is the distinction between such a role and the role of the cerebellum in 'coordinating movement'?


The principal function of the cerebellum, which was detected years ago, is to calibrate detailed movements rather than initiating movements or deciding which movements to execute (Ghez et al, 1985). This was concluded by observing the changes which occurred after damaging cerebellum. Animals and humans with cerebellar dysfunction show, above all, problems with motor control, on the same side of the body as the damaged part of the cerebellum. They continue to be able to generate motor activity, but it loses precision, producing erratic, uncoordinated, or incorrectly timed movements. Thus, cerebellum helps in coordinating fine-tuned movements and inhibits involuntary movements. Apart from this, fMRI studies have indicated that more than half of the cerebellum is intertwined with association areas (Buckner et al, 2011). But since it is out-of-scope here, I'll leave it at that much.

See it like this:

For a more detailed mechanism and circuitry of the cerebellum, you can have a look at this interactive page from the University of Texas. @FilipeRocha have also come up with some fine details in their answer.

References:

  1. Ghez C, Fahn S (1985). "The cerebellum". In Kandel ER, Schwartz JH. Principles of Neural Science, 2nd edition. New York: Elsevier. pp. 502-522.

  2. Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT (2011). "The organization of the human cerebellum estimated by intrinsic functional connectivity". J. Neurophysiol. 106 (5): 2322-2345. doi:10.1152/jn.00339.2011.


When attempting to execute a movement, a signal is not only sent from the motor cortex through the spinal chord and to the muscles, but also one is sent from the same motor cortex to the cerebellum, containing the information of what is the intended movement (this happens via the cortico-pontocerebellar tract, and enters the cerebellum through the middle cerebellar peduncle, in case you are familiar with some neuroanatomy).

At the same time, the cerebellum is receiving information about the current position and forces of the body, called proprioception, through signals that come from proprioceptors located on bones, muscles and joints, which travel up the spinal chord (through the spinocerebellar pathways) and enter the cerebellum (through the inferior cerebellar peduncle). The cerebellum then processes both pieces information - intended movement and current mechanical state of the body - and sends out a signal back to the motor cortex (via the superior cerebellar peduncle) containing information that will improve the overall execution of the movement, by correcting and smoothing out with how much force, how much time and to what extent each component of the movement should be done.

The cerebellum is also implied in the learning process, not only movement-wise (learning to ride a bike or swim), but also cognitively.

To learn more:

http://www.brainfacts.org/brain-basics/neuroanatomy/articles/2012/the-cerebellum/

https://www.youtube.com/watch?v=mpO4lTDr1to&index=21&list=PLp9HSlEm97VXyQ32Uwjfz3dpmQ8nl63zJ


The Cerebellum Isn’t What We Thought

Scientists long believed its function was simply to coordinate movements. Now they suspect it could do much more.

When a 22-year-old college student turned up at a hospital after falling on ice and hitting her head, doctors conducted a CT scan that revealed a surprise: a tumor in her cerebellum, the fist-size structure at the back of the brain. After surgeons successfully removed the mass, the woman started exhibiting strange behaviors. She was emotionally unexpressive and acted inappropriately—undressing in the hospital corridors, for example. She spoke in a fast, high-pitched, unintelligible voice and had trouble doing basic arithmetic, drawing, reading, and writing. Although she began to improve after a few weeks, two years passed before she could take a remedial course through a junior college—and for more than two decades, her decision-making remained impaired.

This unusual case, which was first reported in the 1990s, defied a notion that had persisted for centuries: that the cerebellum’s job is limited to coordinating movements.

For many neuroscientists, the structure took a back seat to the cerebral cortex, the thin layer of cells covering the creased, baseball-glove-shaped lump that most of us think of when we imagine the human brain. The cerebellum was considered so unimportant that many scientists would simply ignore it in neuroimaging studies—or, when they removed animals’ brains for many types of research, they would chop the structure off and throw it away. “That’s how the field has been for a very long time,” says Krystal Parker, a neuroscientist at the University of Iowa.

Things are slowly beginning to change, however, as evidence builds that the cerebellum makes important contributions to cognition, emotion, and social behavior. On top of that, studies suggest that the cerebellum may play a key role in autism, schizophrenia, and other brain disorders. Researchers are now probing the brains of both mice and people to understand how the cerebellum contributes to these conditions.

Investigations of the cerebellum have exploded over the last few years, says Catherine Stoodley, a neuroscientist at American University and a coauthor of a 2019 paper in the Annual Review of Neuroscience on the cerebellum’s role in cognition. “It’s very exciting.”

At first glance, the cerebellum looks a bit like a wrinkly, overgrown walnut shell. A closer look reveals two hemispheres with surface creases that sink down into deep grooves and split off into a network of coral-like branches. Peering through a microscope reveals a uniform pattern of densely packed cells. The cerebellum makes up only about 10 percent of the human brain’s mass but contains more than half of its neurons. Stretched out, the cerebellum’s surface area would be nearly 80 percent that of the cerebral cortex.

The earliest experiments with the cerebellum—Latin for “little brain”—date back centuries. Those investigations weren’t pretty: Scientists simply lopped off the structure from live animals, then observed their behavior. For example, the 19th-century French physiologist Marie-Jean-Pierre Flourens conducted cerebellectomies on pigeons and reported that the animals started to teeter and totter as if intoxicated. These findings led him to propose that the structure was necessary for coordinating motion. Clinical observations of people with cerebellar injuries later confirmed this hypothesis, cementing the cerebellum’s reputation for nearly two centuries as a movement-coordination structure.

A small number of scientists started to challenge this description in the 1980s. Lead among them was Henrietta Leiner, who had initially trained in mathematics, physics, and computer science but later took an interest in neuroanatomy. She became captivated by the cerebellum as she pondered the purpose of the thick tract of nerve fibers that connect it to the cerebral cortex.

Leiner also questioned why the cerebellum evolved to be so much larger in humans than in other animals. (According to one estimate, the human cerebellum is, on average, 2.8 times bigger than expected in primates our size.) Why would that be so, if all it did was coordinate movement? In 1986, Leiner—along with her husband, computer scientist Alan Leiner, and a neurologist named Robert Dow—proposed a radical hypothesis. The human cerebellum, they said, contributed to core thinking skills such as the ability to plan one’s actions.

