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      Possible Involvement of the Hypothalamic Dopaminergic System in the Prolactin-Inhibitory Effects of the Pineal Gland in Blind-Anosmic Male Rats

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      S. Karger AG

      Pineal gland, Dopamine, Rat, blind, Prolactin, Anosmia

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          The purpose of the present study was to assess whether the pineal-induced suppression of prolactin (PRL) cell activity in blind-anosmic (BA) rats was possibly mediated via the hypothalamic dopaminergic system. Prepubertal male rats were divided into the following groups: sham-operated (Sham), BA and blind-anosmic-pinealectomized (BAP). Animals from each group were sacrificed 1, 4 and 8 weeks after the operations. Blinding and anosmia resulted in pineal-dependent decreases in the weight of the testes, accessory organs and anterior pituitaries at 4 and 8 weeks but not 1 week after the operations. Likewise serum PRL levels were significantly decreased in BA rats at 4 and 8 weeks but this effect was not prevented in BAP rats. Hypothalamic dopamine (DA) turnover in BA rats at 1 week was twice that seen in either the Sham or BAP groups at that time; this effect ended by 4 weeks. There were no effects of any treatment on DA turnover at 8 weeks. Finally, PRL cell sensitivity to DA inhibition was determined by measuring the release of PRL from pituitaries incubated in vitro with either vehicle or 5 × 10<sup>–7</sup> M DA. None of the treatments caused significant alterations in the response to DA, though this must be interpreted with caution since only one dose of DA was used. From these data we conclude that: (1) there is an increase in DA neuron activity that precedes the inhibition of both PRL secretion and the reproductive system in BA rats, and (2) the inhibition of PRL cell activity in these animals is apparently not due to an increase in sensitivity to DA.

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          Author and article information

          S. Karger AG
          02 April 2008
          : 48
          : 1
          : 1-7
          Department of Anatomy, College of Medicine, University of Arizona, Tucson, Ariz., USA
          124982 Neuroendocrinology 1988;48:1–7
          © 1988 S. Karger AG, Basel

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          Pages: 7
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