尾仲 達史

Salusin-α, and -β were newly discovered as bioactive endogenous peptides (Shichiri et al., 2003). Salusin-β stimulates the secretion of arginine vasopressin (AVP) from perifused rat hypophysis, and coexists with AVP in the rat hypothalamic magnocellular supraoptic (SON) and paraventricular nuclei. In the present study, we investigated the effects of osmotic stimuli on salusin-β-like immunoreactivity (LI) in the rat hypothalamo-neurohypophyseal system, and also examined the effects of salusin-β on the synaptic inputs to the rat magnocellular neurosecretory cells (MNCs) of the SON and the AVP / oxytocin (OXT) release from the rat freshly dissociated SON and neurohypophysis. We demonstrated that salusin-β-LI exhibited markedly increase in the hypothalamo-neurohypophyseal system after osmotic stimuli, and evoked AVP / OXT releases from the neurohypophysis, but not cause significant changes in the excitatory and inhibitory postsynaptic currents of the MNCs. These results suggest that salusin-β is increased by osmotic stimuli, secreted from nerve endings, acting as autocrine / paracrine modulator to stimulate the AVP / OXT release from the neurohypophysis and involved in the regulation of water balance. [J Physiol Sci. 2007;57 Suppl:S172]

To confirm a role of prolactin-releasing peptide (PrRP) on stress response, we examined the effects of restraint stress (RTS), nociceptive stimulus and acute inflammatory stress in rats on the expression of the PrRP gene in the hypothalamus and medulla oblongata using in situ hybridization histochemistry. Moreover, we examined the effects of pretreatment with indomethacin on acute inflammation-induced PrRP gene expression and pretreatment with an anti-PrRP antibody on nociceptive stimulus-induced c-fos gene expression in the hypothalamic paraventricular nucleus (PVN). RTS, nociceptive stimulus and acute inflammatory stress upregulated the PrRP gene expression in the medulla oblongata. Acute inflammation-induced increase in the PrRP gene expression was significantly attenuated almost completely by prereatment with indomethacin. Pretreatment with anti-PrRP antibody attenuated significantly nociceptive stimulus-induced c-fos gene expression in the PVN. RTS, nociceptive stimulus and acute inflammatory stress activate PrRP neurons. Especially, activation of PrRP neurons by acute inflammation was mediated mainly by prostaglandins. Pretreatment with anti-PrRP antibody attenuated stress response via neurons in the PVN. These results suggested that PrRP is a potent and important mediator of stress response in the hypothalamic PVN in rats. [J Physiol Sci. 2006;56 Suppl:S218]