Jeremy Schmahmann, then a neurology resident at Boston City Hospital, also developed a fascination for the cerebellum around that time. His interest stemmed from emerging evidence that another part of the brain once thought to be involved solely in motor control—the basal ganglia—also contributed to cognition. This led Schmahmann to wonder whether the same could be true of the cerebellum.

To address this question, Schmahmann set out on what he describes as an “archeological dig” through the stacks at Harvard’s Countway Library of Medicine. There, he discovered manuscripts dating to the 1800s documenting instances of cognitive, social, and emotional impairments in patients with cerebellar damage—and in rare cases where people were born without a cerebellum at all. “There was a little counterculture going back right to the beginning that was completely neglected,” says Schmahmann, now a neurologist at Massachusetts General Hospital and a coauthor of the recent review with Stoodley.

The historical reports persuaded Schmahmann to investigate further. In experiments with monkeys, he and his adviser, neuroanatomist Deepak Pandya, found evidence that the cerebellum receives input via the brainstem from parts of the cerebral cortex that, in the parallel areas of human brains, are involved in functions such as language, attention, and memory. “This flew in the face of accepted wisdom,” Schmahmann says. “We had some very strong opponents—but most, once the data became available, came around.”

Also around that time, another group, led by University of Pittsburgh neurobiologist Peter Strick, traced the connections going the other direction—from the cerebellum to the rest of the brain. This two-way communication bolstered the case that the cerebellum does much more than coordinate movements.

Subsequent clinical observations and neuroimaging studies have further strengthened the argument.

In the late 1990s, Schmahmann reported the first description of cerebellar cognitive affective syndrome after observing that people with cerebellar damage—due to degeneration or after tumor removal, strokes, and infection—exhibited a wide array of impairments in cognition and behavior. These included difficulties with abstract reasoning and planning, changes in personality—such as the flattened emotions and inappropriate behaviors he observed in the college student with the cerebellar tumor—and problems with speech. Some patients recovered after several months in others, symptoms persisted for years. This condition, which was later dubbed “Schmahmann’s syndrome,” strengthened the evidence that the cerebellum was indeed involved in a variety of cognitive processes.

Rare cases of people born missing parts of their cerebellum have also hinted at broader functions. In addition to difficulty coordinating their movements, these individuals exhibit signs of Schmahmann’s syndrome, as well as autistic-like traits such as obsessive rituals and trouble understanding social cues.

In another influential study, Harvard neuroscientist Randy Buckner and his colleagues mapped communication between the cerebral cortex and the cerebellum in humans. By scanning the brains of healthy people using functional magnetic resonance imaging, the team revealed that activity in the majority of the cerebellum was in sync with activity in parts of the cerebral cortex responsible for cognitive functions—and not with cortical areas involved in movement. “That paper was incredible for showing that the majority of the cerebellum can actually be accounted for by non-motor functions,” says Ann Shinn, a psychiatrist at McLean Hospital in Massachusetts.

These studies and others are making it increasingly clear that the cerebellum has many roles. But a big question remains: What, exactly, is its overall function?

The highly organized, grid-like architecture of cells in the cerebellum has inspired some scientists to suggest that it carries out a single computation. Schmahmann has dubbed this hypothesis the “universal cerebellar transform.” Exactly which core computation could account for the cerebellum’s involvement in movement, cognition, and emotion remains an open question. But scientists have proposed a variety of possibilities, such as making and updating predictions or the precise timing of tasks.

Given the cerebellum’s myriad roles, some scientists suspect the structure may be involved in several brain-related disorders. The two conditions for which there is currently the most evidence are autism and schizophrenia.

Cerebellar abnormalities are some of the most common neuroanatomical differences seen in people with autism, and physicians have observed that injuries to the cerebellum at birth considerably increase the risk that a child will develop the condition. Recent studies also suggest that the cerebellum may have an outsize influence on development and that early irregularities in this structure may predispose people to conditions like autism.

Sam Wang, a neuroscientist at Princeton, and his team have shown that inactivating the cerebellum in mice during development using chemogenetics—a method for manipulating specific neural circuits using engineered molecules injected into the brain—leads to characteristics in the animals that mirrored those seen in humans with autism. The mice lost the preference to spend time around another mouse instead of an inanimate object, and had difficulty adjusting to a new task. The same manipulation in adult mice had no such effects.

Other researchers have found that it may be possible to modify some of these traits by targeting the cerebellum. Stoodley and her colleagues have demonstrated that stimulating the cerebellum with chemogenetics can reverse social deficits in genetically engineered mice that show autism traits. Her lab is now assessing whether they can modify social learning in both autistic and neurotypical people by targeting the cerebellum with a technique called transcranial direct current stimulation, which uses electrodes placed on the head to modulate brain activity.

The idea that the cerebellum might be involved in schizophrenia has been around for decades, but until recently there was little experimental evidence in humans. In 2019, however, a group including Schmahmann reported that stimulating the cerebellum with a method called transcranial magnetic stimulation (TMS), which uses magnets to create electrical currents in the brain, could alleviate what are known as schizophrenia’s negative symptoms, which include anhedonia (the inability to feel pleasure) and a lack of motivation. If TMS therapy proves effective, it could fulfill a long-standing need. Antipsychotic medications can successfully reduce what are known as schizophrenia’s positive symptoms—in other words, additional behaviors not typically seen in healthy people—such as hallucinations and delusional thoughts. But effective therapies for the negative symptoms remain elusive.

“There’s a lot of things we need to work out before this would become a therapeutic,” says Roscoe Brady, a psychiatrist at Boston’s Beth Israel Deaconess Medical Center who was involved in that trial. That said, he adds, TMS is one of the most promising options he’s seen in the published research.

Brady and his colleagues are now carrying out a follow-up study with a larger group of people. They’re also tackling the question of how, exactly, cerebellar stimulation leads to improvement. At the University of Iowa, Parker and her colleagues are also testing whether cerebellar TMS can improve mood and cognition in people with conditions including schizophrenia, autism, bipolar disorder, depression, and Parkinson’s disease. The abnormalities in working memory, attention, and planning are very similar in many of these conditions, Parker says. Ultimately, she hopes that teasing apart the cerebellar contribution to these conditions will lead to the development of new treatments.

