U5 Lec2 - basal ganglia

Basal Ganglia

a group of nuclei located at the base of the cerebral cortex made of 7 functional parts involved in movement control

what nuclei make up the basal ganglia

caudate

putamen

globus pallidus (interal and external)

sibstantia nigra (paras compacta and paras reticulata)

subthalamic nucleus

whihc nuclei are not anatomocially apart of basal ganglia, but functionaly very interconected

substantia nigra (para compacta and paras reticulata)

subthalamic nucleus

Striatum

the combined structure of the caudate + putamen and the main input area of the basal ganglia

Lentiform (lenticular) nucleus

the combined structure of the globus pallidus + putamen, cone-shaped

Function of basal ganglia

controls movement by planning, sequencing, and regulating VOLUNTARY/ slef initiates movements actions and controls habitual and skill based behaviours

acts as a "brake" that suppresses unwanted movements

what is the basal ganglia interconnected with

acts INDIRECTLY on lower motor neurons and highly interconected with motor cortical areas

what happens if any basal ganglia components get damages

dysfunction in any component leads to dyskinesia (excess or reduced movement) but not paralysis

Eg. movements havppping that you dont want (positive sign) or movements not happing that you do want (negative signs)

Caudate nucleus

a C-shaped input nucleus divided into head, body, and tail, main inphut of the basal ganglia

degenerates in Huntington's disease

Putamen

lateral "shell" oof basal ganglia with cellular bridges to caudate nucleus

also major input in basal ganglia

Globus pallidus (segments, location and roles)

2segments

GPi (internal) → medial

GPe (external) → lateral

Medial to putamen

One of the major outputs

Has inhibitory connections with thalamus

Subthalamic nucleus location and role

Inferior to thalamus

Splidle or lens shaped

Communicates with globus pallidus

Substantia nigra segments and their loaction and role

Pars compacta → contains darkly pigented dopaminergic neurons (more dorsal)

Pars reticulata → involved in output for eye movements, inhibits thalamus (more ventral)

Input nuclei of basal ganglia

striatum (caudate + putamen) serve as the major input structures

Output nuclei of basal ganglia

GPi and substantia nigra pars reticulata which send inhibitory (GABAergic) output

Basal ganglia receives input from

sensory areas, motor areas, association areas, and the thalamus

Basal ganglia outputs to

the thalamus and superior colliculus

what is the basal ganglias default output by what pathway

its out via the GPi and SNpr send inhibatory output signal to the thalamus to reduce signal to a motor neurons --> this output is tonic

what are the 2 main pathways of the basal ganglia

direct --> enable actions

indirect --> stops innapropriate action

direct pathway

cortex, sensory areas, frontal lobe sends excitatory signal --> striatum disinhibits GPi. GPi cannot inhibit thalamus so thalamus send excitatory signal to cortex which send drive along descending tracts to lower motor neurons --> so yes movemnet!

indirect pathway

indirect neurons from cortex send excitatory signals to striatum. striatum disinhibits GPe so it can not inhibit thew subthalamic nucleus. subthalamic nucleus excites the GPi which enhances gpi inhibatory signal to the thalamus decreasing the descending drive to the lower motor neurons disabling movement

2 dif dopamin receptors in striatum

D1 receptor - apart of direct oathway, when recieve dop they send EPSP to striatum axtivating it

D2 receptor - apart of indirect pathway, when recevie dop send IPSP signals to inhibit striatum

what is the effect of dopamine on the direct pathway AND INDIRECT pathway

ACTIVATES DIRECT PATHWAY: by activating D1 receptors --> striatum gets activated --> GPi gets disinhibited --> INC MOVEMENT

INHIBITS INDIRECT PATHWAY: activates D2 receptors which inhibits striatum --> GPe doesnt get inhibited

basal ganglia dysfunction - parkinsons

caused by: neuron death in SN --> loss of dopamine --> underactivation of direct pathways and over activation of indirect pathway --> akinesia and bradykiinesia

sympotoms of parkinsons

- akinesia (lack of movement) and bradykinesia (slowness of movement)

:dopamine isnt helping the stritium to reach threshold than sending the epsps or ipsps is so much harder as cortex has to work harder to get to that same threshold

- resting tremor

there are threshold that manage oscillating system and since these threshold get mess up leads to tremor

-ridgitiy

- posture instability

- stooped poster, shuffling gait - freezing, difficulty turning, diminshed arm swing while walking

- micrographia (writing smaller)

- hyponia (cant speek as loud)

- himinished facial expression

Huntingtons disease - break pedal not push down enough

degeneration of indirect pathway neurons in striatum (caudate) leading to underactive indirect pathway and overactive direct pathways --> less inhibition of movement

symptoms:

hyperkinetic movement like chorea and dystonia

THERE MIGHT BE A CURE