Hippocampal synaptic plasticity as a biological substrate underlying episodic psychosis.
Structural change in the hippocampal formation has become popular as a proposed neurobiological substrate for schizophrenic disorders. It is postulated that behavioral plasticity in the form of long-term potentiation of hippocampal synaptic transmission is an attractive putative mechanism for the mediation of transient psychosis. Moreover, the disturbed hippocampal neuroarchitecture found in schizophrenic brain may be susceptible to potentiation and dysfunctional to the degree that delusions and hallucinations develop. Partial and selective blockade of the receptors mediating potentiation may prove to be an efficient means of preventing psychotic episodes and avoiding further damage to the involved network. Basic research, utilizing experimental models such as intraventricular kainic acid injection, may help to clarify the anatomical and physiological substrate of psychosis.
Port
R L
RL
Department of Psychology, Slippery Rock University, PA, USA.
Seybold
K S
KS
D001143:Arousal / Q000502:physiology; D004298:Dopamine / Q000502:physiology; D006624:Hippocampus / Q000503:physiopathology*; D006801:Humans; D008032:Limbic System / Q000503:physiopathology; D019965:Neurocognitive Disorders / Q000503:physiopathology* / Q000523:psychology; D009473:Neuronal Plasticity / Q000502:physiology*; D010507:Periodicity; D012559:Schizophrenia / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D013569:Synapses / Q000502:physiology*
D004298:Dopamine