Biomedical subjects

M Maltchik

Publications and source records attributed to M Maltchik.

4 recordsLinked to original sources

PubMed1991

Retrieval effects of beta-endorphin and naloxone, and the novelty-induced antinociception in the developing rat.

Three experiments were conducted to assess the retrieval effects of a single dose of beta-endorphin and of naloxone, and of the novelty-induced antinociception response in the developing rat. Wistar rats 30, 45, 60, and 90 days old from our breeding stock were used. Animals were trained and tested, with a 24-h interval between sessions, in a two-way active avoidance task (using 20 presentations of a 5-s, 1-kHz tone and a 0.4-mA footshock) or in a step-down inhibitory avoidance task (using a 60-Hz, 0.2-mA footshock). Saline (1.0 ml/kg), beta-endorphin (2.0 microgram/Kg), or naloxone (0.8 mg/kg), was administered ip immediately after training, and saline or beta-endorphin was administered 6 min before testing. The retrieval enhancing effects of post-training naloxone and pretest beta-endorphin, and the retrieval impairing effect of post-training beta-endorphin, were consistently observed only in 60- and 90-day-old rats, on both tasks. In a third experiment, another group of naive rats was placed for 2 min in a novel environment (the shuttlebox) and nociception was assessed by the tail-flick method. Novelty-induced antinociception was observed only for 60- and 90-day-old rats, and this response was cancelled by naloxone given 6 min before exposure to novelty. These results suggest that both the retrieval effects of naloxone and beta-endorphin, in the doses used, and the novelty-induced antinociception response, which are possibly dependent on the activity of hypothalamic beta-endorphin system, become established between 45 and 60 days postnatal in the rat.

Animals↗

PubMed1990

Retrieval effects of both post- and presession beta-endorphin administration in a three-session paradigm.

Rats were submitted to three sessions, with a 24-hr interval between, of step-down inhibitory avoidance task using a 60-Hz, 0.3-mA footshock, or of two-way active avoidance task using 25 presentations of a 5-sec. 1-kHz tone and a 0.4-mA footshock. Animals received intraperitoneal injections of either saline or beta-endorphin (2.0 microgram/kg) after the first session, and before the second or the third sessions, in a 2 x 2 x 2 design. beta-Endorphin given before the second or the third sessions improved retention for both tasks, but when administered after the first session, it impaired retention for the second session. The administration of beta-endorphin after the first session prevented the retrieval enhancement by the opioid given before the third session. Rats receiving beta-endorphin both after the first and before the second sessions, whilst showing no retrieval impairment on the second session, also did not show the pre-third session beta-endorphin retrieval enhancing effect. These data suggest that the post-first session exaggeration of the endogenous opioid state by beta-endorphin administered after the first session causes a long-lasting change in retrievability for the active and inhibitory avoidance tasks, as shown by the lack of the retrieval enhancing effect of beta-endorphin given before the third session.

Animals↗

PubMed1990

Distinct mechanisms underlying memory modulation after the first and the second session of two avoidance tasks.

Rats were subjected to three consecutive sessions, one session per day, of either a step-down inhibitory avoidance task using a 60-Hz. 0.3-mA footshock, or a two-way active avoidance task using 20 presentations of a 5-s, 1-kHz tone and a 0.3-mA footshock. After either the first or the second training session animals received an intraperitoneal injection of ACTH (0.2 microgram/kg), epinephrine-HCl (5.0 micrograms/kg), or naloxone-HCl (0.8 mg/kg). All these treatments caused memory facilitation on both tasks when administered after the first training session. When administered after the second training session only ACTH and adrenaline were effective, on both tasks. As previous physiological and pharmacological reports point to the activation of the brain beta-endorphin system after the first, but not the second, session of a task, we propose that (a) memory facilitation by naloxone depends on the previous activation of the brain beta-endorphin system; and (b) memory facilitation due to ACTH or epinephrine does not depend on the opioid activity, so their effects are expressed after both the first and the second training sessions. It was also observed that the enhancement of performance in the second training session due to post-training facilitatory treatments carried over to the test session. These results suggest that some form of consolidation occurs both after the first and after the second training session.

Animals↗

PubMed1990

Beta-endorphin enhancement of retrieval in a three-session paradigm.

Rats were submitted to three consecutive sessions, one session per day, of step-down inhibitory avoidance task (60-Hz, 0.3-mA footshock) or of two-way active avoidance task (25 trials of a 5-s, 1-kHz tone and a 0.4-mA footshock). Animals received intraperitoneal (ip) injections of saline or beta-endorphin (2.0 micrograms/kg) before or after the second session and before the third session. beta-Endorphin given before either the second or the third session improved retention of both tasks, while its administration after the second session had no effect upon performance on both tasks. In Experiment 2, it was shown that rats receiving naloxone (0.2 mg/kg) ip after the first session did not exhibit the enhancement of retrieval by beta-endorphin administration before the second session, so a non-state-dependent improvement of retrieval by the opioid seems to be unlikely. In view of these results we can propose that the presession retrieval enhancing effect of beta-endorphin is due to an endogenous state dependency on the opioid that can be expressed either in the second or in the third session of aversive tasks.

Animals↗