kine4505 topic 9: Basal ganglia

what is basal ganglia for

influence movement by modulating activity in upper motor neurons

what makes up the basal ganglia

striatum, globus pallidus, substantia nigra, subthalamic nucleus

does the basal ganglia have direct or indirect influence

indirect, it has no connection to the spinal cord

what makes up the striatum

caudate and putamen

what are the inputs to basal ganglia

cerebral cortex to striatum

cortical signals arrive to what on striatum to integrate signals

medium spiny neurons

where does caudate receive input from

multimodal association cortices + eye movement areas

where does putamen get input from

from primary and secondary somatosensory areas

what are projections from cortex to input area called

corticostriatal pathway

what is the main basal ganglia output

globus pallidal internal via thalamus (for motor areas) and substantia nigra pars reticulata via superior colliculi (for eye movement)

what are the 3 loops between cortex and basal ganglia

1. motor - voluntary movements (our focus)

2. limbic - emotional behaviour

3. executive - cognitive processes

what is the motor circuit for

the initiatioon of voluntary movements

describe tonic inhibitory outflow from the BG

when BG inhibits motor areas during rest, preventing unwanted movements

what must be done to tonic outflow from BG to start movement

inhibition must be removed first

what is the direct vs indirect pathway for BG

direct pathway - stops the inhibition to allow movement (projects to GP(int) and SN pars reticulata)

indirect pathway - inhibits further (projects to GP (ext))

which pathway disinhibits the thalamus in BG

direct pathway

describe direct pathway in BG

Cortex release glutamate --> Excitatory to striatum --> release GABA --> globus pallidus inhibited --> won't release gaba to thalamus --> thalamus is excited --> we get more movement

describe disinhibitory circuit of direct pathway

if the striatum cell receives excitatory input and threshold is reached, it sends inhibition to GPi to disinhibit the thalamus

describe the indirect pathway in BG

Cortex releases glutamate --> SnC releases dopamine --> dopamine is inhibitory --> striatum sends inhibitory gaba to globus pallidus external segment --> gaba is not released --> subthalmic nucleus is not inhibited --> releases nuclei --> excite substantia nigra --> release GABA -->inhibits thalamus --> WE DONT MOVE

describe the hyperdirect pathway

cortex > stimulates STN

> stimulates GPI

> increases inhibitory output from BG

- acts as a very forceful brake, followed by an action

what does dopaminergic input from SN(pc) do?

decreases inhibitory output from BG, inhibiting the indirect and exciting the direct pathway

descrie the receptor subtypes for dopaminergic input

D1: excitatory, part of direct pathway (adds to GPi input)

D2: inhibitory, part of indirect pathway (adds to GPe)

what is hypokinesia vs hyperkinesia

hypo: decrease in the amount and speed of movements (neg sign)

hyper: unwanted movements (pos sign)

what is a positive vs negative sign

positive: action that shouldnt happen and is

negative: action that should happen and isnt

describe parkinsons disease

cell death in SN causing loss of dopamine which leads to overactivity in indirect pathway

is parkinsons hypokinetic or hyperkinetic

hypokinetic

how does parkinsons change circuitry

inhibition to GPe is increased, leading to more tonic inhibition, decreasing excitation on motor cortex

what is akinesia

difficulty initiating movement voluntarily

what is bradykinesia

movements are very slow

what signs does loss of dopamine producing cells in SNc lead to

akinesia, bradykinesia, and a resting tremor in distal limbs

what does loss of ACh producing cells in pedunculopontine nucleus lead to

rigidity- inability to inhibit reticulospinal + vestibulospinal tracts

what are parkinsons treatments

pallidotomy, STN lesion, L-DOPA, and deep brain stimulation

what is pallidotomy

lesion in globus pallidus, so theres less neurons inhibiting thalamus (lets movement occur)

what does STN lesion do

reduces indirect pathway

what does L-DOPA do

acts as dopamine precursor to replace the missing dopamine (since dopamine itself can't cross the BBB)

why does L-DOPA treatment not work longterm?

dopaminergic cells are continually being killed off, so while the balance is maintained for a bit, it's not efficient.

why are lesions used in parkinsons treatment?

to correct balance of the lost dopamine

describe deep brain stimulation treatment

electrodes in the brain which delivers impulses without lesions, so its adjustable and reversible and has good responses

describe huntingtons disease

loss of striatal (mainly caudate) neurons of the indirect pathway, letting unwanted movements occur

is huntingtons hypokinetic or hyperkinetic

hyperkinetic

what is hemiballism

uncontrolled involuntary flinging of limbs on the side contralateral to STN lesion (less output of GPi, cant inhibit unwanted movements)