Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Acute tolerance to the excitatory effects of opioids in the rat hippocampus

Acute tolerance to the excitatory effects of opioids in the rat hippocampus Prolonged iontophoretic administrations of δ‐ and μ‐selective opioid receptor agonists were conducted in the hippocampus of rats, in order to study the possible development of acute tolerance to the excitatory effects of the opioids. Acute tolerance (AT) to the excitatory effects of the 8‐selective opioid receptor agonist Tyr‐D‐Ser‐Gly‐Phe‐Leu‐Thr (DSLET) was observed when the drug was applied locally for 3–5 min in the CA1 hippocampal pyramidal neurons. The acute tolerance was expressed as a decrease in the commissurally evoked spike responsiveness during peptide's administration and led to a long‐lasting potentiation of the population spike (PS) upon its withdrawal. In all cases, where AT and spike potentiation were evident, the population excitatory postsynaptic potential (pEPSP) remained unaltered. Pharmacological studies of AT and long‐lasting spike potentiation showed the following: (1) the non‐selective opioid receptor antagonist, naloxone, while effective in blocking the excitatory effects of DSLET when applied prior and during the application of the latter, failed to exhibit and effect on the long‐lasting potentiating effect of the opioid; and (2) during the spike potentiation phase, administration of DSLET exhibited a depressant effect towards baseline values. This depressant effect of the opioid was evident 2–3 min from the beginning of the application and was completely antagonized by naloxone. The above results show that the development of acute tolerance to the excitatory effects of the DSLET led to long‐lasting spike potentiation, which manifests a withdrawal phenomenon. © 1995 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Research Wiley

Acute tolerance to the excitatory effects of opioids in the rat hippocampus

Loading next page...
 
/lp/wiley/acute-tolerance-to-the-excitatory-effects-of-opioids-in-the-rat-CZqDjduk3b

References (33)

Publisher
Wiley
Copyright
Copyright © 1995 Wiley‐Liss, Inc.
ISSN
0360-4012
eISSN
1097-4547
DOI
10.1002/jnr.490400108
pmid
7714927
Publisher site
See Article on Publisher Site

Abstract

Prolonged iontophoretic administrations of δ‐ and μ‐selective opioid receptor agonists were conducted in the hippocampus of rats, in order to study the possible development of acute tolerance to the excitatory effects of the opioids. Acute tolerance (AT) to the excitatory effects of the 8‐selective opioid receptor agonist Tyr‐D‐Ser‐Gly‐Phe‐Leu‐Thr (DSLET) was observed when the drug was applied locally for 3–5 min in the CA1 hippocampal pyramidal neurons. The acute tolerance was expressed as a decrease in the commissurally evoked spike responsiveness during peptide's administration and led to a long‐lasting potentiation of the population spike (PS) upon its withdrawal. In all cases, where AT and spike potentiation were evident, the population excitatory postsynaptic potential (pEPSP) remained unaltered. Pharmacological studies of AT and long‐lasting spike potentiation showed the following: (1) the non‐selective opioid receptor antagonist, naloxone, while effective in blocking the excitatory effects of DSLET when applied prior and during the application of the latter, failed to exhibit and effect on the long‐lasting potentiating effect of the opioid; and (2) during the spike potentiation phase, administration of DSLET exhibited a depressant effect towards baseline values. This depressant effect of the opioid was evident 2–3 min from the beginning of the application and was completely antagonized by naloxone. The above results show that the development of acute tolerance to the excitatory effects of the DSLET led to long‐lasting spike potentiation, which manifests a withdrawal phenomenon. © 1995 Wiley‐Liss, Inc.

Journal

Journal of Neuroscience ResearchWiley

Published: Jan 1, 1995

There are no references for this article.