Whether cerebellum-based therapies can help people with these wide-ranging conditions remains to be seen. What’s clear, however, is that the cerebellum can no longer be ignored—and that its connections throughout the brain and contributions to brain function may be much broader than scientists had initially imagined.

“What I’m hoping comes out of all of this is that people can’t get away with eliminating the cerebellum from the research that they’re doing,” Parker says. “It’s almost always doing something related to whatever people are studying.”


How Does The Brain Control Movement?

How does the brain control the precision of movement of our body parts? originally appeared on Quora: the place to gain and share knowledge, empowering people to learn from others and better understand the world.

Answer by Fabian van den Berg, Neuroscientist and Psychologist, on Quora:

How does brain control the precision of movement of our body parts? This might get a bit more complicated than you expected, so hold on. Your brain is rather complicated with many different parts and even simplifying it gets confusing. This is going to be a long one since you asked for the brain to movement mechanism (which is more complex than you’d think).

I’ll try to find common ground making it both understandable and accurate. This is about the voluntary control the brain has on muscles, movements like reflexes are excluded.

Initiating a Movement

The first thing we need is to know how movement is initiated. This isn’t as easy as sending a message from the brain to the muscle to make it “move”. Messages originate from the cortex, the outer layer of the brain. These need to go to the muscles, but they make a little stop first. If every message was sent to your muscles you wouldn’t be able to function. This stop happens at the Basal Ganglia. This is a complicated system that selects which “instructions” will be executed and which are inhibited. The reason for a movement can be many things, the specific goal is not important right now.

Important areas in the basal ganglia are the ones below, I’ll hold off on too much detail and just give general descriptions. There are more structures that may or may not be part of the basal ganglia, but let’s stick to these.

Striatum: The striatum is a collective name for several structures. The dorsal (top part) is divided into the caudate nucleus and the putamen. The ventral (bottom part) is divided into the nucleus accumbens and olfactory tubercle.

Globus Pallidus: The Globus Pallidus is divided in two parts, the internal and external globus pallidus. It has a strong role in voluntary movement.

Substrantia Nigra: This translates to “black substance” and is named like that because it is literally darker than the rest. The reason for the dark look is high levels of neuromelanin found in dopaminergic neurons (neurons that produce dopamine). The substantia nigra also has two parts: the pars compacta and the pars reticularis. The substatia nigra plays a large role in both movement, motivation, and learning responses to stimuli.

Thalamus: This is a true master of multitasking. The thalamus is an information hub, receiving and relaying information. It mainly relays information between the subcortical areas and the cortex and in particular relays the sensory information to the relevant association areas.

These have a complex anatomy, so for the sake of clarity I’ll rearrange them a bit to get a clearer image.

We start in the cortex. This is connected to the s triatum via an excitatory (increasing activity) neurotransmitter called Glutamate (with some help from Aspartate). So signals from the cortex increase the activity of the striatum. The striatum then splits into two pathways via inhibitory projections (decreasing activity). There’s the direct pathway and the indirect pathway.

In the direct pathway, the increased activity in the striatum causes an inhibition of the Substantia Nigra Pars Reticularis (SNr) and Globus Pallidus Interna (GPi). Normally these two inhibit the Thalamus, but because they are themselves inhibited (by the striatum), the thalamus is released (disinhibited). So an increase in the Striatum results in an increase in the Thalamus via disinhibition. The thalamus is then free to send its signals back to the cortex, which sends the signal to the brainstem, and eventually to the muscles.

Why this way and not just two excitatory connections? That’s because of white noise. The brain can be pretty noisy, and for two excitatory signals to rise above that they need to be a lot higher. Two inhibitory connections don’t have this problem, it’s easier to take off the brake than to step on the gas.

We once again start in the striatum with higher activity, but this time we follow a different path. In the Indirect Pathway, the striatum inhibits the Globus Pallidus Externa (GPe). The GPe constantly inhibits the Sub Thalamic Nucleus (STN), this inhibition is released when the GPe itself gets inhibited, so here too we have a disinhibition. The STN is then free to send excitatory signals to the SNr-GPi combination. This time these two have their activity increased, so their inhibition of the thalamus remains. Instead of releasing the gas, the indirect pathway slams even harder on the brake.

Modulation Of The Pathways

These two pathways seem at odds, with both of these you are pretty much stuck right? Yes, yes you are. Luckily we have another component, one that modulates the two. The Substantia Nigra pars compacta (SNc) sends dopamine to the striatum. Dopamine can attach to two receptors there: D1 and D2 receptors. D1 receptors stimulate the GABAergic neurons, tipping the scales towards the direct pathway. So more dopamine stimulating D1 receptors means more movement. The GABA neurons that control the Indirect pathway respond to Acetylcholine and Glutamate instead. The D2 receptors decrease the GABAergic neurons of the indirect pathway, soothing the effect and preventing full inhibition of movement.

So through dopamine movement is controlled, maintaining a sensitive balance between excitation and inhibition of movement. Not too much and not too little. Messing this up is bad news, we see this in Parkinson’s and Huntington’s disease.

In Parkinson’s Disease there is not enough dopamine due to damage in the Substantia Nigra. This means the direct pathway cannot initiate movement and the indirect pathway is out of control and inhibiting movement all over the place.

In Huntington’s Disease there is damage in the striatum shifting activity towards the direct pathway and preventing the indirect pathway from functioning. This results in the opposite of Parkinson’s, the inability to prevent unintentional movements.

More Loops, More Problems

Now things get even more complicated, since the system above can be used in different ways using slightly different areas. There’s a Motor Loop for motor control (obviously), an Oculomotor Loop for eye movement, a prefrontal loop for planning/working memory/attention, and a Limbic Loop for emotional behavior/motivation. Different books use different names and some group the motor and oculomotor loop together, this is just how I was taught. These loops can function simultaneously (parallel to each other).

