FE: Lecture 7: The Deep Cerebral Nuclei Flashcards Preview

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

Flashcards in FE: Lecture 7: The Deep Cerebral Nuclei Deck (26):
1

Where is dopamine produced?

Substantia Nigra and Ventral tegmental area

2

What happens to substantia nigra in parkinson's?

cell death in SN, which leads to decreased Dopamine

3

What is the main function of SN?

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

4

What is the antagonist for DA?

halperidol- induces parkinson like symptoms

5

What are the main major deep cerebral nuclei?

caudate, putamen and globus pallidus

6

What are other important nuclei?

claustrum, accumbens, amygdala

7

What are the three capsules of basal ganglia?

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

8

What comprises the corpus striatum?

caudate and putamen

9

What does the neostriatum contain?

caudate, putamen and accumbens

10

What are two different striatal outputs?

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

11

What is direct projection of deep cerebral nuclei?

Corpus striatum to GP internal

GP to motor thalamus

motor thalamus to motor cortex

12

What part of direct projection is excitatory?

thalamus to cortex

activation of this pathway increases motor cortex activation

13

What is lenticular nuclei?

GP and putamen

14

What is limbic striatum?

amygdala and accumbens

15

What are the three major inputs to deep cerebral nuclei?

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

16

What is indirect projection from deep cerebral nuclei to motor cortex

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

In the indirect pathway what two paths are excitatory?

motor thalamus and subthalamus

activation of this pathway leads to decreased activity of motor cortex

18

What are main characteristics of neostrital disorders?

they are disorders of movement initiation

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

additional cognitive symptoms

19

What are characteristics of Parkinson's?

SN cell degeneration, reduces DA in Neo

too little movement hypokinesia, improved with increasing DA

20

What are characteristics of Huntington's?

neostriatal cell degeneration, strong genetic link

too much movement- hyperkinesia

improved by blocking DA

21

What are characteristics of parkinsons hypokinesia?

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

What are characteristics or parkinson's hyperkinesia?

cant stop once movement is started, resting tremor

23

What are names of symptoms in Huntington's?

chorea- involuntary jerking

dystonia- involuntary sustained contracture

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

24

How does DA and movement connect ?

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

What is the net effect of DA decrease in neostriatum?

decreased motor cortex activity in hypokinesia

26

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

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