Marcia Henriques Xavier

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.

Interaction between repeated restraint stress and concomitant midazolam administration on sweet food ingestion in rats

Emotional changes can influence feeding behavior. Previous studies have shown that chronically stressed animals present increased ingestion of sweet food, an effect reversed by a single dose of diazepam administered before testing the animals. The aim of the present study was to evaluate the response of animals chronically treated with midazolam and/or submitted to repeated restraint stress upon the ingestion of sweet food. Male adult Wistar rats were divided into two groups: controls and exposed to restraint 1 h/day, 5 days/week for 40 days. Both groups were subdivided into two other groups treated or not with midazolam (0.06 mg/ml in their drinking water during the 40-day treatment). The animals were placed in a lighted area in the presence of 10 pellets of sweet food (Froot loops). The number of ingested pellets was measured during a period of 3 min, in the presence or absence of fasting. The group chronically treated with midazolam alone presented increased ingestion when compared to control animals (control group: 2.0 +/- 0.44 pellets and midazolam group: 3.60 +/- 0.57 pellets). The group submitted to restraint stress presented an increased ingestion compared to controls (control group: 2.0 +/- 0.44 pellets and stressed group: 4.18 +/- 0.58 pellets). Chronically administered midazolam reduced the ingestion in stressed animals (stressed/water group: 4.18 +/- 0.58 pellets; stressed/midazolam group: 3.2 +/- 0.49 pellets). Thus, repeated stress increases appetite for sweet food independently of hunger and chronic administration of midazolam can decrease this behavioral effect.

Effect of repeated restraint stress on memory in different tasks

The present study investigated the effect of repeated stress applied to female rats on memory evaluated by three behavioral tasks: two-way shuttle avoidance, inhibitory avoidance and habituation to an open field. Repeated stress had different effects on rat behavior when different tasks were considered. In the two-way active avoidance test the stressed animals presented memory of the task, but their memory scores were impaired when compared to all other groups. In the habituation to the open field, only the control group showed a significant difference in the number of rearings between training and testing sessions, which is interpreted as an adequate memory of the task. In the handled and chronically stressed animals, on the other hand, no memory was observed, suggesting that even a very mild repeated stress would be enough to alter habituation to this task. The performance in the inhibitory avoidance task presented no significant differences between groups. The findings suggest that repeated restraint stress might induce cognitive impairments that are dependent on the task and on stress intensity.

The influence of amino acids on mitogen-activated proliferation of human lymphocytes in vitro

Recurrent infections are common features in patients affected by various aminoacidopathies. Since these disorders are biochemically characterized by tissue accumulation of amino acids, it is possible that these compounds may act as immunosuppressants. We therefore investigated the influence of 21 amino acids on in vitro cellular growth of lymphocytes stimulated with phytohaemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM), a recognized test of cellular immunocompetence. Human peripheral lymphocytes were cultured in flat-bottomed 96-well microplates at 37 degrees C for 96 (PHA and Con A) or 144 h (PWM) in the presence of one mitogen at different concentrations and of one amino acid added at doses of 2, 4 or 8 mM. Cell reactivity was measured by the incorporation of tritiated thymidine into cellular DNA and compared to that of identical cultures with no amino acids added (controls). We found that among the 21 amino acids tested, cysteine stimulated lymphocyte growth, whereas glutamate, tryptophan, phenylalanine and glutamine caused significant inhibition. These results may reflect an immunomodulatory role for some amino acids.

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

Abstract 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 mg/kg) 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 ip epinephrine or saline immediately after training. The test session was carried out 48 h after training. Epinephrine (25 or 625 mg/kg) caused an increased glycemia in fed rats, but no effect was observed in fasted animals. Administration of epinephrine 25 mg/kg induced a facilitation of memory, while epinephrine 625 mg/kg 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.