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Behavioral Pharmacology

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Working memory impairment in chronic phencyclidine-treated mice

  • P3-353
  • 有銘 預世布 / Yosefu Arime:1 秋山 一文 / Kazufumi Akiyama:1 
  • 1:獨協医科大学 精神生物学 / Department of Biological Psychiatry and Neuroscience, Dokkyo Medical University of Medicine 

Phencyclidine (PCP) causes psychotic symptoms resembling schizophrenia in healthy subjects and exacerbates psychosis in schizophrenic patients. This robust psychotomimetic action of PCP is considered to be ascribed to its pharmacological profile of the NMDA receptor antagonist. In addition, chronic PCP treatment produces several behavioral deficits such as hyperactivity, impairments in social interaction and cognitive dysfunctions in rodents, indicating the validity of chronic PCP administration as a suitable model for schizophrenia. Recently, it is suggested that in human the prefrontal cortex are predominantly involved in working memory tasks, whereas in animals these tasks are often dependent on the hippocampus (Pratt et al., Nat Rev Drug Discov 2012).
To assess working memory in mice, we used the task modified for mice from the discrete paired-trial variable-delay task for rats (Aultman and Moghaddam., Psychopharmacology 2001), which is dependent on the prefrontal cortex. Mice, which were pre-trained with the discrete paired-trial delayed alternation in T-maze (training session), were chronically administered PCP (10 mg/kg, s.c.) or saline for 14 days. After withdrawal, their working memory was assessed at variable delays (5, 15 or 30 sec) in three consecutive days (test session).
Mice, which were chronically treated with saline, showed delay-dependent change in correct responses. And, mice with repeated PCP treatment displayed significant reduction in correct responses at all retention intervals compared to chronic saline-treated mice.
We here found that chronic PCP-treated mice showed impairment of working memory in the prefrontal cortex-dependent task. These results suggest that these mice might have functional deficits in prefrontal network involving other brain regions. Therefore, we are currently exploring causative neural circuits and cellular basis in this model.

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