What Is The Function Of The Basal Nuclei – The basal ganglia is a subcortical collection of interconnected clusters of cell bodies involved in reward, emotional, and motor circuits. The basal ganglia are central to all brain processing necessary to perform voluntary movement, as they regulate the activity of the motor areas of the cortex. Despite its study, the motor circuitry of the basal ganglia is difficult to understand for many people, especially undergraduates and graduate students. This review article attempts to explain the workings of this circuit in a simple and objective approach, exploring its functional anatomy, neurochemistry, neural pathways, associated diseases, and interactions with other brain regions to coordinate voluntary movement.

Movement is an essential ability to sustain life. Even less complex organisms such as bacteria must move in search of nutrients and ensure their survival (Lodish et al., 2021). In humans, locomotion goes beyond locomotion to include a number of important aspects such as object manipulation, verbal communication, feeding, and vision, as we need eye movements to locate and focus on whatever is the target of our attention. maintain visual focus (Hirs. et al., 2020). Voluntary movement is prepared and initiated in the motor cortex; such preparation mainly involves corticospinal projections, while the initiation of motor action consists of corticospinal projections (Economo et al., 2018). The axons of neurons originating in the motor cortex travel through the spinal cord and make synapses on the motor neurons that innervate the muscle tissue to achieve the desired movement (Jackson, 2018).

What Is The Function Of The Basal Nuclei

Other areas of the brain, such as the cerebellum and basal ganglia, work together with the motor cortex to ensure precise movements. These two structures regulate motor actions through neuronal circuits known as locomotor loops because they regulate movement by regulating the activity of upper motor neurons and do not synapse directly with lower motor neurons (Purves et al., 2017). The brain, despite its much smaller size than the cortex, has a high density of neurons, with 69 of the 86 billion nerve cells forming the encephalon, which is about 80% of the total (Azevedo et al., 2009). From a motor point of view, this huge density in the cerebellum is related to its participation in various afferent and efferent pathways. It receives information about body position and movement through the spinal cord and sends it to the motor cortex and descending motor system, thus responsible for maintaining posture, balance, movement correction, and motor learning (Damiani et al., 2016). For these reasons, the brain is the area of ​​the brain where the planned movement is compared with the executed movement, thereby providing feedback so that the individual can succeed in his future motor actions if the previous movement was not correct (Bear et al. al., 2020).

Basal Ganglia And Hippocampus

The basal ganglia are a subcortical cluster of interconnected cell bodies that communicate with each other through circuits that mainly regulate motor (Parent, 2012), but are also involved in the coordination of behavioral and emotional functions (Lanciego et al., 2012). Because of its significant contribution to motor control pathways, some movement disorders such as Parkinson’s disease, dystonia, and dyskinesias are caused by basal ganglia disorders (Wichman and Dostrovsky, 2011). Although widely studied, the motor pathways of the basal ganglia are complex and difficult to understand for didactic purposes. Therefore, the purpose of this review is to provide a simplified and simplified version for undergraduate and graduate students who wish to contact the topic of the basal ganglia and its role in the control of movement by describing the functional anatomy and neurochemical factors.

According to Steiner and Tseng (2016), the canonical structures that integrate the basal ganglia are: the striatum, which in primates is divided into three structures known as the caudate nucleus, the putamen, which forms the dorsal region of the striatum, and the nucleus accumbens, which they correspond to it. ventral part of the striatum. Other parts are the globus pallidus externus (GPe), the globus pallidus internus (GPi), the subthalamic nucleus (STN), which is part of the diencephalon, and the substantia nigra (SN), which is divided into pars compacta (SNc) and pars reticulata. (SNr), which are part of the midbrain (Fig. 1A). Regarding the projections, the basal ganglia are divided into afferent, efferent and internal nuclei. Afferent nuclei are the regions where information is received. The caudate nucleus and putamen receive corticostriatal input related to the motor pathway and the nucleus ​​​​​​​​​​​from the emotional and reward pathways (Martin, 2012). Efferent nuclei are responsible for transmission to other areas of the brain and include the GPi and SNr. The intrinsic nuclei are involved in circuits between components of the basal ganglia, and it consists of the GPe, STN, and SNc (Lanciego et al., 2012; Figure 1B). To understand how these cores work together, it is important to understand each one individually.

