CSAD 334 Basal Ganglia

for quiz 4

anatomy of basal ganglia

made up of external and internal globus pallidus, the putamen, and the caudate nucleus

functions of basal ganglia

regulates complex motor functions like posture, arm swinging, balance, and locomotion; selects motor responses/programs - inhibits function and coordinates motor behavior; also involved in cognitive processing

striatum

made up of caudate and putamen

basal ganglia loops

each loop has a direct and indirect circuit, and all parts of the loop are set for inhibition (the basal ganglia is an inhibitory system)

basal ganglia loop circuits

like a battery, must have neurotransmitter flow in a specific way for the circuit to be complete

3 main neurotransmitters

GABA, glutamate, and dopamine

GABA

inhibition

glutamate

faciliatory/excitatory

dopamine

faciliatory/excitatory

basal ganglia feedback loops

forms closed feedback loops possessing motor and non-motor operations

motor basal ganglia loops

the movement loop and the oculomotor loop

non-motor basal ganglia loops

the prefrontal loop and the limbic loop

the basal ganglia’s effect on motor behavior

relays and integrates commands from the cortex; implements and selects cortical movement commands; suppresses extraneous movements

where basal ganglia always receives information

cortex

where basal ganglia always sends information

thalamus

basal ganglia sensorimotor effect

implements automatic components of movement such as muscle force (velocity, amplitude), resting muscle tone, and habitual responses

basal ganglia associative effect

connections to the association areas, which aids goal-directed decision making

basal ganglia limbic effect

reward-based learning and conditioning

2 faciliatory structures in basal ganglia

subthalamic nucleus and substantia nigra pars compacta

inhibitory nature of basal ganglia

the basal ganglia is set to be inhibitory; those inhibited signals must be inhibited (with GABA) to get facilitation

functional essence of basal ganglia

output → GABA → thalamus → glutamate → cortex; each area (group of neurons) is regulated by the preceding area (group of neurons)

what happens if the output nuclei (GPi/SNr) reduce their activity

observable behavior is expressed (because output nuclei are inhibitory) which is the condition for movement initiation - the thalamus is “dis”-inhibited (released from inhibition) and allowed to excite motor areas of the cortex more strongly

what happens if output nuclei (GPi/SNr) increase their activity

observable behavior is suppressed (because GPi/SNr is inhibitory) which is the condition for movement termination - thalamus is inhibited more strongly than normal and provides even less excitatory drive to motor areas of the cortex

direct basal ganglia pathway

thalamus is not inhibited and can facilitate a message to the motor cortex = movement!! cortex → striatum → GPi/SNr → thalamus → motor/pre-motor cortex (movement is a go!)

indirect basal ganglia pathway

thalamus is inhibited and can not facilitate a message to the motor cortex = no movement!!; cortex → striatum → GPe → STN → GPi/SNr → thalamus → motor/pre-motor cortex (movement is a no go!)

dopamine

acts as a neuromodulator in the basal ganglia; operates simultaneously on both pathways and has a counterbalancing effect; makes neurotransmitters work better or less effectively

what dopamine increases

increases the efficacy of striatopallidal projections in the direct pathway → heightens the influence of glutamate (from cortex) on striatal cells

what dopamine decreases

decreases the efficacy of striatopallidal projections in the indirect pathway → lessens the effect of glutamate (from cortex) on the striatal cells

symptoms of basal ganglia dysfunction

dyskinesias and akinesias

dyskinesias

involuntary, erratic movements; tremors, athetosis, chorea, ballismus, and tics

akinesias

absence or loss of movement; rigidity, dystonia, and bradykinesia

parkinson disease

a progressive neurological disease first described by dr james parkinson in 1817; known as “shaking palsy”; caused by degeneration of midbrain’s substantia nigra and loss of dopamine to the basal ganglia

symptoms of parkinson disease

muscle rigidity, dyskinesias, resting and pill-rolling tremors, shuffling gait, weak voice, dysarthria, flat affect, poor posture, and dysphagia

hypokinetic basal ganglia disorders

related to indirect pathway dominance from substantia nigra compacta and dopamine loss; characterized by lack of movement; parkinson disease

parkinson disease treatment

includes medication, surgery, deep brain stimulation, and pallidotomy

parkinson disease medication

levodopa/carbidopa medications; sinemet, parcopa, and stalevo

deep brain stimulation (DBS)

surgical insertion of a brain pacemaker that stimulates the basal ganglia, reducing parkinsonian symptoms

pallidotomy

cells in the globus pallidus are selectively destroyed using a heated probe, reducing parkinsonian symptoms

huntingdon disease

a progressive, hereditary neurological disease due to degeneration of the basal ganglia; average onset is around 35 years of age; has an autosomal dominant pattern of inheritance

symptoms of huntingdon disease

severe chorea, athetosis, emotional and personality changes, torticollis (twisting of the neck), dysarthria, dysphagia, and dementia

hyperkinetic basal ganglia disorders

related to direct pathway overactivity caused by degeneration between the striatum and globus pallidus external; characterized by an excess of movement; huntingdon disease

other basal ganglia problems that can occur

emotional processing problems (most consistent sign); disinhibition, impulsivity, and inappropriate behavior