AJP - Regu Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 269: R463-R468, 1995;
0363-6119/95 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lowes, V. L.
Right arrow Articles by Ferguson, A. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lowes, V. L.
Right arrow Articles by Ferguson, A. V.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 2 463-R468, Copyright © 1995 by American Physiological Society


ARTICLES

Vasopressin actions on area postrema neurons in vitro

V. L. Lowes, K. Sun, Z. Li and A. V. Ferguson
Department of Physiology, Queen's University, Kingston, Ontario, Canada.

The area postrema (AP) is a circumventricular organ located on the dorsal surface of the medulla. Substantial evidence suggests that the AP is an important site involved in cardiovascular regulation. Arginine vasopressin (AVP) is thought to act at the AP to increase the sensitivity of the baroreceptor reflex. We have therefore examined the effects of AVP on AP neurons with the use of extracellular single unit recordings in vitro. Coronal medullary brain slices (thickness = 400 microns) were obtained from male Sprague-Dawley rats and maintained in oxygenated artificial cerebrospinal fluid (aCSF). The slices were perfused with AVP (10(-8) to 10(-6) M), and the effect on single AP neurons was recorded. A total of 79 AP neurons was tested of which 50 (63.3%) were excited by AVP and 5 (6.3%) were inhibited, whereas the remaining 24 (30.3%) cells were unaffected. The excitatory effects of AVP were dose dependent: firing rate increased 92.6 +/- 25.8% at 10(-8) M, 289.4 +/- 53.9% at 10(-7) M, and 456.8 +/- 113.1% at 10(-6) M, respectively. We also examined whether these effects of AVP resulted from direct actions of this peptide on AP cells by testing if responses were retained during blockade of synaptic transmission (achieved by perfusion with a low Ca(2+)-high Mg2+ aCSF) in 11 cells excited by AVP. Nine of these cells were excited by AVP during such synaptic blockade. Finally, we demonstrated that the excitatory responses of five AP cells to AVP were all totally abolished by perfusion of slices with aCSF containing the V1 antagonist ([1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid,2-(O-methyl)tyrosine]-Arg8-vasopressin; Peninsula Laboratories, 10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
J. Neurophysiol.Home page
X. Chen and Q. J. Pittman
Vasopressin and Amastatin Induce V1-Receptor-Mediated Suppression of Excitatory Transmission in the Rat Parabrachial Nucleus
J Neurophysiol, October 1, 1999; 82(4): 1689 - 1696.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
M. Kolaj and L. P. Renaud
Vasopressin-Induced Currents in Rat Neonatal Spinal Lateral Horn Neurons Are G-Protein Mediated and Involve Two Conductances
J Neurophysiol, October 1, 1998; 80(4): 1900 - 1910.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online