Search

The effect of right- and left-sided intra- amygdaloid injection of kainic acid on the hypothalamo- hypophyseal-testicular axis was studied in rats. Both right- and left-sided injection of the neurotoxin into the amygdala resulted in a significant decrease in basal testosterone secretion in vitro of both testes and in serum testosterone concentration. In addition, left-sided administration of kainic acid significantly suppressed serum luteinizing hormone level, while right-sided intervention did not alter this parameter. The results of the present study provide further evidence on the involvement of the amygdala in the control of testicular steroidogenesis. Furthermore, the observations suggest functional asymmetry of the amygdala concerning the mechanism of suppressed testosterone secretion.

Somatostatin, and the recently discovered neuropeptide cortistatin, exert their physiological actions via a family of six G protein-coupled receptors (sst1, sst2A, sst2B, sst3, sst4, sst5). Following the cloning of somatostatin receptors significant advances have been made in our understanding of their molecular, pharmacological and signaling properties although much progress remains to be done to define their physiological role in vivo. In this review, the present knowledge regarding neuroanatomical localization, signal transduction pathways, desensitization and internalization properties of somatostatin receptors is summarized. Evidence that somatostatin receptors can form homo- and heterodimers and can physically interact with members of the SSTRIP/Shank/ProSAP1/CortBP1 family is also discussed.

Le polyendocrine-polyneuropathie syndrome (PEPNS, OMIM #616113) est dû à une diminution de l’expression de DMXL2 qui code pour la rabconnectin-3α (rbcn-3α). Ce syndrome comprend notamment un déficit gonadotrope. Les premières investigations de la caractérisation moléculaire de ce déficit chez des souris invalidées pour Dmxl2 dans le cerveau (Nes-Cre;Dmxl2-/+) ont montré une baisse de l’expression et/ou des neurones GnRH. Néanmoins, cette baisse ne suffit pas à expliquer l’infertilité des souris Nes-Cre;Dmxl2-/+ce qui suggère un déficit fonctionnel associé. Le but de ce travail était de caractériser ce déficit fonctionnel.