Neurochemical mechanism for the behavioral disturbances in the Se-deficient mice : an evaluation with in vivo microdialysis.

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We have previously reported that a prolonged Se deficiency in mice results in behavioral alteration. Elucidation of the underlying neurochemical mechanism for this behavioral effect of Se deficiency was the goal of the present study.A model for postweaning Se deficiency was developed using mice ; in this process, we have found that decrease in Se concentration was significantly more pronounced in cerebrum than in cerebellum or in brain stem. Taking this result as well as the results from preceding studies into account, we have examined the extracellular concentration (as an index of release) of dopamine (DA) in the striatum of Se-deficient mice with in vivo microdialysis. In vivo microdialysis was selected to evaluate possible neurochemical effect (s) of Se deficiency because of its direct link to behavioral output. After aporox.4 weeks on low-Se-diet regimen, the Se-deficient group was not different from the control (Se-adequate) group regarding the extracellular concentration of DA under a "basal" condition or under a depolarizing stimulus with high-K^+ perfusion. After 12 week of Se deficiency, the deficient group showed a DA increase upon high-K^+ perfusion, which was significantly greater than the one observed in the control group. To determine whether this alteration in the DA metabolism is related with any behavioral effects of Se deficiency, an open-field test with or without nomifensine (NOM), a selective inhibitor for the DA transporter, was conducted. After 14 week of Se deficiency, the activity in the open-field apparatus was significantly greater in the Se-deficient group than in the control group. Prior administration of NOM increased the activity of both the groups, the effect being slightly exaggerated in the deficient group. In addition, this dose of NOM increased extracellular DA in the striatum. Taken together, these results suggested that the Se deficiency increased the open-field activity by an enhanced DA release in the striatum.