HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Silinsky, E M Articles by Redman, R S Search for Related Content PubMed PubMed Citation Articles by Silinsky, E M Articles by Redman, R S

Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, IL 60611-3008, USA.

1. It has been suggested that ATP is released together with the neurotransmitter acetylcholine (ACh) and, after hydrolysis to adenosine, is the primary physiological mediator of prejunctional neuromuscular depression. To evaluate whether ATP is released with sufficient rapidity to mediate prejunctional depression, outside-out patches containing both ATP-gated and ACh-gated ion channels were made from acutely dissociated guinea-pig sympathetic neurons and used to detect the co-release of nucleotide and neurotransmitter in frog cutaneous pectoris nerve-muscle preparations. 2. In a normal bathing solution in which muscle nicotinic receptors were blocked, a single stimulus to the motor nerve produced channel openings in the detector patch characteristic of both ATP and ACh. 3. In the remaining experiments, preparations were treated with sufficient hexamethonium (200 microM) to block nicotinic responses in the detector patch. In these experiments, a single temporally isolated nerve impulse caused the synchronous opening of ATP-gated channels in the detector patch with a latency of < 5 ms when patches were placed within 10 microns of the motor nerve ending. This multichannel phasic response was followed by trail of discrete channel openings characteristic of ATP-gated channels. 4. The selective ATP antagonist suramin (50 microM) reversibly eliminated the response to nerve stimulation. 5. The results suggest that ATP is released synchronously together with the neurotransmitter ACh in response to an individual nerve impulse and with a brief latency characteristic of quantal release from synaptic vesicles.

This article has been cited by other articles:

				E. M. Silinsky Selective disruption of the mammalian secretory apparatus enhances or eliminates calcium current modulation in nerve endings PNAS, April 29, 2008; 105(17): 6427 - 6432. [Abstract] [Full Text] [PDF]

				G. Burnstock Physiology and Pathophysiology of Purinergic Neurotransmission Physiol Rev, April 1, 2007; 87(2): 659 - 797. [Abstract] [Full Text] [PDF]

				J. D. Tompkins and R. L. Parsons Exocytotic release of ATP and activation of P2X receptors in dissociated guinea pig stellate neurons Am J Physiol Cell Physiol, November 1, 2006; 291(5): C1062 - C1071. [Abstract] [Full Text] [PDF]

				G. Wollmann, C. Acuna-Goycolea, and A. N. van den Pol Direct Excitation of Hypocretin/Orexin Cells by Extracellular ATP at P2X Receptors J Neurophysiol, September 1, 2005; 94(3): 2195 - 2206. [Abstract] [Full Text] [PDF]

				S. G. Baryshnikov, O. A. Rogachevskaja, and S. S. Kolesnikov Calcium Signaling Mediated by P2Y Receptors in Mouse Taste Cells J Neurophysiol, November 1, 2003; 90(5): 3283 - 3294. [Abstract] [Full Text] [PDF]