title: A computer model of neuronal pathways in the basal ganglia.
abstract: Disorders of the basal ganglia and the extrapyramidal motor system exhibit an imbalance of neurotransmitter concentrations in affected neurons. For three synapses with dopamine, acetylcholine, and gamma-amino butyric acid (GABA), mathematical models of synaptic transmission are developed. To describe the kinetics of transmitter substances, compartment analysis is used. Membrane potential behaviour is described by the Hodgkin-Huxley equations with an additional equation accounting for a presynaptic calcium current mediating transmitter release. At the postsynaptic site, activated receptor molecules control the activity of ion channels, eliciting either inhibitory or excitatory postsynaptic potentials. A simple model of the feedback loop connecting the caudate nucleus and the substantia nigra is simulated on a digital computer using the simulation language ACSL. A comparison of the control case with a model of Parkinson's disease shows a shift of eigenvalues towards zero in the diseased state.
mesh_terms: D000109:Acetylcholine / Q000502:physiology; D001479:Basal Ganglia / Q000502:physiology*; D003201:Computers; D004298:Dopamine / Q000502:physiology; D005246:Feedback; D006801:Humans; D008564:Membrane Potentials; D008959:Models, Neurological; D010300:Parkinson Disease / Q000503:physiopathology; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D004298:Dopamine