These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The impairment of retention induced by beta-endorphin in mice may be mediated by a reduction of central cholinergic activity.
    Author: Introini IB, Baratti CM.
    Journal: Behav Neural Biol; 1984 Jul; 41(2):152-63. PubMed ID: 6148931.
    Abstract:
    beta-Endorphin (0.03 to 1.00 microgram/kg, ip) impaired retention of a one-trial inhibitory avoidance task in a dose-dependent manner when injected into male Swiss mice immediately post-training, as indicated by retention performance 48 h later. The doses of 0.03 and 0.10 microgram/kg significantly impaired retention while the two higher doses (0.30 and 1.00 microgram/kg) did not significantly affect retention as compared with the control group, but tended to increase retention as compared with the dose of 0.10 microgram/kg. Thus, the dose-response curve shows an U-shaped form. The simultaneous injection of naloxone (0.1 mg/kg, ip) not only shifted the dose-response curve to the right but also prevented the tendency to increase retention latencies of the two higher doses. The two lower doses of beta-endorphin did not lengthen latencies to step-through of mice that had not received a footshock during the training while, under these conditions, the two higher doses of the peptide significantly increased latencies to step-through. This effect was prevented by naloxone (0.1 mg/kg). Taken together these results suggest that the effects of beta-endorphin on retention are the consequence of an interaction with opioid receptors and indicate that the right ascending arm of the dose-response curve would probably be due to a punitive effect of beta-endorphin which was also prevented by naloxone. The impairing effect of post-training administration of beta-endorphin (0.10 microgram/kg) on memory was time-dependent, since it was decreased as the training-treatment interval was increased. These results rule out a pharmacological proactive effect of beta-endorphin on retention performance and suggest that beta-endorphin affects memory consolidation. The simultaneous administration of beta-endorphin (0.10 microgram/kg) with the central muscarinic agonist oxotremorine (12.5 or 50.0 micrograms/kg) completely prevented the impairment of retention induced by beta-endorphin, while the simultaneous administration of the central-acting anticholinesterase physostigmine (17 or 68 micrograms/kg) only partially but significantly attenuated the effect of beta-endorphin on retention. Further, the peripheral-acting anticholinesterase neostigmine (68 micrograms/kg) and the nicotinic blocker hexamethonium (5 mg/kg) modified neither retention nor the behavioral effects of beta-endorphin. These results suggest that the impairment of retention induced by beta-endorphin is probably due to an inhibition of acetylcholine release at central cholinergic synapses which are critical for memory formation.
    [Abstract] [Full Text] [Related] [New Search]