Basal Ganglia

Front 1

role of basal ganglia

Back 1

selectively adaptive. What is the best adaptive way to do the movement wanted. For planning and initiating movement 'Adaptive control of action' . Gets input from the cerebral cortex and output goes to the thalamus back to cortex

Front 2

lesions of basal ganglia

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loss of full voluntary control of movement. from no movement to uncontrollable movement

Front 3

pathway of basal

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inputs from all entire cortical mantle to VaVL thalamic nucleus to primarily the prefrontal/preomotor cortices

Front 4

corpus striatum

Back 4

caudate + putamen

Front 5

pallidum

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globus pallidus internal (GPi) and external (GPe)

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substantia nigra

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SNc (compacta) (dopamine) SNr (reticulata) (extension of GPi)

Front 7

projection of the cortical mantle to the striatum is toptgraphically organized

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creates multiple functional loops running in parallel ; so depending on the behavior these loops may operate separately or concerted

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3 main loops plus one

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Sensorimotor, associative, limbic, plus intralaminar thalamic nuclei sending inputs ot the striatum

Front 9

Sensorimotor loop

Back 9

projects to the putamen from frontal and parietal cortex. operates in fine motor control

Front 10

associative loop

Back 10

projects to the caudate from association cortex and prefrontal cortex. Involved in cognitive functions

Front 11

limbic loop

Back 11

projects to the ventral striatum from the frontal and temporal cortices and is involved in motivated behaviors

Front 12

gluatamate corticostriatal pathway

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in the simple loop causes disinhibtion drive to the thalamus via 2 GABA nneurons in series

Front 13

striatal neurons

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lack spontaneous activity. activated from cerebral cortex output or thalamus

Front 14

pallidal neurons

Back 14

tonically active. therefore tonically inhibiting the thalamus; when striatal is activated, it takes away this inhibition

Front 15

Direct pathway what do the striatal GABA neurons contain?

Back 15

P.dynorphin

Front 16

In the indirect pathway what do the striatal GABA neurons contain?

Back 16

enkephalin

Front 17

direct pathway

Back 17

disinhibiting winning competitors

Front 18

indriect pathway

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increasing inhibitory control over losing competitors

Front 19

medium spiny neuron

Back 19

the main cell type in the striatum. Corticospinal inputs synpases onto the heads of these spines. Dopamine projections synapse on the necks of the same spines causing triadic arrangement

Front 20

triadic arrangement

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convergence of cortical and dopamine input on the medium sping neuron. Which places dopamine in the position to modulate corticostriatal transmission

Front 21

dopamine on D1 receptors

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firing response of the striatal neurons are enhanced

Front 22

dopamine on D2 receptors

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firing response is reduced on the striatal neurons

Front 23

what neuronal cells are GABA firing inhibitory

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striatum, GPi, GPe

Front 24

what neuronal cells are GLut firing excitatory

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cortex, subthalamic nucleus, thalamus to prefrontal/premotor cortex

Front 25

Parkinsons Disease

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associated with loss of dopamine neurons in the midbrain. Can manifest until 80-90r% of projections are deteriorated due to such high resevior in the system. Cause is idiopathic (unknown)

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Parkinsons may results from

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head trauma, viral encephalitis, environmental neurotxins such as methamphetamine, antipyschotic medications which block dopamine receptors

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methamphetamine

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neurotoxin than is toxic to dopamine neurons

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main symptoms of Parkinsons

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hypokinesia
-bradykinesia
-akinesia
-resting tremor
-rigidity
-postural inastability
- cognitive deficits
-paradoxical kinesia

Front 29

hypokinesia

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difficulty in the initiation of movement and lack of spontaneous movements

Front 30

bradykinesia

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slow execution of movements

Front 31

akinesia

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loss ability to perform movement

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hypertonia

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=rigidity , increase in muscle tone, tense

Front 33

cause of tremor and rigidity

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cortical transmission is impoverished. tremeor and rigidity seem to be of cortical orgiin (with excessive drive to A alpha motor nuerons)

Front 34

paradoxical kinesia

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patient overcomes hypokinesia when provided a sufficient enough ammount of sensory stimuli because basal gang is most important or regulating the spontaneous movements rather than sensory evoked movement (so someone can run when they are caught in a fire because it is sensory provoked)

Front 35

treatment for parkinsons

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L-DOPA is a precursor of dopamine. LDOPA can cross the blood brain barrier into the dopmaine neurons and then produce dopamine. Though over time dopamine neurons diminish so more and more LDOPA is needed. The treatment does not stop progression and loses effectiveness (on-off phenomenon) .
Can produce dyskinesia and lead to akinesia

Front 36

dyskinesia

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uncoordinated movement

Front 37

Huntingtons disease

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autonomal dominant genetic disorder. Loss of striatal GABA neurons in the indirect pathway. THe removal of GABA neurons removes the balance between the two pathways and causes a more complete disinhibition of thalamocortical drive.
-removes the abilityof the basal gang to suppress maladaptive motor programs.
- There is a mutation on the short arm of chromosome 4 and codes for the protein huntingtin. This short arm consists of series of CAG trinucleotide repeats. The more repeats the more early on andsevere the disease and this is the polyglutamine tail.

Front 38

huntingtin

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protein that is coded in chromosome 4 and consists of a polyglutamine tail

Front 39

polyglutamine tail

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trinucleotide repeats of CAG that causes an accumulation of the protein in the nucleus boggled up.

Front 40

symptoms of huntingtons

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-hypotonia
-hyperkinesia
-chorea
-mood changes
-dementia

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hypotonia

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decrease in muscle tone

Front 42

hyperkinsia

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over movement stimulation

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chorea

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dance like movements that represent the intrusion of fragments of unwanted motor programs into the normal flow of motor acts