Instead of going into detail about the specific differences and similarities of the functional loops, an example might be better. Let’s say you want to touch a glass globe (to see if it’s nice and smooth):

  • The limbic loop plays its part in the decision to move due to activation caused by your desire to see if it’s actually smooth glass (motivation).
  • The prefrontal loop forms a movement plan: the how, where, and when of your reach and perhaps grab.
  • The oculomotor and motor loops play their part in the execution and programming of the behavior to reach the target: so the movement of the eyes, arms, and hands to get a hold of that glass globe.

From the Brain Down the Spine

Ok, we’re nearly there. The instructions have gone through all the areas and have reached the cortex once again. Here we have two pathways: The Lateral or Pyramidal Pathways for voluntary movement and the Ventromedial or Extrapyramidal Pathways for unconscious movements like posture.

Lateral Pathways/Pyramidal Tracts

The more important one is the Corticospinal Tract which innervates the muscles of the body. Neurons of one side controls the muscles on the other side. We start in the neocortex, about 66% motor cortex and 33% somatosensory.

  • Axons move through the capsula interna and continue through the cerebral penducle (a large collection in the midbrain).
  • Then they move through the pons and come together to form a tract at the base of the medulla. The tract forms the medullary pyramid, on account of the pyramid-like shape.
  • At the transition of the medulla to the spine, the majority crosses over to the other side, so the left side controls the right and vice versa.
  • In the lateral column of the spine we now have a nice corticospinal tract that goes all the way to the ventral horns. Here they connect to motor and interneurons that control the muscles.

The second one is the Corticobulbar Tract which controls the muscles of the head and neck. Neurons control muscles on both sides. We again start in the motor cortex.

  • Axons decend down through the capsula interna and down into the midbrain to the penducles.
  • The Corticobulbar Tract exits at different levels of the brainstems to connect to lower motor neurons of the cranial nerves.
  • The Corticobulbar tract does not fully move to the other side of the body, it rather splits in two innervating both sides of the muscles in the head.

Ventromedial Pathways/Extrapyramidal Tracts

There are four ventromedial tracts that originate in the brainstem and end at spinal interneurons connected to the muscles. The extrapyramidal system is concerned about the modulation and regulation of movement. The tracts below are all affected by various other structures like the Nigrostriatal Pathway, the Basal Ganglia, and the cerebellum. The cerebellum in particular is important to smooth out fine movements (alcohol affects the cerebellum, hence the problem of touching your nose). The cerebellum doesn’t initiate nor inhibit movement, it’s more of a modulator using sensory information to make slight adjustments to movements. More in depth information about the cerebellum can be found here: Cerebellum .

    Rubrospinal Tract is still a bit of a mystery, but it’s thought to be involved in fine motor control of hand movements.

  • Red Nucleus → Switches to the other side of the midbrain → Descends into the lateral tegmentum → Through the lateral funiculus of the spinal cord (alongside the corticospinal tract).
  • Vestibular nuclei (input from the balance organs) → Remains ipsilateral (does not cross) → Down through the lumbar region of the spinal cord.
  • Superior Colliculus (receives input from the optic nerves)→ Switches sides and enters the spinal cord → Terminating at the cervical levels.
  • Caudal and Oral Pontine Reticular Nucleus (in the pons) → Lamina VII & VIII of the spinal cord.
  • Medullary Reticular Formation (in the Medulla from the gigantocellular nucleus) → Lamina VII & IX of the spinal cord.

From Neuron to Muscle

Regardless of the pathway taken, we have now a signal that travelled from the brain through the spine and some nerves. This signal still needs to activate a muscles. Muscles are controlled using motor units, which are composed of an upper and a lower motor neuron. The tracts above are the upper motor neurons, which is the neuron that sends the signal from the brain.

Upper Motor neurons then connect to Lower Motor neurons, which in turn connects to the muscle.

Your muscles are basically fibers within fibers within fibers. When we get to the smallest level we have Sarcomeres which are composed of sections divided by Z-lines. Between the Z-lines we have two filaments, actin and myosin. Actin is a long thin filament attached to the Z-line, Myosin is a thick filament attached to the middle called the M-line. What is going to happen is that the Myosin is going to pull on the Actin, causing the Z-lines to contract in towards the M-line. If many of these small fibers do this at the same time the larger structures will follow, causing the entire muscle to contract. This is called the Sliding Filament Model of contraction.

If we zoom in to a single actin and myosin pair it looks a bit like this. When your muscles are at rest actin and myosin don’t touch, but they have a high affinity (they really want to touch). They would touch if it wasn’t for two proteins (tropomyosin and troponin) attached to the actin filament.

We zoom out a little bit now, as we still have a neuron waiting.

  • The lower motor neuron sends an action potential that releases Acetylcholine into the synapse, causing an influx of Sodium which alters the voltage and propagates the signal.
  • The action potential is now inside the muscle, no longer in the neuron. As the action potential makes its way along the muscle cells it hits the Sarcolemma.
  • The Sarcolemma has tubes going deep into the cell (T-Tubules). These tubes lead the action potential towards the Sarcomeres.
  • The Sarcoplasmic Reticulum which encases the sarcomeres is constantly pumping calcium out of the cell (these pumps use ATP as energy). It is also lined with voltage-gated calcium channels which are still closed.
  • When the T-Tubules provide an action potential the Voltage Gated Calcium channels open up causing an influx of calcium into the cell.

The calcium now triggers the two proteins that surround the Actin. Calcium binds to troponin causing it to change shape (as proteins do when they bind). The troponin pulls towards tropomyosin, exposing the acting strands.

The myosin is now free to attach itself to the exposed actin sites. But it can’t just do this on its own, no, only myosin that took some ATP and broke it down into ADP and Phosphate are able. This “charged” m yosin stretches into an extended position. Here it stays, holding onto ADP+Phosphate like a loaded gun.

  1. Now that the actin is exposed and the myosin is primed and ready it releases its energy and shoots towards the actin. It changes shape again pulling on the acting, sliding it inwards.
  2. With the bullet fired, all the energy it got from separating ATP into ADP and Phosphate has been used up and it released the split compounds back into the cell (the release occurs because myosin changed it shape and in this state no longer has a strong affinity for them). Here they will be re-used and turned into ATP again by the mitochondria.
  3. In this state myosin does have a high affinity for ATP, leading to ATP binding to it again. This binding causes another shape change that releases myosin from the actin. This resets the myosin back to its primed and ready state. It can fire again and pull actin in a little bit more.

