Divyan Bavan
The control of movement is one of the most sophisticated processes in the brain. Although many areas help coordinate this process, two in particular stand out: the cerebellum and basal ganglia. These structures play crucial, but separate, roles in the control of voluntary movement. While the cerebellum is primarily involved in error correction and feedforward corrections, the basal ganglia are mostly insinuated with the initiation of movement. These differences can be seen through the circuits that these areas form; inhibitory and excitatory inputs shape the roles that these areas play in the brain. These roles can also be discerned by observing the effects of diseases. Thus, understanding the differences between these areas is critical for understanding the coordination of movement.
Initiation versus Control
When looking at the basal ganglia and cerebellum, there is an obvious dissociation in their roles: initiation versus control of movement. The basal ganglia form a network that is concerned with gating movement; the cerebellum uses mismatches in sensory and cortical input to correct errors. Looking at the similarities and differences between these two processes enables a more nuanced understanding of movement.
The basal ganglia have two pathways: direct and indirect. The direct pathway starts off in the striatum. This area of the brain receives cortical input to its medium spiny neurons (MSNs). These neurons are GABAergic and inhibit the GPi/SNr. Inhibition of these centres leads to reduced inhibition of the thalamus. This leads to the excitation of the cortex and the initiation of movement. In the indirect pathway, inhibitory input to GPe from the striatum leads to reduced inhibition of the STN. This causes excitation of the GPi/SNr, leading to the inhibition of movement. Therefore, these two pathways oppose each other. To modulate both, dopaminergic input from the SNc causes inhibition and excitation of the indirect and direct pathways, respectively. This is due to the expression of D1 receptors on direct MSNs, versus D2 expression on indirect MSNs. Thus, dopamine release leads to the initiation of movement.
Once movement has been initiated through the basal ganglia, the cerebellum modifies it. This is through the process of error correction. Like the basal ganglia, the cerebellum receives input from the motor cortex. This is through mossy fibres, granule cells, and eventually, parallel fibres. These parallel fibres synapse onto Purkinje cells, the most important cell in the cerebellar cortex. Purkinje cells provide GABAergic input to the deep cerebellar nuclei—the primary output centre of the cerebellum. To correct for errors, it is important to have sensory input as well. This enables a comparison to be made between the motor plan and the execution. Sensory afferents reach the Purkinje cells through the climbing fibres. These fibres form multiple contacts with the Purkinje cells, enabling a large EPSP when an action potential occurs. This leads to a complex spike in the Purkinje cell. When this spike occurs simultaneously with input from the parallel fibre, a process called long term depression (LTD) occurs. This calcium-mediated process leads to inhibition of the Purkinje-parallel fibre synapse, reducing its input. Since Purkinje cells are inhibitory and parallel fibres are excitatory, this leads to reduced inhibition of the deep cerebellar nuclei. The result of this is input to the motor cortex, correcting for errors.
Diseases Affecting the Cerebellum and Basal Ganglia
Another way to elucidate the differences between the basal ganglia and cerebellum is through observing diseases which affect them. This gives an understanding for what gap exists when one area functions while the other doesn’t.
A disease which affects the basal ganglia is Parkinson’s Disease (PD). PD is caused by the degeneration of dopaminergic neurons in the SNc. It is marked by reduced pigmentation in this area. The result of this degeneration is difficulty initiating movement. As mentioned previously, dopamine is responsible for exciting the direct pathway and inhibiting the indirect pathway. When dopamine is not present, this causes the indirect pathway to dominate and movement to be inhibited. When L-DOPA, a precursor to dopamine is given to these patients, movement can be restored. This shows how the basal ganglia are critical for movement initiation.
On the other hand, patients with cerebellar ataxia often don’t have issues initiating movement. Instead, they often show signs of clumsiness and discoordination. This is due to issues in the cerebellum causing improper error correction. This illustrates how the cerebellum is key in this process.
Conclusion
By looking at how the cerebellum and basal ganglia control movement, it becomes evident that both play key, but separate roles in this process. The basal ganglia are more concerned with initiating movement. This is done through a defined circuit which uses two pathways to control whether movement is initiated or inhibited. In contrast, the cerebellum is more concerned with correct errors during movement. This is done through LTD, a process which is coordinated by inputs from parallel and climbing fibres to the Purkinje cells. Although looking at these circuits gives a mechanistic explanation for these differences, diseases can also help elucidate them. For example, PD leads to difficulty in initiating movement, a result of damage to the SNc. On the other hand, cerebellar ataxia leads to issues in correcting errors, presenting as clumsiness in the patient. These are just some examples of how these structures influence voluntary movement. It is critical that we continue to explore these differences to better understand how we can treat diseases that come out of their malfunction.