The stimulatory effect of male agouti (Dasyprocta prymnolopha) on the onset of female puberty

O objetivo desta pesquisa foi analisar a puberdade em fêmeas de cutias. Não foi observado o inicio da puberdade quando as fêmeas foram mantidas sem os machos. Se um macho adulto era mantido com as fêmeas adultas e não ciclantes, o inicio do ciclo estral era observado após um período de 10 a 60 dias. Quando as fêmeas jovens eram mantidas com o macho, a puberdade se estabelecia aos nove meses. Concluindo que o macho de cutia influencia o inicio da puberdade das fêmeas, e as fêmeas dominantes, aparentemente, inibem ou atrasam a puberdade de outras do grupo. Sugerem-se estudos futuros sobre o controle social na reprodução deste animal.

Stimulatory effects of adenosine on prolactin secretion in the pituitary gland of the rat

We investigated the effects of adenosine on prolactin (PRL) secretion from rat anterior pituitaries incubated in vitro. The administration of 5-N- methylcarboxamidoadenosine (MECA), an analog agonist that preferentially activates A2 receptors, induced a dose-dependent (1 nM to 1 µM) increase in the levels of PRL released, an effect abolished by 1,3-dipropyl-7-methylxanthine, an antagonist of A2 adenosine receptors. In addition, the basal levels of PRL secretion were decreased by the blockade of cyclooxygenase or lipoxygenase pathways, with indomethacin and nordihydroguaiaretic acid (NDGA), respectively. The stimulatory effects of MECA on PRL secretion persisted even after the addition of indomethacin, but not of NDGA, to the medium. MECA was unable to stimulate PRL secretion in the presence of dopamine, the strongest inhibitor of PRL release that works by inducing a decrease in adenylyl cyclase activity. Furthermore, the addition of adenosine (10 nM) mimicked the effects of MECA on PRL secretion, an effect that persisted regardless of the presence of LiCl (5 mM). The basal secretion of PRL was significatively reduced by LiCl, and restored by the concomitant addition of both LiCl and myo-inositol. These results indicate that PRL secretion is under a multifactorial regulatory mechanism, with the participation of different enzymes, including adenylyl cyclase, inositol-1-phosphatase, cyclooxygenase, and lipoxygenase. However, the increase in PRL secretion observed in the lactotroph in response to A2 adenosine receptor activation probably was mediated by mechanisms involving regulation of adenylyl cyclase, independent of membrane phosphoinositide synthesis or cyclooxygenase activity and partially dependent on lipoxygenase arachidonic acid-derived substances.