The myosin thus pulls on the actin, pulling the two Z-lines towards the middle and the sarcomere contracts. In the meantime: the calcium pumps of the Sarcoplasmic Reticulum are busy pumping calcium out, so eventually calcium unbinds from Troponin. This resets the protection and causes actin to become inaccessible to myosin. Now the fun is over, myosin can no longer attach to the actin and the cycle starts anew when an action potential hits.

There you have it, the full pathway of movement from brain to muscle (in a very short and condensed version). A movement plan has been made, this can be for big movements like walking or fine movements like softly touching something. This goes trough a lot of structures, some motor tracts, gets some assistance from the cerebellum and your senses, and then it ends up in your torso, arm, hand, and finger where the muscles move to make it all happen.

Important and convenient sources are:

Mancall, E. L., & Brock, D. G. (2011). Gray’s Clinical Neuroanatomy: The Anatomic Basis for Clinical Neuroscience. Elsevier Health Sciences.

Middleton, F. A., & Strick, P. L. (2000). Basal ganglia and cerebellar loops: motor and cognitive circuits. Brain research reviews, 31(2), 236-250.

Lanciego, J. L., Luquin, N., & Obeso, J. A. (2012). Functional Neuroanatomy of the Basal Ganglia. Cold Spring Harbor Perspectives in Medicine, 2(12), a009621. http://doi.org/10.1101/cshperspe.

And my own summary of the courses concerning the brain and interaction with the environment. The summary is a mix of articles, books, lectures, talks, and group discussions. Sorry, no online source for that.

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Where is the Cerebellum located? What parts does it consist of?

The Cerebellum is located in the back of the brain at the level of the brainstem bridge, under the occipital lobe (slightly above the nape of the neck). It binds to the rest of the brain through the lower, middle and upper cerebral peduncles, which are a set of nerve fibers that carry information from the rest of the body to the Cerebellum (afferent), or from the Cerebellum to the rest of the body (efferent). In fact, if it weren’t for the cerebral peduncles, it would be separated from the rest of the brain.

Cerebellum

Mining the cerebellum for its role in speech

The following comes from Adityarup Chakravorty, a science writer at the Waisman Center at the University of Wisconsin–Madison:

To be able to speak aloud the word you picked needs exquisite coordination between several parts of the body. The brain, lungs, throat, voice box, tongue and lips must work together to make sure we are saying what we intend to communicate.

How do we do it? Researchers have long thought that a specific part of our brain – the cerebellum – plays a key role in the muscle control we need to speak.

What they don’t know is how the cerebellum influences our speech.

The Cerebellum. Located in the back of the brain, it is involved in central regulation of basic movement, like balance and posture.//From Serendip Studio, Bryn Mawr College

“We know that when the cerebellum is damaged, it causes movement disorders in both speech and non-speech actions,” says UW–Madison Waisman Center investigator Ben Parrell. “What we don’t understand is why cerebellar damage leads to these disorders.”

So Parrell, who is a new assistant professor of communication sciences and disorders at UW-Madison, set out to investigate.

In a recent study, he and his colleagues discovered that damage to the cerebellum diminishes our ability to predict consequences of an action and issue specific motor commands to the body – what researchers call “feedforward control.”

Diminished feedforward – or predictive – control could explain speech difficulties often faced by individuals with cerebellar damage.

“If you can correctly predict what will happen after an action – like trying to say a specific word, for example – you can do things more fluidly, more rapidly because you don’t need to monitor outcomes in real time,” says Parrell.

In contrast, without properly functioning feedforward control, we have to instead exercise “feedback control,” which is reactive rather than predictive and it takes more time. “You do things a little bit at a time, monitor what happened, then do a little bit more and monitor again, and so on,” says Parrell.

Imagine trying to carry out a conversation while having to slow down and make sure that each word is being pronounced correctly.

“For the human nervous system, monitoring outcomes and correcting for them takes between 50-200 milliseconds,” says Parrell. Many actions, including speaking, happen in a much shorter time span. “So the idea is that we can’t rely only on the feedback – or reactive – system to produce these actions because it will be just too slow.”

Ben Parrell//Courtesy of the Waisman Center at the University of Wisconsin–Madison

Parrell, who conducted the bulk of the study during his time as a postdoc at the University of California, Berkley, tested both the predictive (feedforward) and reactive (feedback) systems in individuals with and without damage to the cerebellum.

Study participants were asked to read specific words, such as “head,” into a microphone. Their voices were recorded, run through a computer program and played back through headphones. This entire process took 12 milliseconds – an imperceptible nugget of time.

When their voices were played back through headphones, the study participants didn’t always hear what they expected. The researchers subtly changed the words they spoke – “head” would sound more like “hid,” for example.

In tests for predictive control, the researchers introduced these changes over multiple trials. It was up to the participants to compensate, changing how they subsequently pronounced the intended word to get it closer to sounding like “head.” For instance, in the next trial, the speaker might say something that sounded more like “had.”

How well participants were able to do this depended greatly on whether they had experienced cerebellar damage.

“We wanted to ask if people with cerebellar damage could adjust their behavior to incorporate this consequence of their action over time,” says Parrell, noting that individuals with cerebellar damage could adjust their behavior, but not to the same degree as those without any damage. “We take that as evidence that their ability to change their predictive control system is impaired, which indicates that the cerebellum is critical for this process.”

But the tests for reactive control said something else entirely.

In these experiments, the changes to the spoken words were varied. “Sometimes ‘head’ sounded like ‘head,’ sometimes it sounded like ‘hid’ and sometimes it sounded like ‘had,’” says Parrell. “We made the change random and unpredictable.”

That meant the study subjects had to depend on their reactive system. “We found that the folks with cerebellar damage responded to these unpredictable changes to a larger extent than those without any damage,” says Parrell. “It was totally unexpected.”

Parrell’s research shows that the cerebellum plays a vital role in our predictive systems, which in turn greatly affects how we speak and communicate. He is now exploring why those with cerebellar damage have improved reactive systems and what that means for their ability to speak the words they want to use.


