GSBS Student Publications

Title

Endogenous ATP potentiates only vasopressin secretion from neurohypophysial terminals

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Physiology; Program in Neuroscience

Date

5-16-2008

Document Type

Article

Medical Subject Headings

Action Potentials; Adenosine Triphosphate; Animals; Antineoplastic Agents; Arginine Vasopressin; Male; Nerve Endings; Oxytocin; Patch-Clamp Techniques; Pituitary Gland, Posterior; Platelet Aggregation Inhibitors; Pyridoxal Phosphate; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P2; Suramin; Vasopressins

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

Exogenous ATP induces inward currents and causes the release of arginine-vasopressin (AVP) from isolated neurohypophysial terminals (NHT); both effects are inhibited by the P2X2 and P2X3 antagonists, suramin and PPADS. Here we examined the role of endogenous ATP in the neurohypophysis. Stimulation of NHT caused the release of both AVP and ATP. ATP induced a potentiation in the stimulated release of AVP, but not of oxytocin (OT), which was blocked by the presence of suramin. In loose-patch clamp recordings, from intact neurohypophyses, suramin or PPADS produces an inhibition of action potential currents in a static bath, that can be mimicked by a hyperpolarization of the resting membrane potential (RMP). Correspondingly, in a static versus perfused bath there is a depolarization of the RMP of NHT, which was reduced by either suramin or PPADS. We measured an accumulation of ATP (3.7 +/- 0.7 microM) released from NHT in a static bath. Applications of either suramin or PPADS to a static bath decreased burst-stimulated capacitance increases in NHT. Finally, only vasopressin release from electrically stimulated intact neurohypophyses was reduced in the presence of Suramin or PPADS. These data suggest that there was sufficient accumulation of ATP released from the neurohypophysis during stimulations to depolarize its nerve terminals. This would occur via the opening of P2X2 and P2X3 receptors, inducing an influx of Ca2+. The subsequent elevation in [Ca2+](i) would further increase the stimulated release of only vasopressin from NHT terminals. Such purinergic feedback mechanisms could be physiologically important at most CNS synapses.

Rights and Permissions

Citation: J Cell Physiol. 2008 Oct;217(1):155-61. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal Title

Journal of cellular physiology

PubMed ID

18481265