Figure 1. (A) Coronal section of the brain showing structures that are part of the basal ganglia and motor cortex (Created at biorender.com). (B) Afferent, intrinsic and efferent nuclei of the basal ganglia. Globus pallidus externus (GPe), globus pallidus internus (GPi), substantia nigra (SNc) and substantia nigra (SNr). (C) Immediately after dopamine binds to the D1 receptor, the α subunit of the Gs protein moves to adenylate cyclase, stimulating this enzyme to produce more cAMP. Elevated cAMP levels activate PKA, which phosphorylates L-type calcium channels and potassium channels, phosphorylation activates calcium channels and inhibits potassium channels, making the neuron more sensitive to depolarization. (D) Upon D2 receptor activation, the α subunit of the Gi protein moves to adenylate cyclase, inhibiting this enzyme to generate cAMP. Low levels of cAMP inactivates PKA, thereby dephosphorylating L-type calcium channels and potassium channels, making the neuron less sensitive to depolarization. It can also be seen that a second pathway is activated by the D2 receptor. PLC catalyzes the hydrolysis of PIP2 to DAG and IP3, DAG activates PKC, and IP3 causes an increase in cytosolic Ca

Causes activation of calcineurin, which in turn activates other protein kinases that suppress L-type activity.

Neuronal Oscillations In The Basal Ganglia And Movement Disorders: Evidence From Whole Animal And Human Recordings

The striatum consists mainly of GABAergic (aminobutyric acid) projection neurons, known as medium-sized neurons because of the large number of spines on their dendrites. These cells also produce and release some neuropeptides, such as enkephalin, substance P and dynorphin (Fazl and Fleisher, 2018), which increase the inhibitory action of GABA. In the striatum, there are less interneurons that contain GABA, acetylcholine, somatostatin, nitric oxide, and neuropeptide Y as neurotransmitters. Striatal interneurons act mainly by modulating medium-sized interneurons, determining whether they are activated or not (Kawaguchi, 199). ; Asus and Tepper, 2019).

The striatum is the main area for input to the basal ganglia, which receives several projections from the cortex, thalamus, and brainstem. Cortico-striatal projections exert a greater influence on the striatum via glutamatergic synapses, they are mainly excitatory. Another structure that contributes to glutamatergic input to the striatum is the thalamus, but it does not influence striatal activity in the same way as cortical inputs. The pedunculopontine nucleus and the dorsolateral tegmentum pontinum are structures in the brainstem and provide cholinergic projections to both striatal interneurons and interneurons, however, their functions are not yet fully understood. In addition, the midbrain sends large dopaminergic outputs to the striatum (Silberberg and Bolam, 2015). Dopaminergic signaling is essential for basal ganglia motor circuitry. Thus, among the intermediate dopaminergic nuclei, the SN plays a key role in this pathway, as one of its units, the SNc, is directly connected to the striatum in a pathway called the nigrostriatal pathway (Rice et al., 2011; Norrara et al., 2018). ; Rocha et al., 2022).

When it receives large amounts of dopaminergic input, the striatum has a high density of dopamine receptors. Dopamine receptors are divided into D

Species that are metabotropic and have a modulatory effect on neuronal activity. Both types of receptors are coupled to G proteins (GPCRs) and trigger a response through an intracellular signaling cascade. It activates or inhibits key proteins in specific pathways that affect the rate of neuronal depolarization (Tritch and Sabatini, 2012; Steiner and Tseng, 2016).

The Expanding Universe Of Disorders Of The Basal Ganglia

Agonists bind, displacing α subunits from G protein to the enzyme adenylyl cyclase, causing its activation. It then catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). An increase in the intracellular concentration of cAMP leads to the activation of protein kinase A (PKA), which phosphorylates other proteins, including some ion channels, and changes the kinetics of their opening. As a result, PKA promotes the opening of calcium channels (Ca

Receptors leads to a phosphorylation cascade that increases the activity of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) (Xue et al., 2017) and N-methyl-d-aspartate (NMDA) receptors ( Hallett, 2006) and therefore enhances the excitatory responses of glutamatergic projections from the cortex (Figure 1C).

A protein that inhibits the activity of adenylyl cyclase. Because of this, the intracellular accumulation of cAMP is disrupted. Therefore, there is no PKA activation, which cannot trigger a phosphorylation cascade that makes the neuron more prone to depolarization (Neve et al., 2004; Beaulieu and Gainetdinov, 2011). In addition to this way, there is a second way

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