The Cerebellum Is the Body's Little Brain

In an average week, how many times would you say you walk across a room? Drive your car? Try and potentially fail to learn dance choreography off of YouTube? Chances are, you're doing at least one of those on a regular basis, and you have one small but mighty brain structure to thank: the cerebellum.

How Big Is the Cerebellum?

Named for the Latin term for "little brain," and hanging off the back of the main brain, the adorable sounding anatomical feature packs a major punch for its diminutive size. "The brain weighs about 3 pounds (1.36 kilograms) and the cerebellum makes up about 10 percent of that," says Janice Wiesman, M.D., clinical associate professor in the department of neurology at the NYU School of Medicine, in an email interview. "It's made up of three lobes, the vermis in the center ('vermis' means 'worms' in Latin and it is a long, thin, structure that looks like a worm), and a cerebellar hemisphere on each side of that."

"It weighs about 5 ounces (147 milliliters)," adds Pediatric Neurophysiology Fellow at Nationwide Children's Hospital, Daniel Freedman, D.O., in an email. "It's the coordination center of the brain and receives a large amount of sensory input from the spinal cord and brain regarding the body's movements and position. It uses this information to maintain smooth coordinated movements."

We'll get to how the cerebellum translates all that input into action in a second, but let's go deeper on the brain structure's super distinctive appearance. "It has a beautiful branched appearance which is very unique," says Parneet Grewal, a fellow at RUSH University Medical Center, in an email interview. "It has a complex circuitry and is divided into midline vermis (named for its worm-like appearance) and two cerebellar hemispheres on either side of the vermis."

"The vermis is most associated with coordinating movement of the trunk and legs and the cerebellar hemispheres work to coordinate the movement of the arms, hands and fingers," Weisman says. "The cerebellum coordinates voluntary movements like posture, balance, coordination, and speech, resulting in smooth muscle movements."

"When cut in half, the branching pattern of the cerebellar white matter required to connect all the 'folia' (Latin for leaves) can be seen," Freedman says. "This resembles a head of cauliflower or broccoli and is referred to as the 'arbor vitae' (Latin for 'tree of life')."

What Does the Cerebellum Do?

Appearances aside, the cerebellum plays a major role in a variety of everyday functions. "The function most doctors think about is smooth, coordinated control of movement," Wiesman says. "The cerebellum gets sensory input from the joints in the limbs and the trunk and also from the motor areas of the brain – the parts that plan and direct movement. The cerebellum matches those two inputs to make sure that the limb or trunk is doing what the motor cortex in the brain wants it to. This is how you can walk a straight line or close your eyes and touch your nose without missing! It coordinates the movement of your eyes so that you can smoothly track an object. It also coordinates the muscles of swallowing and speech so you don't choke on your food and so you can say 'Peter Piper picked a peck of pickled peppers.'"

But according to research published in October of 2018 in the journal Neuron, all these important functions are just part of the picture — the cerebellum is apparently capable of a whole lot more. "Recently, scientists have found that this most well-known function may be only one of many functions of the cerebellum and only involve 20 percent of it," Wiesman says. "Other functions include modulation of emotion, memory, language and abstract thinking. Like with movement, the cerebellum monitors these functions to make sure they are being done the right way — it's been referred to as the 'editor' of the brain."

What Happens if the Cerebellum Is Damaged?

With all this responsibility, you can't help but wonder what might happen if the cerebellum were to suffer any kind of damage.

"The primary symptom of a damaged cerebellum is 'ataxia' or uncoordinated movement," Freedman says. "Permanent damage to the cerebellum can come from stroke, tumors, infection, or alcohol use. Ataxia can also be temporary as seen in alcohol intoxication. When police officers conduct a roadside sobriety test, they are checking cerebellar function by having you touch finger to nose or walk a straight line."

"Symptoms and signs of cerebellar disease include difficulty coordinating movements, such as walking, moving the arms, and coordinating the muscles of swallowing and speech into a smooth pattern," Wiesman says. "People can have trouble with balance, moving the arms and hands in the way they want, swallowing and coordinating the voice when they speak and the speech can sound slurred. Cerebellar damage can cause a tremor of the limbs, trunk, or voice."

Because the cerebellum also regulates smooth movements of the eyes, people with cerebellar damage may also experience double vision or abnormal eye movements. And because the cerebellum is apparently a player in cognitive and emotional function, researchers believe damage could contribute to mental illnesses like schizophrenia.

"Trouble with speech, eye movements and onset of a tremor can also be seen in cerebellar disorders," Grewal says. "These symptoms are often accompanied by intense nausea, vomiting and vertigo, with lesions that can lead to herniation sometimes presenting with depressed consciousness."

What Causes Damage to the Cerebellum?

So how can such a tiny structure incur so much damage? "The cerebellum can be damaged a number of ways," Wiesman says. "In a person with high blood pressure, a blood vessel can burst and cause a hemorrhagic stroke. A clot in the heart or large arteries can break off and cause an ischemic stroke. Accidents can cause physical trauma to the cerebellum. Degenerative brain diseases affect the cerebellum. Some are inherited like the spino-cerebellar ataxias or Friedreich's ataxia, some occur sporadically like multiple systems atrophy, some are caused by infectious proteins called prions and that are known to be the cause of mad-cow disease in cows and humans or Creutzfeldt-Jacob disease in humans. Some toxins, like alcohol and some medications can cause atrophy of parts of the cerebellum. Rarely as a side effect of cancer, antibodies are made to cells in the cerebellum and damage those cells."

While all this sophisticated circuitry certainly may seem exclusively reserved for human brains, the cerebellum predates us by a longshot. "The cerebellum is an evolutionarily old structure, hundreds of millions of years old, found in fish and reptiles as well as mammals," Weisman says. "After all, fish have to swim straight!"

"The cerebellum is present in other species also and is not unique to humans," Grewal says. "It performs important functions in all species. Circuits of cerebellum are similar in vertebrates with variation in size and shape. The largest cerebellar size is present in elephants."

Weisman adds some food for thought: "Since the cerebellar vermis and hemispheres coordinate different parts of the body, as you look up the evolutionary scale, as animals begin to use their hands in a way different from their legs, their cerebellar hemispheres get larger – but which came first – the structure or the action?"

