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neuroscience > basal ganglia > Flashcards

basal ganglia Flashcards

1
Q

what is are the primary subdivisions of the striatum and their respective secondary subdivision?

A

primary subdivision: doral striatum ( secondary sub divion = caudate and putamen) and the ventral striatum ( nucleus accumbens )

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2
Q

what is are the primary subdivisions of the globus pallidus and their respective secondary subdivision?

A

1˚: external segment, internal segment ( 2˚: outer and inner portion)

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3
Q

what is are the primary subdivisions of the substantia nigra and their respective secondary subdivision?

A

1˚:pars compacta,

1˚:pars reticulata ( 2˚ pars lateralis)

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4
Q

what is the most common neuron in the basal ganglia and where specifically is it found?

A

the medium spinal stellate neuron and it is found in both the striasome (caudate and putamen) and the matrix

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5
Q

what are the main input structures in the basal ganglia and where do they receive projections from?

A

the striatum: caudate and putamen, and the subthalamic nucleus

they receive direct input from the cerebral cortex

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6
Q

what are the main output structures of the basal ganglia and where do they project to ?

A

the globus palidus : internal segment and the substantia: nigra pars reticulata

they project back to the cerebral cortex via the thalamus

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7
Q

what are e.g.s of intermediate structures that modify the activity of input or output structures?

A

substantia nigra pars compacta and the subthalamic nucleus

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8
Q

Where is dopamine made?

A

in the substantia nigra pars compacta

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9
Q

cognition IS supported by basal ganglia true or false?

A

TRUE

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10
Q

Depending on the receptor type dopamine can be _ ______ or ________

A

a positive influence or negative influence

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11
Q

what does dopamine receptor d1 do?

A

increase adenylate cyclase therefore increasing excitation and turns the brake off ( the thalamus is the brake)

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12
Q

what does dopamine receptor D2 do?

A

it is inhibitory and decreases adenylate cyclase and ramps the brake up ( it is the indirect pathway) ( the thalamus is the brake)

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13
Q

what does releasing the brake in the bicyle analogy mean?

A

disinhibition i.e. excitation as seen in the direct pathway with D1 receptor

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14
Q

the subthalamic nucleus is rich in ______ and therefore ______________ the brake

A

glutamate ( which is excitatory and therefore ramps up the brake) ( the brake is the thalamus )

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15
Q

D1 receptors are always doing what to the thalamus?

A

inhibiting it

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16
Q

what are the 2 motor loops in the basal ganglia?

A

the body movement loop and the oculomotor loop

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17
Q

describe the body movement loop

A

1.starts in the primary , premotor, and somatosensory corticies

  1. putamen
  2. lateral globus pallidus, internal segment,
  3. ventral lateral and ventral anterior nuclei
  4. cortical targets
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18
Q

describe the oculomotor loop

A

1.starts in the posterior parietal lobe and prefrontal cortex
2. goes to the caudate
3. globus pallidus, internal segment, substantia nigra pars reticulata
4 mediodorsal and ventral anterior nuclei
5. cortical targets

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19
Q

what are the nonmotor loops in the basal ganglia?

A

the prefrontal loop and the limbic loop

20
Q

describe the prefrontal loop

A
  1. dorsolateral prefrontal cortex
  2. anterior caudate
  3. globus pallidus internal segment; substantia nigra pars reticulata,
  4. cortical targets
21
Q

decsribe the limbic loop

A
  1. amygdala, hippocampus, orbitofrontal , anterior cingulate, temporal cortex
  2. ventral striatum,
  3. ventral pallidum
  4. mediodorsal nucleus
  5. cortical targets
22
Q

the substantia nigra is very involved in simple movements of the ________ and ________ ________ movements

A

movement of the limbs and visually guided movements

23
Q

the globus palidus is part of the non-motor loops receiving input from and projecting back to the

A

prefrontal areas involved in short term working memory ( the globus palidus also has motor loops)

24
Q

globus palidus works in _________ control tasks? as seen in example with the blocks

A

visuomotor control tasks

25
Q

what 2 other pathways of basal ganglia arise from the libim function areas?

