FE: Lecture 7: The Deep Cerebral Nuclei Flashcards
Where is dopamine produced?
Substantia Nigra and Ventral tegmental area
What happens to substantia nigra in parkinson’s?
cell death in SN, which leads to decreased Dopamine
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
What is the antagonist for DA?
halperidol- induces parkinson like symptoms
What are the main major deep cerebral nuclei?
caudate, putamen and globus pallidus
What are other important nuclei?
claustrum, accumbens, amygdala
What are the three capsules of basal ganglia?
internal (anterior, posterior, genu), external, extreme
What comprises the corpus striatum?
caudate and putamen
What does the neostriatum contain?
caudate, putamen and accumbens
What are two different striatal outputs?
- Neo to GP
1b. GP internal to motor thalamus (pallidothalamic tract), GP external to subthalamus
2a. Neo to SN
these are all inhibitory- GABA
What is direct projection of deep cerebral nuclei?
Corpus striatum to GP internal
GP to motor thalamus
motor thalamus to motor cortex
What part of direct projection is excitatory?
thalamus to cortex
activation of this pathway increases motor cortex activation
What is lenticular nuclei?
GP and putamen
What is limbic striatum?
amygdala and accumbens
What are the three major inputs to deep cerebral nuclei?
- cerebral cortex- almost all of it except auditoty and visual
- brainstem to SN and raphe nuclei
- thalamus to midline and intralaminar nuclei
main targets are neostriatum and provide serotonin
What is indirect projection from deep cerebral nuclei to motor cortex
- neostriatum to GP external
- GP external to subthalamus
- Subthalamus to GP internal
- GP internal to motor thalamus
- motor thalamus to motor cortex
In the indirect pathway what two paths are excitatory?
motor thalamus and subthalamus
activation of this pathway leads to decreased activity of motor cortex
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
What are characteristics of Parkinson’s?
SN cell degeneration, reduces DA in Neo
too little movement hypokinesia, improved with increasing DA
What are characteristics of Huntington’s?
neostriatal cell degeneration, strong genetic link
too much movement- hyperkinesia
improved by blocking DA
What are characteristics of parkinsons hypokinesia?
- cant initiate movements- “stuck in door way” or visual stimuli
- decreased spontaneous movements- bradykinesia- mask like face
- Gait- slow and shuffling
- cogwheel rigidity- parking brake rigidity
What are characteristics or parkinson’s hyperkinesia?
cant stop once movement is started, resting tremor
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
How does DA and movement connect ?
DA produces two effects on striatum
one transmitter two effects
- DA is excitatory to direct path- D1 receptors
- DA is inhibitory to indirect pathway- D2
What is the net effect of DA decrease in neostriatum?
decreased motor cortex activity in hypokinesia
In Huntington’s how does destruction of indirect neurons affect movement?
less activity of indirect neostriatal neurons leads to more activity of motor cortex