"If a person has bleeding into one cerebellar hemisphere, the cortex of that hemisphere can be removed and the person will typically recover their motor function over time, with very little disability," Weisman says.


ANATOMICAL CONSIDERATIONS

Motor Functioning

Lesions of the midline area of the cerebellum, the vermis, are associated with disorders of the trunk, whereas lesions of the lateral areas, the hemispheres, produce limb asynergia. 1 Cerebellar diseases can be generally localized by their clinical features: Lesions in the flocculonodular lobe are seen to cause disequilibrium with ataxic gait, a wide-based stance, and nystagmus lesions of the anterior lobes are associated with an even more impaired gait and abnormal coordinated movements of the lower limbs lesions of the lateral posterior lobes are associated with hypotonia, dysmetria, dysarthric speech, and dysdiadochokinesia. 1

Nonmotor Functioning

From an anatomical standpoint, it should not be surprising that the cerebellum may play a role in nonmotor brain functioning. Although the cerebellum constitutes only 10% of the total brain weight, it contains more than half of all the neurons in the brain. 1 The cerebellum is connected to the cerebrum via three cerebellar peduncles. There are connections, largely via the thalamus, to many brain areas relevant to cognition and behavior, including the dorsolateral prefrontal cortex, the medial frontal cortex, the parietal and superior temporal areas, the anterior cingulate, and the posterior hypothalamus. 2,3 There are also noradrenergic, serotonergic, and dopaminergic inputs to the cerebellum from brainstem nuclei. 2 Given these connections, a role for the cerebellum in nonmotor functioning would seem likely. Gao et al. 4 recently suggested that the lateral cerebellum is involved in the acquisition and discrimination of sensory information. Behavioral aspects of the cerebellum have not been directly examined until recently.


Classical Conditioning𠅎yeblink Conditioning: Evidence in Animals (JM. Delgado-Garcia)

The classical conditioning of eyelid responses has a long trajectory going back to the 1930s of the past century [33�]. Those early studies carried out in human volunteers provided basic information regarding the different types of eyelid response evoked by the conditioning (true conditioned responses, sensitization, pseudoconditioning, alpha responses, etc.) depending on the selected conditioned (CS) and unconditioned (US) stimuli or on their temporal relationships. For example, in delay conditioning, the US is presented in the presence of the CS and co-terminates with it, while in trace conditioning there is a time interval between the end of the CS and the beginning of the US. The latter has the advantage of allowing the formation of the conditioned response in the absence of any sensory stimulus [36, 37], although in this regard, it is frequently overlooked that sensory receptors are activated by changes in the stimulus presented to them and not by its sustained presence. Thus, delay conditioning could be considered a particular case of trace conditioning.

Gormezano’s group and many others popularized the classical conditioning of the nictitating membrane/eyelid response in animals (mostly rabbits) during the 1960s [37]. In a seminal paper, Schneiderman et al. [38] had already noticed that the eyelid reflex can easily be conditioned using Pavlovian procedures ( Fig. 1 ), although they did not mention that facial muscles belong to a special type of visceral muscle, a fact that could explain why eyeblinks are so easily conditioned as compared with other types of motor response involving skeletal muscles.

Mean percentage of responses collected in rabbits during classical conditioning of the nictitating membrane response. The conditioned stimulus (CS) consisted of an 800-Hz, 72-dB tone lasting for 600 ms. The unconditioned stimulus consisted of a 100-ms air puff directed at the right cornea. Nictitating membrane responses were recorded with the help of a potentiometer attached to the ipsilateral nictitating membrane. Experimental groups were as follows: the CS–UCS group received paired CS–UCS presentations. CA-A and UCS-A groups received sole presentations of CS or UCS stimuli, respectively. CS-R and UCS-R groups received unpaired presentations of CS and USC stimuli. Figure taken with permission from [33]

Indeed, both the orbicularis oculi (the muscle that closes the eyelids) and the retractor bulbi (the muscle retracting the eye in the orbit, allowing the passive displacement of the nictitating membrane in mammals) are peculiar in the sense that they are devoid of a stretch reflex (they have no proprioceptors). As a consequence, motoneurons receive no signal indicating the position of the lids on the eye [39]. Finally, these muscles have a constant mass (no extra weights on them), and their innervating motoneurons have no axon collaterals and control eyelid velocity only during reflexively evoked blinks [39]. Although the recording of nictitating membrane responses has provided valuable information about the biomechanics of eyeblink conditioning, it has been the use of the search coil in a magnetic field technique that has allowed a quantitative study of reflex and conditioned eyelid responses in humans [40], cats [41], and rabbits [42]. Recently, the magnetic distance measurement technique has enabled similar studies in the small eyelid of behaving mice [43]. Those quantitative studies of eyeblink kinematics have allowed the determination of the main sequence of eyelid responses [40�] and of their oscillatory properties. The latter are dependent on eyelid mass and compliance [43] and are nicely tuned to the firing properties of facial motoneurons [39]. It should be stressed that a proper understanding of eyelid kinematics and of the firing properties of innervating facial and accessory abducens motoneurons is necessary to understand how acquired eyeblinks are generated and the functional possibilities offered by this motor system for the acquisition of new motor responses [44]. Another important requisite for understanding the organization of the eyelid motor system is knowing the location of the neural premotor system controlling spontaneous, reflex, and acquired eyelid responses. This was achieved recently using attenuated rabies virus injected as a transneuronal retrograde tracer in the orbicularis oculi muscle of the adult rat [45]. As expected, many brainstem, cerebellar, and cerebral cortex structures mediating reflex, voluntary, and limbic related eyelid responses were labeled, indicating the neuronal complexity of this apparently simple motor system.

