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53 Cards in this Set

  • Front
  • Back
which two areas control the motor cortex output?
1. basal ganglia
2. cerebellum

refine raw motor output
what are the BG and cerebellum associated with?
1. initating
2. terminating movement
3. muslce tone
(4)generally refining
what are the BG mainly known for? contains?
motor connections
streams of info going to the motor and limbic systems
which NT do the BG use?
1. GABA- inhib
2. Ach
3. Peptides: enkaphalins, SubP, Dynorphin, somatostatin, neuropeptide Y
Lenticular Nucleus



Striatum
lateral to IC
putamen+GP
lenticulstriate vessels

caudate+putamen
order of capsules
IC->Ext Capsule->Claustrum->extreme
what is GP anatomic location?
lateral to IC and medial to striatum
embryological demarcations for GP/Striatum
line lat to GP=end of brainstem
GP is from diencephalon
Striatum grows down from cortex
how do you definitely know youre in a rostral coronal slice?
there is no thalmus
see the ant commissure(connects 2 temporal lobes)
Nucleus Accumbens Septi
in ant part of brain
connection of caudate and putamen

addiction behavior
anatomical funnel
striatum and GPi/GPe
mainly inhibitory output, GABA
Corpus Striatum
BASAL GANGLIA
caudate+putamen+GP
caudate/putamen/GP + Amygdala Subthalmic nucleus + SN
Putamen in general is more motor
it receives input from...
motor and somatosensory cortex

*Motor fxn of BG
Putamen projects via what and to what?
via GP and Thalmus
1. M1
2. pre-motor
3. supplementary M2
The Caude is more what?

receives what?
More Limbic/Cognitive

receives mainly motor association cortex
what is almost gone in HD patients?
the caudate
motor and behavioral disease
input nuc

processing nuc

output nuc
caudate, putamen, nuc accumbens

GPe, Subthal nuc, vent teg area

GPi, SNpr, ventral pallidum
Input Nuclei

NT used in input
Caudate and Putamen
receive info from cortex
ALL Glutaminergic
Main NT of output in BG

Wild-card modulating NT
GABA

Dopamine- from SN
Substantia Nigra
Pars Compacta

Pars Reticulata
magnocellular, rel dopamine to striatum
smaller cells- lumped in w/ GPi
what is the main output of the BG?
GPi (SNpr lumped in w/ it)

go from GPi->VA/VL of thal-> to PreMC and SMA
what are the two pathways out of GPi?
1. Ansa Lenticularis (Vent Gpi)
2. Lenticular Fasiculus (Dorsal Gpi)

ALV LFD
What are the two major pathways with in the BG?
1. Direct Path- initiates movement
2. Indirect Path- suppresses mvmt
Direct Pathway

primarily Glu-initiates mvmt
1. Glu input from cortex to striatum
2. Straitum gives GABA input to GPi, directly
3. Gpi sends GABA via ALV or LFD to thalmus
4. THalmus is excitatory back to cortex
Indirect Pathway

primarily GABA- inhibits mvmt
1. cortex Glu to striatum
2. Striatum GABA tp GPe
3. GPe GABA to STN
4. STN Glu to GPi
5. rest follows direct
how do the direct and indirect pathways work together?
they work together to influence GPi, which is the main output

GPi recieves excitatory(Glu) input from STN, and inhib input from Striatum
Wildcard SN modulation

where are the D receptors?
Dopamine- Neither inhib or excit- receptor determines it

medium spiny (GABA) neurons found in the striatum have D rec
D1 and D2
D1 rec

D2 rec
excitory- inc cAMP

inhibitory- blocks cAMP
Striatum Cells both GABA

S1
S1 rel GABA to GPi, to the thal, back to the cortex= DIRECT PATH

primarily have medium spiny neurons w/ D1 rec on them
S2
indirect pathways
primarily D2 inhibitory
so when Dopamine hits the D2 rec, there is less GABA putout.
what does the direct pathway give the GPi/SNpr?

indirect?
direct-->GABA to GPi/SNpr

indirect-->Glu to GPi/SNpr
Chorea
dancing, continous rapid movements
assoc w/ HD
Athetosis
slow writhing movements
lesion of the GP or its projectsions

Chorea+Athetosis=choreoathetosis
Dyskinesia

what PD drug induces it?
abnormal movements

Levodopa induces dyskinesia
Ballismus


Hemiballismus
Flailing movements, NOT a seizure
stroke in STN
lesion in STN or its projectsion
Parkinson's Disease

Huntington's Disease
degen of SNpc (no Dopamine)
hypokinetic mvmt disorder
lesion to Striatum, or projections. CAG repeat, w/ anticipation
what happens in the BG to cause hemiballismus?
lose the Glu input that usually stim GABA.

overall, less GABA and more Thalamic input to Cortex
hyperkinetic mvmt disorder
Parkinson's effects
Direct Pathways

Indirect
degen of SNpc
shows less GABA output

take away inhib input, there is more GABA output
glu coming out of STN is more than it should be, therefore put out too much GABA to thal
Substantia Nigra
two black streaks in mid brain

due to neuromelanin

projects to Striatum
Direct pathway effects in PD

Indirect path effects in PD
less DA, less GABA output
take brake off of GPi
*same result as direct
not enough of an inhib on STN, you then get too much Glu to Gpi
put the foot on gas for Gpi, which is in hib
*Get HYPOkinetic mvmt disorder
Pigmented Structrues that degen in PD

what is this infering?
1. SNpc
2. Locus Ceruleus

PD is an overall MONOAMINERGIC disease
PD problems
motor, sleep, mood
Ach Interneurons
serotonin input to striatum
LC projects to SN
ALL of these areas are affected
Spasticity

Rigidity
1. velocity dependent, UMN disease- see w/ stroke, damaged retiulospinal tr

2. Rigidity is velocity independent. BG disease
muscle tone is set by what?
Muscle spindle- unique end organ that is part muscle and part nervous system
Muscle Spindle
talks to gamma motor neuron in SC
gamma MN set stretch sensitivity
-controlled by Reticulospinal tract
what does the reticulospinal tract normally do?

in sroke?
inhibits the gamma motor neurons of SC, ms

in stroke, the gamma mn are disinhibited and fire too much and are now inc sensitivity to stretch-->hyperreflexes
internal capsule is confluent with what?
cerebral peduncle
2 ways to get from BG to VA/VL
1. thru IC: Fields of Forel
2. under IC: Ansa Lenticularis
Fields of Forel
go from Gpi/SNpr to H2, to H1, to H, to VA/VL

H2- Lenticular fasiculus
H1- Thalamic fasiculus
what do the fields of Forel have to loop around?
Zona Inserta
Ansa Lenticularis
sneaks under IC
very ant portion of thalmus
ventral?
what is H(0) in the Fields of FOrel
where the H1 of the Fields of Forel and Ansa Lenticularis meet before they enter VA/VL
1. Tremor on opp side of body, DBS
2. Gpi DBS

3. STN DBS
1. Ventral Intermedial Nuc
essential hereditary tremor
2. dystonia twist, pallidotoomy for PD patients
3. stimulated for PD, bilaterally