Nolte Chapter 19: Basal Ganglia

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Nolte Chapter 19: Basal Ganglia

The putamen, caudate, and nucleus accumbens are all referred to as the straitum. Their main cell types are the medium spiny neurons. The putamen and globus pallidus are referred to as the lenticular nucleus.

The putamen is coextensive with the insula, which is where the telencephalon and diencephalon first meet during development.

The putamen is sperated from the globus pallidus by the lateral medullary lamina.

The globus pallidus has an internal and external segment which is divided by a medial medullary lamina

The caudate tail is continuous with the amygdala, which, in turn, is continuous with the putamen.

The substantia nigra has two parts: compact, with closely packed pigmented neurons and the reticular part that is more loosely packed and nonpigmented. The compact is what sends dopaminergic projection and the reticular part serves as an output nuclei.

Globus Pallidus internal and Substantia nigra internal are the two output centers of the basal ganglia. Outputs are GABA(inhibitory).

Projections from the cerebral cortex reach the striatum and subthalamic nucleus. Inputs are glutamate.

Somatosensory and motor areas project to the putamen, mainly. This in turn projects by way of GPi to the VA/VL thalamic nuclei.

The only prominent source of excitatory (glutamate) projections is the subthalamic nucleus.

Putamen – Somatosensory and motor. Neurons fire in conjunction with particular movements or positions.

Caudate – association areas (primarily prefrontal). Associated with cognitive functions.

Ventral Striatum – limbic, hippocampus, and amygdala. Associated with drive-related behaviors.

Ventral Tegmental Area (VTA) projects to all areas of the stratium. As does the SNc. They both use dopamine and the VTA makes up the nigrostriatal pathway.

Intralmainar nuclei also project to the stratium.

GPe received inhibitory inputs from the striatum and excitatory inputs from the subthalamic nucleus.

GPi and SNr receive inhibitory inputs from the straitum and excitatory inputs from the STN. Also receive inputs from GPe.

This system projects mainly to the thalamus by way of:

The lenticular fasciuculs runs through the internal capsule and then passes medially as a sheet of fibers between the STN and zona inverta.

the ansa lenticularis loops aroung the medial edge of the internal capsule and joins the lenticular dfasciculus and GABAergic fibers from the SNr in the thalamic fasciculus.

Fibers from caudate go to the dorsomedial nuecleus to get back to prefrontal.

Fibers related to movement go to VA/VL

Efferents from GPi and SNr have a branch that descends to midbrain to the peduncolopontine nucleus. Another branchs reaches the superior colliculus and the habenula.

The globus pallidus and the STN are connected by the subthalamic fasciculus.

SNr receives inputs from striatum, GPe and STN. It projected to the VA/VL and dorsomedial and to the superior colliculus and reticular formation.

The direct pathways operates as a success of inhibitory synapses that leads to the disinhibition of thalamocortical loops. Direct excited movement. Indirect inhibits.

This chart is missing the Cerebral cortex to STN input which is the fastest route from cortex to output nuclei.

Lenticulostraite, a branch of the middle cerebral artery, basically supplies blood.

Chorea is a series of nearly continuous rapid movements of the face, tongue, or limbs.

Huntington’s is a hereditary disorder that is characterized by neuronal damage to the striatum and caudate and causes involuntary choreform movements and alteration of mood or cognitive function. Thought to knock out the D2 receptors(the ones that are inhibitory once they receive dopamine). This would account for the spastic movements.

Dementia- caudate and cortical destruction

chorea- stratium

Athetosis is a slow writhing movement with an inability to keep the affected limb in a fixed position. Thought to be caused by striatum problems.

Hemiballismus is characterized by wild flailing movements and we see it caused by lesions in the STN.

Parkinson’s is characterized by rigidity, slow, and reduced movements, stooped posture, and tremor. The rigidity is cause by an increase tone in all muscles. The resting tremor (pill rolling) shows that there is a diminished voluntary movement that increases during emotional stress.

Dystonia has hand cramping and twistic and is usually a result of corticostriate interruption.

Bradykinesia – slow movements

hypokinesia – few movements

Positive signs – motor neurons fire when they should not

Negative signs – motor neurons cannot easily be made to fire by their owner.

Parkinson’s disease has damage that is most consistently evident in the substantia nigra where we see a degeneration of pigmented nigral cells. L-dopa can help reverse some of the functional abnormalities. Sometimes lesions of the GPi can help relieve the tremor and rigidity and faliling movements.Deep brain stimulation to the SNc can help as well.

Increase in dopamine to straitum – chreiform and athetoid movements

Decrease is parkinsons systems. With a loss of opamine, we get the loss of enhancement of the disinhibition circuit and an enhancement (loss of inhibition) of the brake since SNc goes to straitum, which has deifferent responses to dopamine.

The BG could be working a “center-surround” fashion that releases wanted movements and inhibits unwanted movements.

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