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29 Cards in this Set
- Front
- Back
Most obvious structures of the basal ganglia
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Caudate nucleus, Putamen and Globus pallidus
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Main fxn of basal nuclei
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initiation and control of voluntary movement
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Name the 4 structures of the basal ganglia (two of them have components to them) that help basal nuclei carry out their integrative fxns
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• Striatum - Caudate nucleus, putamen, ventral striatum
• Globus Pallidus - External/lateral part and Internal/medial part • Subthalmic nucleus • Substanti nigra - Pars reticulata and Pars compacta |
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The Basal Ganglia have Direct and Indirect motor loops. Describe 4 common features they share.
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• Corticalstriatal fibers (Fibers projecting from the cortex to the striatum) will excite striatal neruons with Glu.
• Fibers from the Substantia nigra will either excite/inhibit Striatal cells through dopamine release • The substantia nigra receives inhibitory GABAergic input from the striatum • GABAergic output from the from the GPi inhibts cells of the ventral (anterior + posterior) thalamic nuclei • Thalamic cells excite the motor cortex through the release of Glu |
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The Direct Basal Ganglia motor Loop:
• The over goal of the pathway • Describe the Direct Basal Ganglia Motor Loop. Remember that the pathway features these areas: • The Cortex • Substantia nigra • Neostriatum • Medial/Internal Globus pallidus • Thalamus |
• Increase cortical activity and facilitate movement
• The Direct Motor Loop - Cortex and the Striatum excite the Neostriatum > The cortex releases Glu > The Substatia nigra releases dopamine which binds to D1 excitatory receptors - The Neostriatum releases the neurotransmitter, GABA, which inhibits GPi - GPi normally inhibits the Thalamus however, since it is now inhibited by the Neostriatum, the Thalamus is free to excite the cortex |
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Indirect Basal Ganglia Motor Loop:
• The overall goal of the pathway • Describe the Indirect Basal Ganglia Motor Loop. Remember that the pathway features these areas: - Substantia nigra - Cortex - Lateral/External & Medial/Internal Globus pallidus - Subthalamic nucleus - Thalamus |
• The goal is to decrease cortical activity and diminish movement
• The Indirect Motor Loop - The Cortex and Substantia nigra influence the activity of the Neostriatum to ultimatley secrete GABA > The cortex excites it with Glu > The Substantia nigra inhibits it the dopamine binding to D2 receptors - GABA secreted from the Neostriatum inhibits the GPe - The fxn of the GPe is to inhibit the subthalmic nucleus via its own GABA secretion however, since it is inhibited by the Neostriatum, the subthalamic nucleus is free to excite GPi via Glu. - GPi is stimulated to releases GABA which inhibits Thalamic fxn. The Thalamus fxns to excite the cortex, however it cannot because of GABA inhibition. |
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Parkinson's Disease
• Features this level of movement • Pathological description |
• Features hypokinesis
• Diminished release of striatal dopamine, secondary to degeneration of the dopaminergic nigrostriatal tract |
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Describe the Basal Ganglia motor loop in Parkinson's
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• Degeneration of the Substantia nigra pars compact leads to diminished levels of dopamine release
• This has two effects on the Neostriatum - Excitatory D1 receptors do not bind dopamine. GABA is not released and GPi is not inhibited - Inhibitory D2 receptors do not bind dopamine. GABA is released and GPe is inhibited • GPi is allowed to release GABA via the direct and indirect basal gangliar pathways - Because GPe is inhibited in the indirect pathway, the subthalamic nucleus is permitted to release Glu and excite GPi - GPi is excited by way of the direct pathway since it is not inhibited by the Neostriatum • Because it is excited, GPi releases GABA which inhibits the ventral lateral and anterior thalamic nuclei • the frontal cortex is not stimulated (decrease in cortical activity) and hypokinesis results |
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Other than genetic and idiopathic origins, name 5 other causes behind Parkinsonism
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• Drug-induced
• Vascular • Dementia pugilistica • Postencephalitic • Neoplastic |
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Three modes of drug-induced Parkinsonism
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• Blocking D2 receptors --> diminishes the dopamine-mediated inhibition of striatal neurons --> hypokinesia
• Depletion of dopamine stores within nerve endings affects the release of dopamine in the niagrastriatal pathway • A metabolite of the neuortoxin MPTP damages niagral mitochondria |
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Artery that supplies the Substantia nigra
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Posterior cerebral artery
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Dementia Pugilistica
• categorized as this type of a disease • cause |
• midbrain disease
• traumatically induced acceleration to the forebrain (e.g. blows o the head) causes the midbrain to flex , tearing small mesencephalic blood vessels and shearing axons |
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Huntington's Disease
• Features this level of movement • These muscles are often affected early * These components of the brain degenerate * Hallmark feature of ventricles • Pathology • The net effect on the Basal Ganglia Motor Pathway |
