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Tanaka, S. et al.

Tanaka, Okuno, Numazawa, Yamamoto, Shioda, Yoshida,

Brain responses to acute withdrawal in phenobarbital-dependent rats.

Heat shock proteins (HSP) such as HO-1 and HSP27 have been implicated as functioning in a protective manner against oxidative and physical stress. The objective of the current study was to determine the role of HSPs in drug-withdrawal stress induced in phenobarbital-dependent rats. Increased expression of HO-1 and HSP27 was observed in the hippocampus and the cerebral cortex of phenobarbital-withdrawn rats. Gene expression was measured by Northern and Western blot analyses and in situ hybridization. The induction of HO-1 mRNA was suppressed by the administration of the NMDA receptor antagonist, (+)-5-methyl-10,11-dihydro-5H-dibenzo (a,d) cyclohepten-5,10-imine (MK801). Despite significant upregulation of glutamatergic transmission, neuronal cell degeneration was not apparent. These findings suggest that the induction of HO-1 and HSP27 during withdrawal from phenobarbital dependence may play a role in protection against glutamate toxicity.[1]

References

Brain responses to acute withdrawal in phenobarbital-dependent rats. Tanaka, S., Okuno, Y., Numazawa, S., Yamamoto, T., Shioda, S., Yoshida, T. Eur. J. Pharmacol. (2001) [Pubmed]

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