Sensory gating in a computer model of the CA3 neural network of the hippocampus

We have developed a unique computer model of the CA3 region of the hippocampus that simulates the P50 auditory evoked potential response to repeated stimuli in order to study the neuronal circuits involved in a sensory processing deficit associated with schizophrenia. Our computer model of the CA3 h...

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Bibliographic Details
Published in:Biological psychiatry (1969) 1996-12, Vol.40 (12), p.1230-1245
Main Authors: Flach, Karen A., Adler, Lawrence E., Gerhardt, Greg A., Miller, Christine, Bickford, Paula, MacGregor, Ronald J.
Format: Article
Language:English
Subjects:
acetylcholine
Adult and adolescent clinical studies
Animals
Attention - physiology
Biological and medical sciences
computational model
Computer Simulation
Evoked Potentials, Visual - physiology
Hippocampus - physiology
Humans
medial septus nucleus
Medical sciences
Models, Neurological
Nerve Net - physiology
Neurons - physiology
nicotine
Nicotinic Agonists - pharmacology
Nicotinic Antagonists - pharmacology
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Rats
Receptors, Nicotinic - drug effects
Receptors, Nicotinic - physiology
Schizophrenia
Schizophrenic Psychology
Synapses - physiology
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Summary:We have developed a unique computer model of the CA3 region of the hippocampus that simulates the P50 auditory evoked potential response to repeated stimuli in order to study the neuronal circuits involved in a sensory processing deficit associated with schizophrenia. Our computer model of the CA3 hippocampal network includes recurrent activation from within the CA3 region as well as input from the entorhinal cortex and the medial septal nucleus. We used the model to help us determine if the cortical and septal inputs to the CA3 hippocampus alone are responsible for the gating of auditory evoked activity, or if the strong recurrent activity within the CA3 region contributes to this phenomenon. The model suggests that the medial septal input is critical for normal gating; however, to a large extent the activity of the medial septal input can be replaced by simulated stimulation of the hippocampal neurons by a nicotinic agonist. The model is thus consistent with experimental data that show that nicotine restores gating of the N40 evoked potential in fimbria-fornix lesioned rats and of the P50 evoked potential in schizophrenic patients.
ISSN:0006-3223
1873-2402
DOI:10.1016/0006-3223(95)00624-9