Biomedical subjects

C B Oliveira

Publications and source records attributed to C B Oliveira.

4 recordsLinked to original sources

PubMed1990

Effect of atropine and propranolol on retrieval enhancement by a novel experience or by injection of beta-endorphin prior to testing in rats.

Wistar rats were trained in step-down inhibitory avoidance and tested 24 h later. One h prior to testing they were exposed to an open field or to an open field with flashing light (OFL) for 2 min. The OFL-exposed group showed retrieval enhancement for the avoidance task. This effect was mimicked by an injection of beta-endorphin (2.0 micrograms/kg) 1 h prior to testing, and both effects were blocked by the concomitant administration of naloxone (0.8 mg/kg, ip). Propranolol (2.0 mg/kg, ip) and atropine (0.5 mg/kg, ip) injected 6 min before the test completely blocked the retrieval-enhancing effect of both beta-endorphin and OFL. These results suggest that: 1) in rats, novel experiences may induce retrieval enhancement provided they are alerting; 2) the retrieval-enhancing effect of pre-testing exposure to OFL is probably due to activation of the brain beta-endorphin system which triggers late beta-noradrenergic and cholinergic mechanisms acting at the moment of retrieval.

Analysis of Variance↗

PubMed1989

Beta-endorphin and electroconvulsive shock alter the retrieval of two avoidance tasks when given after the first, but not the second, training session.

1. Rats were submitted to three consecutive sessions, one session per day, of two-way active avoidance or of step-down inhibitory avoidance, and received 1 microgram/kg beta-endorphin intraperitoneally or an electroconvulsive shock immediately after the first or after the second training session. 2. Administration of either treatment after the first session caused a reduction of performance in the second session in both tasks. There was no impairment of performance in the third session. 3. Administration of either treatment after the second session did not affect performance during the third session. 4. Therefore the effect of beta-endorphin and of electroconvulsive shock on active and inhibitory avoidance performance was expressed only when treatments were administered after the first, i.e., novel, training experience. We suggest this effect is on mechanisms acting on retrieval, since the retention performances of all groups for the third session were identical.

Animals↗

PubMed1989

Chronic ethanol ingestion selectively affects memory modulation in rats.

Post-training treatment alters memory by different mechanisms. Naloxone enhances memory by antagonism of endogenous beta-endorphin-induced state dependency. Epinephrine facilitates consolidation at low doses and generates state dependency at high doses. Exposure to a session of tones causes retroactive interference through a cognitive effect. The present data show that chronic ethanol ingestion, in rats, inhibited the post-training effect of naloxone and of a high dose of epinephrine on the retention of an inhibitory avoidance task but did not inhibit retrograde interference by a session of tones or retrograde facilitation by a low dose of epinephrine. Therefore, ethanol appears to selectively affect post-training influences related to state dependency.

Animals↗

PubMedDate not supplied

Pre-test administration of beta-endorphin, or of electroconvulsive shock reverses the memory disruptive effect of posttraining electroconvulsive shock.

Memory disruption by posttraining electroconvulsive shock was studied in adult Wistar rats using three different tasks: step-down inhibitory avoidance, two-way active avoidance, and habituation of rearing to an open field. The animals were given training and test sessions 24 hours apart in each of these tasks. Immediate posttraining transcorneal, 15 mA, 60 Hz, 2 sec electroconvulsive shock disrupted memory of the three tasks. The effect was completely reversed by the IP administration of beta-endorphin (2.0 micrograms/kg), 6 min prior to testing, or of another electroconvulsive shock, 30 min prior to testing. These findings indicate that the posttraining electroconvulsive shock did not affect memory storage. In view of the fact that electroconvulsive shock has been previously shown to cause a pronounced decrease of brain beta-endorphin immunoreactivity, attributable to a release of the peptide, the present findings can be interpreted as showing that memory disruption by posttraining electroconvulsive shock results from the induction of state dependency on beta-endorphin.

Animals↗