A

the hyperdirect and striosomal area which are cincerned with reward and therefore impact dopamine release

26
Q

which cells are most involved in habit learning in the basal ganglia?

A

TANS ( tonically active neurons which are giant cholernergic interneurons in the striatum which interact with opamineanertic neurons in the substania nigra pars compacta

27
Q

Ach stimulates________ ________?

A

dopamine release

28
Q

whatis the major symptom of basal ganglia damage?

A

dyskinesia

29
Q

what types of dyskinesia are there?

A 
hyperkinetic ( excessive movement) 
and hypokinetic ( reduced movement)
30
Q

what is hyperkinetic disorder related with?

A

abnormally low levels of basal ganglia output which disinhibits i.e. excites the thalamus turning the thalamus off e.g. huntington’s, tics,

31
Q

hyptokinetic disorders are attributed to

A

inhibition of the basal ganglia = too much braking of the thalamus i.e. thalmus turned on too much and you get impaired initiation of movement and lack of movement

32
Q

what is sydenham’s chorea?

A

a hyperkinetic basal ganglia disorder an autoimmune reaction caused by the childhood infection w/ group a beta hemolytic strep

33
Q

what is messed up in the basal ganglia circuit in huntington’s disease?

A

the indirect pathway: D2 is knocked out leaving D1 unchecked

34
Q

what is an example of a hypokinetic disease?

A

parkinson’s

35
Q

what are some symptoms of parkinsons?

A

shuffing gait, resting trempr .difficulty initiaing movement, slpw movements, muscular rigidity, expresionless faces, postural abnromalities. dyautonomia ( problems with the autonmic fnc due to effects on locus coreleus which relases norepi )

36
Q

what is messed up about the basal ganglia circuit in parkinson’s?

A

there is a loss of dopamine soo indirect pathway is is taken which leads to more brakeing of the thalamus

37
Q

what are higher order consequences of basal ganglia damage in huntington’s disease :

A

cognitive deficits

38
Q

what are higher order consequences of basal ganglia damage in sydenham’s chorea:

A

emotional and behavioral, ocd

39
Q

are there higher order consequences of basal ganglia damage in parkinson’s disease?

A

common in advanced stages cognitive deficits

40
Q

are there higher order consequences of basal ganglia damage in wilson’s diseas

A

almost always cognitive deficits

41
Q

are there higher order consequences of basal ganglia damage in syndrome of corpus luys ( subthalamic lesion)

A

most of the time ( cognitive defecits)

42
Q

WHAT ARE SOME CAUSES OF BASAL GANGLIA LESIONS?

A

carbon monoxide posioning, wasp stings ( produce antibodies, adverse drug reactions, high altitude sickness

43
Q

what are some methods of treating huntington’s and sydenhams’s chorea?

A

block the excess action of the direct pathway with anti dopaminergic or dopamine depleting drugs but side effects are that pts often devleop tardive dysinesia w/ chronic treatment

44
Q

even though parkinson’s pts lack dopamine why don’t you give dopamine to parkinson’s pts to treat them?

A

because it can’t cross the blood brain barrier and isn’t well tolerated so we give L-DOPA instead which metabolizes to dopamine but this is only for improvement in the dhort term because in the long term the pt will continue to need higher and higher doses because the dopamine making cells continue to die

45
Q

what are some methods of treating parkinsons:

A

L-DOPA: metabolizes to dopamine
dopamimetics: ( longer acting than L-DOPA ) but stronger side effects

MAO inhibitors: prevent basal degradation of dopamine

anticholenergics which reduce the side effects of the tremor ( not really for the dopamine b/c this would further reduce dopamine)

46
Q

what is the best treatment do far for parkinson’s?

A

a surgically implanted stimulator which decreases the thalamus activity and enforces a normal rhythm of discharge

47
Q

ipsc derived dopaminergic cells are promosing for parkinsons patients but what is the problem?

A

they can’t regulate dopamine regulation

neuroscience (32 decks)

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