• Hyperkinesia
• Facial/oral muscles followed by the hands • Bilateral degeneration of D2-expressing striatal-pallidal neurons, ultimately affecting the indirect pathway * Striatal cells, efferent tracts and frontal cortices * Lateral ventricles enlarge, called "boxcar ventricles" • Increased thalamic output, increased cortical activity --> hyperkinesis |
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Discuss the Basal Ganglia Motor Loop in Huntington's Disease
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• Although the Substantia nigra is intact and releases dopamine at appropriate levels, it is the D2-expressing striatal-pallidal neurons that are degenerating and as a result GABA is not secreted by these cells
• The GPe is not inhibited and is free to release its own GABA to inhibit the Subthalamic nucleus. • The subthalamic nucleus does not excite the GPi via this indirect pathway and GPi is further inhibited via the direct pathway from the GABA secretions of the Neostriatum • The VA & VL thalamic nuclei are not inhibited by the GPi and is free to activate the Frontal lobe, unregulated --> hyperkinesia |
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Sydenham Disease
• is this type of a d/o • occurs after recovery from this sickness • Features these type of movements • State of the basal ganglia |
• Autoimmune d/o
• rheumatic fever • features choreoform movements • basal ganglia is inflammed |
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These two drugs can can induce chorea
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L-dopa and anti-convulsants
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Athetosis
• description of movements • these areas of the brain are often injured |
• slow, continuous writhing movements
• striatum or thalamus * can overlap w/ other movements |
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Hemiballismus
• Type of movements involved • most common cause • This part of the basal ganglia motor pathway is affected • This area of the brain typically decreases its excitatory output, ultimately resulting |
• flinging movements of the arm and/or rotational movements of the leg
• unilateral stroke-related injury to the subthalamus • Indirect pathway • GPi |
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Describe the how the Basal Ganglia Motor Pathway is affected in Hemiballismus
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• In a normal pathway, the Neostriatum inhibits GPe which allows the Subthalamic nucleus to excite GPi
• However because the Subthalamic nucleus is damaged, GPi is understimulated as it is alos being inhibited by the Neostriatum. •This leaves the VA & VL Thalamic nuclei to increases cortical activity |
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Parkinson's Disease
• Name two types of cells that degenerate and are associated with this d/o. Include the location of where the cells would be found |
• Dopaminergic cells in the substantia nigra, Catecholaminergic cells in the pontine locus ceruleus or even peripherally in the heart
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Two front-line therapy drug for Parkinson's and their mechanism of action
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L-dopa: a precursor to dopamine, helps increase its synthesis in the remaining cells of the Substantia nigra
Carbidopa: A peripheral decarboxylase inhibitor, reducing the metabolism of L-dopa |
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Anticholinergics can be used in the tx of Parkinson's. Name the general category of drugs used in tx and their mechanism of action.
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• Muscarinic antagonists
• Because ACh can excite D2 receptors on the Neostriatum, these antigonists can inhibit the fxn of he neostriatal cells and ultimately decrease output from the GPi, leaving the thalamus free to excite the cortex |
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In the tx of Parkinson's, these receptors are often targets in the Basal Ganglia motor loop
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D1 and D2 receptors of the Neostriatum
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Another form of tx in Parkinson's is to target/inhibit Dopamine metabolism. Name two enzymes usually targeted.
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MAO-B and COMT
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Anticholinergics can be used in the tx of Parkinson's. Name the general category of drugs used in tx and their mechanism of action.
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• Muscarinic antagonists
• Because ACh can excite D2 receptors on the Neostriatum, these antigonists can inhibit the fxn of he neostriatal cells and ultimately decrease output from the GPi, leaving the thalamus free to excite the cortex |
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Two surgically ablative areas in the tx for Parkinson's
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* Subthalamic nucleus
- This reduces the excitatory input to the GPi via the indirect pathway. The thalamus is not as inhibited by GPi secreted GABA and can excite the cortex * GPi - This reduces the inhibitoryinput to the thalamus and the cortex can be excited |
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High frequency electrical stimulation of these areas has been shown to benefit patients w/ Parkinson's (3)
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Thalamus, Globus pallidus and Subthalamus
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Two categories of drugs in the tx of Huntington's
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Antidepressants, Anti-chorea drugs
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Antichorea drugs
* mechanism of action * Overall goal of these drugs |
* D2 receptor antagonists increase GABA output from the striatum to the GPi
* Decrease thalamic-dependent excitation of the cortex and ultimately reduce choreic activity |