basal ganglia

functions of basal ganglia

1. control movement

2. regulate cortical output

3. set the gain of movement 

4. plays a role in action selection and motor control 

cerebral cortex

primary excitatory input for basal ganglia; loop involves the thalamus

action selection

aiding in the choice of behaviors to execute

forebrain

striatum and globul pallidus

caudate nucleus

nucleus accumbens

putamen

striatum:

external segment

internal segment

globus pallidus:

diencephalon

subthalamus 

thalamus

midbrain

substania nigra

compact

reticular

components of substania nigra:

internal capsule

separates the putamen and caudate nucleus

medium spiny neurons

neurons of the straitum 

• GABAergic

• contain dopamine receptors 

D1 medium spiny neurons

depolarization and excitation of medium spiny neuron; project to internal segment of Globus Pallidus (-)

D2 medium spiny neurons

hyperpolarization and inhibition of medium spiny neurons; project to external segment of Globus Pallidus (-)

substania nigra pars compacta

dopamine is released from here; medium spiny neurons receive input from here

• contains dopamergic neurons that project to putamen and caudate nucleus

globus pallidus internal segment

GABAergic; primary output of basal gaglia - neurons here project to the thalamus 

• D1 medium spiny neurons in straitum project to this structure

globus pallidus external segment

GABAergic, critical for regulating output via connections with subthalamus

• D2 medium spiny neurons of straitum project to this structure

subthalamus

glutamergic; located between the thalamus and the substania nigra - only intrinsic source of excitation in the basal ganglia

• projects to globus pallidus internal segment

• receive inhibitory information from GP(e)

inhibiting

thalamus

disfacilitation

background levels of activity

• putamen = low activity

• GP(i) = high activity

GP(i) is BLANK neurons in the BLANK leading to BLANK of the cortex = little or no movement 

active 

decreased 

decreased

decreased 

BLANK GP(i) leads to BLANK thalamic activity - this leads to BLANK activity in the motor cortex, and in turn, BLANK activity in the spinal cord/CST

basal ganglia circuitry

modulate output of GP(i); made up of opposing parallel pathways that adjust the magnitude of inhibiting GP(i) in order to increase or decrease movement

center-surround organization

theory of basal ganglia function; cortical output movements associated with particular voluntary output and reinforce the ongoing movement - permit desired movements and inhibit unwanted competing movements 

• invalid theory because it does not account for dopamine released from SN(pc) that impacts the direct/indirect pathway 

dopamine

present in both direct and indirect pathway; leads to greater cortical output - increased movement

ACH

present in both direct and indirect pathay; leads to decreased cortical output - decreased movement 

ACH and direct pathway

inhibit strial cells in direct pathway

ACH and indirect pathway

excite straital cells (indirect pathway)

dopamine and direct pathway

excite straital cells (direct pathway)

dopamine and indirect pathway

inhibit striatal cells (indirect pathway)

loss of dopamine

direct pathway; removes excitatory drive on D1 expressing cells in striatum which results in slight decrease in suppression of GP(i)

• ACH inhibition of D1 neurons is unchecked and this causes decreased input to GP(i) - this results in decrease in motor activity (BRADYKINESIA)

loss of dopamine

indirect pathway; removes inhibitory drive on D2 expressing neurons, this results in increased inhibition of GP(e) and decreased suppression of subthalamus —> this increases excitation in GP(i) and decreases thalamic activity

• ACH excitation of D2 neurons is unchecked; further suppression of GP(e) and there is greater output to subthalamus → results in decreased activity (BRADYKINESIA)

parkinsons

movement disorder - loss of dopaminergic neurons in SN(PC)

• bradykinesia (loss of dopamine) - reduced amplitude and velocity of voluntary movement

• indirect pathway affected

treatments for parkinsons

1. L-DOPA (con: not localized; may cause systematic effects)

2. lesions in GP(i) or subthalamus

3. deep brain stimulation