Opioid involvement in the adaptive change of 5-HT1 receptors induced by chronic restraint.
L Cancela, M Volosin, V A Molina
European journal of pharmacology February 13, 1990 DOI: 10.1016/0014-2999(90)90025-2 via PubMed
Summary
AI-generated from the abstractRats immobilized for 2 hours daily over 7 days developed a heightened behavioral response to a serotonin receptor agonist, 5-MeODMT, measured by forepaw treading and hind-limb abduction. Giving naloxone before each stress session fully blocked this increased reactivity. Conversely, pairing morphine or beta-endorphin with immobilization for 3 days produced an even stronger response than immobilization alone. Chronic immobilization did not affect shaking behavior induced by another serotonin precursor, 5-HTP. These findings suggest chronic stress selectively adapts the 5-HT1 serotonin site and activates an opioid mechanism likely involved in that adaptation.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Naloxone Morphine Beta-endorphin |
| Duration | 7-day immobilization period, 24-hour post-stress testing |
| Citations | 31 |
| Key finding | Chronic stress selectively increases behavioral reactivity to a 5-HT1 agonist through an opioid-dependent mechanism. |
Abstract
Rats immobilized for 2 h daily for 7 days showed an increased behavioral response (forepaw treading and hind-limb abduction) to 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) 24 h after the last stress session. An injection of naloxone before each stress session fully antagonized the increased behavioral reactivity to 5-MeODMT. Treatment with morphine or beta-endorphin associated with each immobilization session for 3 days produced a response to 5-MeODMT higher than that of animals subjected to immobilization only. Chronic immobilization for 7 days did not affect the shaking behavior induced by 5-hydroxytryptophan (5-HTP) 24 h after the last restraint session. These findings suggest that chronic stress may induce a selective adaptive change of the 5-HT1 site and activate an opioid mechanism that is most likely to be involved in the development of this adaptive change.