Basal Ganglia
Here’s the text version:
General Info
Neural clusters in peripheral nervous system are ganglia. In the central nervous system, they are called nuclei. Should be called Basal Nuclei but usually called Basal Ganglia.
Works on disinhibition principle
It’s the brain’s brake
If no input = steady fire at high rates
Neurotransmitters
Inputs use glutamate
Outputs use GABA
Internal connections use dopamine or ACh
Group of nuclei
Distinct masses of gray matter
Left-right sides mirror each other
Work together as functional unit
Interact with cortex, thalamus, etc
FOUR PARTS
Striatum
Dorsal
caudate & putamen
Ventral
nucleus accumbens & olfactory
Pallidum
globus pallidus (dorsal)
ventral pallidum
Substantia nigra (pons)
Subthalamic nucleus (below thalamus)
Two large parts
Striatum & Pallidum
Two smaller parts (& farther back)
Substantia Nigra & Subthalamic
Disorders
Huntington’s disease
Major loss of medium spiny neurons in striatum
Inability to prevent parts of the body from moving unintentionally
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Striatum
Largest
Looks striped
Looks like two blobs of gray separated by large white stripe
input from many brain areas
only outputs to other parts of basal ganglia
Complex internal organization
Direct pathway (D1)
Indirect (D2)
Organized in 3D
Cortex is layered; organized 2D
Coordinates multiple aspects of cognition
action planning
decision making
motivation
reinforcement
reward
Interneurons
Release acetylcholine
Many types of interneurons
include fast-spiking interneurons
Continuously produce new neurons in striatum
Striatum is activated by stimuli associated with reward
aversive
novel & unexpected
intense stimuli
Ventral striatum composed of olfactory tubercle & nucleus accumbens
As a whole, major role in cognitive processing of
aversion & pleasure
motivation
reward & reinforcement
addiction
As a whole, minor role
cognitive processing of:
fear (type of aversion)
impulsivity
placebo effect
Also involved in
encoding of new motor skills
Nucleus accumbens
Two, one in each hemisphere
Each has two structures:
Nucleus accumbens core
Increased density of dendritic spines
Increased branch segments
Increased terminal segments
Processes
motor function related to reward
encodes new motor programs that help get future rewards
Nucleus accumbens shell
Lower density of dendritic spines
Less terminal segments
Less branch segments
Processes
want (motivational salience)
reward perception
positive reinforcement
drugs & naturally rewarding stimuli
addictive drugs affect dopamine in shell more than core
Function
Reward
Subset of VTA neurons
Dopamine (D1) medium spiny neurons in shell
Drugs
Increase dopamine in shell & core; more pronounced in shell
morphine
cocaine
amphetamines
at high levels, increase dopamine level to similar levels in both shell & core
Drug rewards
has abnormal strengthening effect on stimulus
drug associations
increases drug-reward stimuli’s resistance to extinction
effect was more pronounced in shell than core
Addiction
Links to addictions to
alcohol, cannabinoids, cocaine
nicotine, opioids & amphetamines
Links to
Depression
OCD
Placebo effect
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Pallidum
Input from striatum
Sends inhibitory output to a number of motor-related areas
Globus Pallidus
Latin for “pale globe“
AKA, paleostriatum or dorsal pallidum
Output to substantia nigra
Very large neurons
Very large dendritic arbors
3-dimensional shape of flat discs
Involved in plan & inhibit move
regulation of voluntary movement
regulate subconscious movements
If damaged, can cause movement disorders
Balances excitatory action of cerebellum
allow people to move smoothly
even & controlled movements
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Substantia Nigra
Located in pons
Important role in reward, addiction & movement
Latin for black substance
due to high levels of neuromelanin found in dopaminergic neurons
Discovered in 1784
Largest nucleus in midbrain
Two substantiae nigrae; one on each side
Function
eye movement
motor planning
reward-seeking
learning
addiction
Mediated thru striatum
Co-dependence between striatum & substantia nigra
Looks like a continuous band
Two parts with very different connections and functions:
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Pars Compacta
Supplies striatum with dopamine
Heavily involved in learned responses to stimuli
Activity increases when new $ is presented
Partial dopamine deficits do not affect motor control
Can lead to disturbances in the sleep-wake cycle
Especially in hippocampus
Parkinson’s
Neurodegenerative disease
tremor, stiffness, akinesia
bradykinesia, fatigue, depression
Death of dopaminergic neurons in pars compacta
Impacts motivation
Hunger fails to initiate movements
“Paralysis of will”
kinesia paradoxica
Moves easily in emergency
Immobile after issue passed
Animal with severe basal ganglia damage won’t move toward food
Even if placed within inches
Chew & swallow if put in mouth
Why neurons die is unknown
unique susceptibility?
abnormalities in mitochondrial?
result in abnormal protein handling and neuron death
Dopaminergic neurons in pars compacta contain less calbindin
protein involved in calcium ion transport within cells
excess calcium in cells is toxic
Plasticity of pars compacta is robust
no symptoms until 50-80% of pars compacta dopaminergic neurons have died
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Pars Reticulata
output to rest of brain
spontaneously fire action potentials
inhibits targets of basal ganglia
decreases in inhibition are associated with movement
Parkinson’s and epilepsy
Altered patterns of firing
single-spike
burst firing
Schizophrenia
Patients have increased levels of dopamine
dopamine antagonists remain a standard and successful treatment for schizophrenia
Substantia nigra’s pars compacta
reduction in synaptic terminal size
more active NMDA receptors
reduced dysbindin expression
Wooden Chest Syndrome
aka, fentanyl chest wall rigidity syndrome
rare side effect of synthetic opioids (ie Fentanyl)
generalized increase in skeletal muscle tone
increased dopamine release and decreased GABA release in substatia nigra/striatum
most pronounced on chest wall muscles
leads to impaired ventilation
most common in anesthesia where rapid and high doses given intravenously
Cocaine
inhibition of dopamine reuptake
cocaine is more active in VTA than substantia nigra
increases metabolism in substantia nigra
altered motor function
also inhibits spontaneous firing by the pars compacta
inactivation of substantia nigra as treatment for cocaine addiction?
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Subthalamic nucleus (also called Luys’ Body)
Input from striatum & cerebral cortex
Output to the globus pallidus
Small lens-shaped nucleus; major part of subthalamus
Functionally part of basal ganglia
Location
ventral to thalamus
dorsal to substantia nigra
medial to internal capsule
Discovered 1865, by Jules Luys
Structure
long sparsely-spiny dendrites
elliptical dendritic arbors
Spontaneously firing cells
Pace-maker of the brain?
Oscillatory and synchronous activity
Stimulated to treat Parkinson’s
causes nearby astrocytes to release ATP
precursor to adenosine
catabolic process
Damage
small vessel stroke in patients with diabetes, hypertension, or a history of smoking
produces hemibaliismus
uncontrollable flinging movements of arms and legs
Functions
impulse control
OCD cause?
action selection?
Basal ganglia all work together
Impacts
Eye movements
Action selection
Voluntary motor control
Inhibits motor systems
Procedural learning
Eye movements
Habits
Lots of brain regions work
Basal ganglia impacts implicit learning
Action selection?
Which behavior to do when?
Parkinson’s
Cerebral palsy
Damage to basal ganglia during 2nd and 3rd trimester
Foreign accent syndrome
Some combination of problems in cerebellum, Broca’s area & basal ganglion
Caused by stroke or injury
Mispronunciation of words
Listener’s hear it as accent
Not new vocabulary
Sufferer’s may imitate other aspects to normalize syndrome
