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Neuroscience Final Exam > FE: Lecture 7: The Deep Cerebral Nuclei > Flashcards

FE: Lecture 7: The Deep Cerebral Nuclei Flashcards

1
Q

Where is dopamine produced?

A

Substantia Nigra and Ventral tegmental area

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2
Q

What happens to substantia nigra in parkinson’s?

A

cell death in SN, which leads to decreased Dopamine

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3
Q

What is the main function of SN?

A

this is the brains reward zone, VTA releases dopamne

when you do cocaine DA uptake and its addicting

however too much can cause hallucinations or psychiatric disorders

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4
Q

What is the antagonist for DA?

A

halperidol- induces parkinson like symptoms

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5
Q

What are the main major deep cerebral nuclei?

A

caudate, putamen and globus pallidus

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6
Q

What are other important nuclei?

A

claustrum, accumbens, amygdala

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7
Q

What are the three capsules of basal ganglia?

A

internal (anterior, posterior, genu), external, extreme

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8
Q

What comprises the corpus striatum?

A

caudate and putamen

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9
Q

What does the neostriatum contain?

A

caudate, putamen and accumbens

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10
Q

What are two different striatal outputs?

A
  1. Neo to GP
    1b. GP internal to motor thalamus (pallidothalamic tract), GP external to subthalamus
    2a. Neo to SN

these are all inhibitory- GABA

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11
Q

What is direct projection of deep cerebral nuclei?

A

Corpus striatum to GP internal

GP to motor thalamus

motor thalamus to motor cortex

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12
Q

What part of direct projection is excitatory?

A

thalamus to cortex

activation of this pathway increases motor cortex activation

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13
Q

What is lenticular nuclei?

A

GP and putamen

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14
Q

What is limbic striatum?

A

amygdala and accumbens

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15
Q

What are the three major inputs to deep cerebral nuclei?

A
  1. cerebral cortex- almost all of it except auditoty and visual
  2. brainstem to SN and raphe nuclei
  3. thalamus to midline and intralaminar nuclei

main targets are neostriatum and provide serotonin

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16
Q

What is indirect projection from deep cerebral nuclei to motor cortex

A
  1. neostriatum to GP external
  2. GP external to subthalamus
  3. Subthalamus to GP internal
  4. GP internal to motor thalamus
  5. motor thalamus to motor cortex
17
Q

In the indirect pathway what two paths are excitatory?

A

motor thalamus and subthalamus

activation of this pathway leads to decreased activity of motor cortex

18
Q

What are main characteristics of neostrital disorders?

A

they are disorders of movement initiation

no UMN or LMN paralysis or sensory loss- too much or too little movement

additional cognitive symptoms

19
Q

What are characteristics of Parkinson’s?

A

SN cell degeneration, reduces DA in Neo

too little movement hypokinesia, improved with increasing DA

20
Q

What are characteristics of Huntington’s?

A

neostriatal cell degeneration, strong genetic link

too much movement- hyperkinesia

improved by blocking DA

21
Q

What are characteristics of parkinsons hypokinesia?

A
  1. cant initiate movements- “stuck in door way” or visual stimuli
  2. decreased spontaneous movements- bradykinesia- mask like face
  3. Gait- slow and shuffling
  4. cogwheel rigidity- parking brake rigidity
22
Q

What are characteristics or parkinson’s hyperkinesia?

A

cant stop once movement is started, resting tremor

23
Q

What are names of symptoms in Huntington’s?

A

chorea- involuntary jerking

dystonia- involuntary sustained contracture

Cognitive- difficulty planning, lack of flexibility or get stuck in thought, depression

24
Q

How does DA and movement connect ?

A

DA produces two effects on striatum

one transmitter two effects

  1. DA is excitatory to direct path- D1 receptors
  2. DA is inhibitory to indirect pathway- D2
25
Q

What is the net effect of DA decrease in neostriatum?

A

decreased motor cortex activity in hypokinesia

26
Q

In Huntington’s how does destruction of indirect neurons affect movement?

A

less activity of indirect neostriatal neurons leads to more activity of motor cortex

Neuroscience Final Exam (10 decks)

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