Abstract：
:The N-methyl-D-aspartate channel blocker phencyclidine is known to induce psychotic episodes in normal subjects and exacerbate psychosis in schizophrenics; however, its site of action is not clear. The prefrontal cortex, hippocampus, and basal ganglia are brain regions that appear to play a role in the pathophysiology of schizophrenia, and therefore are the most likely to be involved in the psychotomimetic action of phencyclidine. In this study, systemic administration of phencyclidine reduced the frequency and duration of the spontaneously occurring depolarized plateaus observed in the membrane potential of accumbens neurons recorded intracellularly in vivo. Furthermore, recordings from rats pretreated with phencyclidine yielded proportionately fewer neurons showing depolarized events compared with untreated animals. These results suggest that phencyclidine may interfere with the generation of the depolarized ("up") state of the accumbens neuron membrane potential, which we had previously shown is dependent upon hippocampal input and is necessary for action potential discharge in these neurons. This action of phencyclidine is proposed to impair the flow of cortical information through the nucleus accumbens, and thereby mimic the consequences of the hippocampal deficit proposed to contribute to the pathophysiology of schizophrenia.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
O'Donnell P,Grace AAdoi
10.1016/s0306-4522(98)00190-0subject
Has Abstractpub_date
1998-12-01 00:00:00pages
823-30issue
4eissn
0306-4522issn
1873-7544pii
S0306452298001900journal_volume
87pub_type
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