Series of subcortical structures that are intimately involved with various aspects of movement. They are super important but mostly communicate amongst themselves and eventually signal with the motor cortex (but never directly with the spinal chord)
Striatum
Biggest + main input site of the BG. Inputs from cortical and lymbic structures like the thalamus and amygdala. Most of its neurons are GABAergic and called spiny projection neurons (SPNs) with different types of dopamine receptors (some i some e). Divided into dorsal and ventral
Dorsal striatum
Made up of caudate nucleus and putamen, which are indistinguishable in rodents. Contributes to learning of habitual behaviors.
Dorsal striatum
Receives excitatory glutamatergic input from the thalamus and the motor cortex. Receives dopaminergic projection from the substantia nigra pars compacta
Nigrostriatal pathway
Pathway connecting the substantia nigra pars compacta to the dorsal striatum
Caudate
Part of dorsal striatum for goal-oriented actions, sets of motor behaviors made because we know what consequences we want and how to get them. OPERANT CONDITIONING
Putamen
Part of dorsal striatum for motor-associated procedural learning tasks, like the mirror tracing task, which involves learning how to draw while only seeing a reflection of your hand
dSPNs (direct) = express dopamine D1 receptors and go into the internal globus palladus (GPi). When activated it increases motor activity.
iSPNs (indirect) = express dopamine D2 receptors and go into the external globus palladus (GPe). Activation decreases motor activity.
We need dSPNs to drive intended motor functions and iSPNs to inhibit competing ones. Issues in this, like in Parkinson's, lead to motor dysfunction
Spiny projection neuron
SPN (on the GABAergic dopamine producing cells in the striatum)
Ventral striatum includes the olfactory tubercule and the nucleus accumbens (divided into a core and shell)
Ventral striatum
Important for reward, motivation, and aversion. Uses dopamine as a "learning signal" and also in response to unexpected rewards, like sex or sugar. Drugs of abuse artificially drive up these signals and cause addiction
Ventral striatum inputs = glutamatergic afferents from prefrontal cortex and limbic areas like thalamus, hippocampus, and amygdala. Dopaminergic inputs come from the ventral tegmental area of the midbrain
Globus Pallidus (GP) looks like a pale globe when you dissect it. 2 components.
interior (GPi) = movement promoting, dSPNs from DS
exterior (GPe) = movement inhibiting, iSPNs from DS
Subthalamic nucleus (STN)
Part of indirect pathway. Inputs = inhibitory GABAergenic projections from the GPe. Outputs = glutamatergic signals into the GPi. Deep brain stimulation here helps with the symptoms of Parkinson's
Deep brain stimulation (DBS)
Puts electrodes into the brain with a preprogrammed external battery pack that helps get the brain to work properly. Can alleviate Parkinson's symptoms when you put it in the STN
Substantia nigra (SN)
Largest midbrain structure, appears dark in dissection because of heavy neuromelanin expression. Divided into pars compacta (SNpc) and pars reticulata (SNpr)
Substantia nigra pars compacta
Contains dopamine expressing neurons that project into the dorsal striatum. Degenerates with Parkinson's disease.
Substantia nigra pars reticulata
Part of the SN that gets GABAergic inputs from DS and excitatory inputs from the STN. Output = GABAergic and axons terminates in the thalamus
Bradykinesia
Slowness of movement
Hyperkinesia
Uncontrolled movement
Huntington's disease
Rare neurodegenerative disease (hyperkinesia + cognitive changes + less coordination = dementia) that is fatal within 15 years. Presents between 30 and 50, and is caused by too many repeats of glutamine in the huntingtin (htt) gene. The more repeats, the more severe and early onset the case is. Theory is htt accumulates in neurons causing neurodegeneration.
Parkinson's disease
Affect 1% of people over 60, and has strong genetic and environmental components. Caused by less SNpc dopamine entering the dorsal striatum, which means dSPNs are more active than iSPNs, causing motor deficiencies. Cause is unknown, but Lewy bodies and oxidative stress leading to neurodegeneration are leading theories