Vasopressin(4-9) fragment activates V1a-type vasopressin receptor in rat supraoptic neurones

Abstract

The effect of vasopressin fragment 4-9 (AVP(4-9)) was investigated on freshly dissociated rat supraoptic neurones by measuring changes in intracellular calcium concentration ([Ca2+]i) using fura-2 microspectrofluorimetry. In 60% of neurones responding to vasopressin, AVP(4-9) induced a transient rise in [Ca2+]i that was dose-dependent in the concentration range 10 nM to 1 microM AVP(4-9) and strongly decreased in Ca2+-free buffer (84% inhibition). This [Ca2+]i response was completely and reversibly abolished by SR 49059 (1O nM), a specific V1a receptor antagonist, but not by SR 121463A, a specific V2 receptor antagonist. Our results demonstrate the presence of functional receptors activated by AVP(4-9) on vasopressin-sensitive neurones that possess the apparent pharmacological profile of the V1a-type vasopressin receptor.

Regulation of activity‐dependent dendritic vasopressin release from rat supraoptic neurones

“…However, the physiological consequence of vesicle priming in vasopressin cells has yet to be determined. Neuropeptides released from dendrites are at very high local concentrations (Ludwig & Leng, 1997) and might have long half‐lives, and even degradation produces shorter, but still active, fragments (Gouzenes et al 1999). Not only can their local actions be prolonged, but diffusion through the brain extracellular fluid might allow them to act on receptors on neurones at a distance from their sites of release (Landgraf & Neumann, 2004), including regions involved in behaviour regulation that are known to be influenced by oxytocin and vasopressin, but which have no direct anatomical connection with magnocellular neurones (see Engelmann et al 1996; Ferguson et al 2002).…”