The effects of acute and repeated restraint stress on the nociceptive response in rats.

The effects of acute and repeated restraint stress on nociception, as measured by the tail-flick latency, were studied in adult male and female rats. After the exposure to a single restraint session, both male and female rats presented an increased latency in the tail-flick test. On the other hand, chronically stressed females presented a performance similar to the control group, whereas chronically stressed male rats responded to restraint with a decrease in the tail-flick latency. This response could be determined by the chronic treatment itself or by the restraint done just before the measurement. Thus, the effect of chronic stress upon basal tail-flick latency was evaluated. In male rats, this latency was significantly decreased in the stressed animals compared with the control group. In female rats, no difference between those groups was observed. Therefore, the results suggest that: (a) acute restraint stress induces an analgesic response in both male and female rats, and (b) there is a gender-specific nociceptive response induced by repeated restraint stress with a hyperalgesic effect in response to stress only in males.

Epinephrine effects on memory are not dependent on hepatic glucose release.

Epinephrine released or administered soon after a given training task modulates memory processes. Since epinephrine does not readily cross the blood-brain barrier, studies have suggested that some of the central effects of epinephrine might be mediated by peripheral release of glucose. These experiments examined the involvement of blood glucose levels in the posttraining effects of peripherally administered epinephrine. The effects of the administration of epinephrine (25 and 625 microg/kg) [corrected] on memory of an inhibitory avoidance task were evaluated in fed and fasted rats (depleted glycogen stores in liver). Blood glucose levels after the task in each group were also measured. Female Wistar rats were divided in two groups. Fed and 48-h-fasted animals were submitted to the inhibitory avoidance task and received i.p. epinephrine or saline immediately after training. The test session was carried out 48 h after training. Epinephrine (25 or 625 microg/kg) [corrected] caused an increased glycemia in fed rats, but no effect was observed in fasted animals. Administration of epinephrine 25 microg/kg [corrected] induced a facilitation of memory, while epinephrine 625 microg/kg [corrected] impaired retention (either in fasted or in fed animals). There was no relation between increased glycemia induced by epinephrine and its effects on memory, since this drug presented its classical effects independently of the previous state of the animal (fed or fasted). The results of the present study suggest that the effects of systemic released or administered epinephrine on memory processes are not dependent on hepatic glucose release.