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24 Cards in this Set
- Front
- Back
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Basal ganglia
1. what are they? 2. what the two divisions? |
1. gray matter nuclei deep to cerebral cortex
2.-Striatum (input/neostriatum): caudate, putamen, n. accumbens -Pallidum (output/paleostriatum): globus pallidus externa and interna, substantia nigra |
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Substantia Nigra
1. what is it? 2. what are its two parts, are they ventral/dorsal, what do they do? |
1. nucleus of the upper mesencephalon (midbrain)
2. -pars reticulata (ventral): connects to GPi -pars compacta (dorsal): makes dopamine |
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Input to and Output of Basal Ganglia
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wide spread areas of cerebral cortex > striatum > pallidum > thalamic nuclei > (back to) cerebral cortex
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4 functional circuits of the basal ganglia
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1. sensory-motor
2. occulomotor 3. association 4. limbic |
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Closed vs. Open Circuits
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Closed: begins w/ input from single appropriate cortical area (initiating circuit)
Open: basal input from other cortical areas that modify closed circuit input (modifying circuit) |
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Thalamic Inputs
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all inputs (ex: ascendding reticular activiating system-ARAS) to thalamus, Gpi, and SNpr are excitatory giving these structures intrinsic rhythmycity
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1. basal ganglia input is...and uses...as a neurotransmitter
2. basal ganglia output is...uses... 3. function....regulate overall actions of basal ganglia |
1. excitatory; glutamate
2. inhibitory; GABA 3. b/n corticalstriatal input and pallidothalamic output |
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Direct Loop
1. effect on thalamic drive 2. how does that happen? |
1. increases thalamic drive
2. excited striatum inhibits Gpi and SNpr which disinhibits the thalmus |
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Indirect Loop
1. effect on thalamic drive 2. how does that happen? |
1. decreases thalamic drive
2. excited striatum inhibits GPe, disinhibitng subthalamus, which can now excite GPi and SNpr that send inhibitory signals to thalamus |
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Dopamine
1. what makes it? 2. what are the most important subtypes 3. what effect does it have on thalamic drive |
1. neurons in the pars compacta of the substantia nigra
2. DA1 (excitatory) and DA2 (inhibitory) 3. always increases |
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Relationship b/n dopamine, direct loop, and thalamic drive
-how does this happen? |
Dopamine enhances thalamic drive by exciting the direct loop
-dopamine binds DA1 exciting striatum which inhibits GPi/SNpr, disinhibiting thalamus |
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Relationship b/n dopamine, indirect loop, and thalamic drive
-how does this happen |
Dopamine enhances thalamic drive by inhibition of the indirect loop
-dopamine binds DA2 which inhibits sriatum, disinhibiting GPe, allowing the inhibition of the subthalamus, preventing activation of GPe/SNpr, so no inhibitory signals sent to thalamus |
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Sensory-Motor circuits
1. influences... 2. carries out... 3. example 4. open circuit 5. closed circuit |
1. UMNs in frontal lobe
2. learned motor activities 3. picking up a pen 4. S1, M1 > putamen 5. supplementary motor cortex (SMA) > putamen > pallidum > thalmus > SMA |
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Oculomotor circuit
1. controls 2. open circuit 3. closed circuit |
1. volluntary (saccadic) eye movements to contralateral side
2. prefrontal cortex, posterior parietal cortex > caudate body 3. frontal eye field > caudate > GPi, SNpr > VAmc, DM thalamus > FEF |
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Association circuit
1. involved in... 2. example 3. open circuit 4. closed circuit |
1. planning, directionality, and force of new/modified movements
2. chess move 3. premotor cortex, posterior parietal cortex > caudate head 4. prefrontal cortex > caudate head> GPi, SNpr > VApc, DM thalamus > prefrontal cortex |
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Limbic Circuit
1. involved in.. 2. open circuit 3. closed circuit |
1. emotional posturing (changes of facial expression and body posture)
2. temporal lobe, hippocampus, amygdala, entorhinal cortex > caudate, n. accumbens 3. ant cing gyrus, orbitofronal cortex > caudate, n. accumbens > GPi, SNpr > VA, DM thalmus > ant cing gyrus, orbitofrontal cortex |
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Dyskinesia
1. what is it? 2. what are the two types? |
1. difficulty controlling voluntary movements in absence of paralysis, paresis, or apraxis
2. -hyperkinesia (spontaneous movement CAN'T be controlled) -hypokinesia (decreased movements with muscular ability intact) |
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5 types of hyperkinesia
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chorea, athetosis, dystonia, ballismus, tic
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chorea
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spontaneous rapid RANDOM movements
-hyperkinesia -huntington's -damage to head of caudate nucleus -indirect pathway/DA2 receptors not activated |
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athetosis
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writing combination of movements (usually in hands in feet)
-hyperkinesia |
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dystonia
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joint or postural freezing due to coactivation of antagonist muscles
-hyperkinesia -spasmodic torticollis |
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ballismus
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rapid flailing movements of the extremities
-hyperkinesia -subthalamic degeneration |
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tic
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spontaneous repeated single movements (NOT random)
-hyperkinesia -Tourette's |
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Parkinson's disease
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Hypokinesia
-loss of substantia nigra pars compacta -lack of dopamine causes decreased thalamic drive |
