0907 - Basal Ganglia Flashcards
What are the constituents of the basal ganglia?
Striatum - Caudate, Putamen, (n. accumbens)
Pallidum - Globus pallidus - medial (internal) and lateral (external) segments - (includes substantia nigra pars reticulata).
Subthalamic nucleus
Substantia nigra (pars compacta)
Outline the neostriatum
Connects to various areas of the cortex. Comprises caudate and putamen.
Inputs come from SNpc and Cortex. Outputs to GPi and GPe.
Caudate - mainly connected to frontal and pre-frontal areas and posterior parietal cortex, influence on social/moral behaviours. More active during acquisition of new motor skills.
Putamen - mainly connected to somatic cortical areas and has a mapped representation of the body.
Describe the basic circuitry involving the basal ganglia, thalamus, and cerebral cortex.
Basal ganglia basically works to connect one part of the cortex to another and integrate everything between them. Decision or plan of what to do comes from frontal/parietal and input from temporal/insular/cingulate. This goes to basal ganglia, which links it with ‘regulators’ and other cortical systems. Outputs to thalamic nuclei, then SMA, M1, and Action performed.
Outline the different motor loops and their main putative roles in regulating a range of behaviours
Motor Loop
Putamen-based.
Allows scaling strength of muscle contractions in collaboration with SMA. Putamen provides a reservoir of learned programs.
Outline the different motor loops and their main putative roles in regulating a range of behaviours
Cognitive loop
Caudate based. Prefrontal/PPC inputs to putamen/caudate and GP, which outputs to ventral-anterior of thalamus and then to supplementary motor area.
Planning ahead for an learning motor intentions. Once learned, they move to motor loop.
Outline the different motor loops and their main putative roles in regulating a range of behaviours
Limbic loop
Limbic Cx outputs to N Accumbens, which outputs to medial-dorsal thalamus and inferior pre-frontal Cx. Involved in motor responses to environment - rich in dopamine.
Reward/motivational behaviours and memory. Motor expression relevant to emotions (smiling/gesturing). Parkinsons Disease leads to problems with expressions - also pathologically addictive behaviours.
Limbic Cx inputs to N accumbens, goes to MD of thalamus, and inferior pre-frontal Cx (limbic system).
Outline the different motor loops and their main putative roles in regulating a range of behaviours
Occulomotor loop
Frontal eye fields and PPC inputs to caudate and SNr, as well as superior colliculi. Caudate and SNR inhibit SC, and output to ventral anterior thalamus, which outputs to frontal eye fields.
Parkinsons leads to problems with saccades.
Outline the Direct and indirect pathways to cortex
Direct pathway (Go! pathway) feeds information from cortex to thalamus via neostriatum and GPi, resulting in increased muscle activity.
GPi tonically inhibits the thalamus, direct pathway disinhibits certain areas, allowing some movements to occur.
Indirect (Stop!) pathway includes a ‘side loop’ from GPe to STN to GPi. Keeps GPi active, meaning inhibition continues and net effect is to suppress muscle activity.
Modulatory (via) SNc - adjusts balance between them, allowing for an appropriate level of activity.
What is the Role of Dopamine in the basal ganglia?
Allows ‘fine tuning’ of the circuits - directly activating or inhibiting cortical inputs in the striatum. Enables preferred pathways to be ramped up or inhibited, ensuring the right balance is struck between the direct and indirect pathways.
Underlying anomalies Parkinson’s Disease
PD - Dopaminergic cells in the SNc are lost, leading to eventual death of neurons in the striatum and the disengagement of the direct (Go) pathway. As a result, the indirect pathway prevails by default, leading to decreased inhibition of GPi and thus enhanced inhibition of the thalamus - hypokinesia.
Underlying anomalies Huntington’s Disease
Huntington’s - GABA-ergic cell death in the neostriatum means that the brakes are applied harder to the STN, meaning less stimulation of the GPi/SNr, so they can’t inhibit Thalamus as effectively anymore. Means that suppressed motor behaviours are no longer suppressed. Corticostriatal neurons retrogradely degenerate because the DA1 cells are dead, so loss of cortex.
How does the reticular formation influence locomotion? Which area of it?
Pedunculo-pontine RF via reticulospinal tracts that terminate at all cord levels. The medial component facilitates extensors, and lateral releases them.