While a large number of neural regions are implicated in various aspects of eyelid responses, the cerebellum has been the primary focus in the study of eyeblink conditioning. Indeed, hundreds of research studies and reviews have been devoted to determining the involvement of cerebellar structures in the acquisition and storage of this type of associative learning [46�]. In an influential series of studies, Thompson’s group has popularized a basic brainstem�rebellar circuit certainly involved in the generation and control of classically conditioned eyelid responses [46, 49] that is not completely in agreement with anatomical [45], kinematic [41], and electrophysiological and pharmacological [50, 51] findings. For example, the precise latency analysis (using both delay and trace conditioning paradigms) of identified cerebellar interpositus neurons indicates that they start firing after the beginning of the eyelid conditioned response [50]. Moreover, it is still under discussion whether cerebellar structures are involved in learning (i.e., in the acquisition and storage of newly acquired eyelid responses) or in the proper performance of eyelid responses independently of their reflex or acquired nature [51�]. As illustrated in Fig. 2 , learning and performance of conditioned eyeblinks can easily be differentiated in alert behaving cats [51]. Recently, it has been proposed [55] that the cerebellar output represented by the activity of interpositus neurons plays a modulating role in the dynamic control of eyeblink learned responses, i.e., they could be considered a phase-modulating device helping to reinforce, as well as to damp, the oscillatory properties of facial motoneurons ( Fig. 3 ).

Effects of muscimol injection in, and microstimulation of, the posterior interpositus nucleus on the percentage and amplitude of conditioned eyelid responses (CRs) collected from alert behaving cats. a Diagram illustrating the experimental design. Animals were implanted with electromyographic recording electrodes in the orbicularis oculi muscle (O.O. EMG) and with a chronic guide cannula in the posterior interpositus nucleus (PIN) allowing neuronal recording (Rec), microstimulation (St), and microinjection (Inj). Animals were also implanted with stimulating electrodes in selected brain sites for antidromic identification of recorded facial motoneurons and posterior interpositus neurons [46, 50]. Delayed eyeblink conditioning was achieved by the paired presentation of a 370-ms tone used as a conditioned stimulus (CS), followed 270 ms from its start by a 100-ms air puff as an unconditioned stimulus (US). b Representative examples of CRs evoked by the sole CS presentation, collected from the fourth, fifth, and seventh conditioning sessions. Muscimol (a GABAA agonist, 1.25 μg/kg) was injected 20 min before the fifth session. The double-arrowed line (a) indicates CR amplitude. c Quantitative analysis of data collected from three animals (mean ± SEM). Muscimol was injected before the fifth and sixth sessions. Note that, according to the selected CR criterion [dashed blue line in b], the expected percentage of CRs (blue circles and dotted line) was not modified by muscimol, but the amplitude of the evoked CRs (red circles and dashed line) was significantly decreased (***pπ.001 ANOVA). d Representative examples of CRs evoked by single CS presentations without (fourth and seventh sessions) and with (fifth session) microstimulation (20 Hz for 1 s pulses of 50 μs and 50 㯊) of the posterior interpositus nucleus. e Quantitative analysis of data collected from three animals (mean ± SEM). Microstimulation was applied during the fifth and sixth sessions in trials in which the CS was presented alone. Note that, according to the selected CR criterion, the expected percentage of CRs (blue circles and dotted line) was not modified by the microstimulation, but the amplitude of the evoked CRs (green circles and dashed line) was significantly increased (**p< 0.01 ANOVA). Data collected from [46]. Figure reproduced with permission from [39]

Schematic representation of the reinforcing–modulating role of cerebellar interpositus neurons (IP n) during the acquisition of an associative learning task such as the classical eyeblink conditioning. This representation is based on data published elsewhere [23]. The experimental design is illustrated in Fig. 2 . Neuronal inputs (green set of premotor nuclei) arriving at the orbicularis oculi motoneurons (OO MNs) and carrying eyeblink conditioned signals p(t) need the reinforcing–modulating role of cerebellar nuclei signals m(t). In order to be efficient, IP neuronal signals need to go through a learning process in order to become 180° out-of-phase with OO MN firing. Thus, IP neuronal activities (following a relay in the red nucleus) reach OO MNs right at the moment of maximum motoneuronal hyperpolarization [34], and IP neurons facilitate a quick repolarization of OO MNs, reinforcing their tonic firing during the performance of those classically conditioned eyelid responses. Abbreviation: VIIn facial nucleus. Figure reproduced with permission from [50]

Even if the debate about the contribution of cerebellar circuits to the acquisition of new eyelid responses remains open for a while, we should keep in mind that many other brain structures, such as the hippocampus [44] or the amygdala [56], are also involved in this type of associative learning, and that, surprisingly, only a few studies have been devoted to the most important center for the generation of voluntary and acquired movements namely, the motor cortex [57].


What Does the Frontal Lobe Do?

The frontal lobe is the slowest part of the brain to mature, continuing to create and prune neural connections until a person's mid-twenties. This means that brain damage early in life renders the frontal lobe particularly vulnerable, potentially affecting behavior and cognition forever.

The frontal lobe is involved in a wide range of “higher” cognitive functions. Although all mammals have a frontal lobe, highly social mammals, such as dolphins and primates, tend to have more developed frontal lobes. This suggests that our social interactions may play a key role in the development of intelligence, and that the brain must devote significant resources to responding to the demands of social interactions. Humans have larger and more developed frontal lobes than any other animal.

Some of the many functions of the frontal lobe include:

  • Coordinating voluntary movements, such as walking and reaching for objects. The frontal lobe is home to the primary motor cortex.
  • Assessing future consequences of current actions. Thus the frontal lobe plays a vital role in impulse control, including decisions about when to spend money and eat, and whether a particular decision is morally or socially acceptable.
  • Assessing similarities and differences between two objects.
  • Formation and retention of long-term memories, particularly emotional memories derived from the limbic system.
  • Language: The frontal lobe plays a role in understanding language, linguistic memories, and speaking.
  • Emotional expression and regulation, in addition to understanding the emotions of others empathy may derive from the frontal lobe.
  • The development of personality. Because of the frontal lobe's roles in memory, emotional regulation, expression, impulse control, and other key functions, it plays a key role in personality. Damage to the frontal lobe can spur sudden and immediate alterations in personality.
  • Managing reward. Dopamine, a neurotransmitter that plays a role in reward and motivation, is heavily active in the frontal lobe because most of the brain's dopamine-sensitive neurons located here.
  • Attention regulation, including selective attention. Frontal lobe difficulties can lead to executive functioning issues, as well as disorders such as ADHD.


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