The effects of the nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester (L-NAME) were investigated in two animal models of anxiety: the elevated plus-maze and the social interaction test. In the elevated plus-maze, L-NAME (12.5-50 mg/kg) had an anxiogenic-like profile as indicated by dose-dependent reductions in the time spent on the open arms, open arm entries, the percentage of open arm entries and head dips, but there was no significant effect on the number of stretch attend postures. In contrast, L-NAME (12.5-50 mg/kg) failed to modify time spent in social interaction but did reduce a measure of vertical activity. The differential effects of L-NAME in the two anxiety paradigms are discussed.
Subchronic (6 days) but not acute injections of nicotine (0.4 mg/kg SC) increased spontaneous activity (P less than 0.01) in an elevated X-maze composed of two open and two enclosed runways. Neither acute nor subchronic nicotine altered significantly the ratio of open:enclosed runway entries (O/E ratio). Diazepam (5 mg/kg PO) had no significant effects on spontaneous activity but increased the O/E ratio (P less than 0.05). Acute nicotine increased (P less than 0.01) whereas subchronic nicotine caused a small decrease (P less than 0.05) in the plasma corticosterone concentration. Both acute and subchronic diazepam decreased the levels of the hormone (P less than 0.01 and P less than 0.05, respectively) although the reduction elicited by chronic diazepam was less than that caused by acute diazepam (P less than 0.05). In the experiments with diazepam the plasma corticosterone concentration correlated negatively with the O/E ratio (r = -0.58; P less than 0.05), whereas in the experiments with nicotine plasma corticosterone correlated negatively (r = -0.46; P less than 0.05) with enclosed runway entries. Nicotine injections were associated with a regionally-selective reduction in the 5-hydroxyindole acetic acid (5-HIAA) concentration in the hippocampus (P less than 0.05) and a reduction in hippocampal 5-hydroxytryptamine (5-HT) which approached statistical significance. Chronic, but not acute, diazepam increased (P less than 0.01) hypothalamic 5-HT. The changes in 5-HT and 5-HIAA did not appear to be directly related to the behavioural or adrenocortical responses to either of the drugs.
This study investigated the action of chlordiazepoxide (CDP), on the social interaction (SI) of adult rats maintained in one of three housing conditions: (i) group-reared, (ii) isolated from weaning or (iii) paired during adulthood after initial isolation at weaning (pair-housed former isolates; PHFIs). Group-reared rats and PHFIs rats were housed in pairs starting 21 days prior to the first experiment. For these two groups, CDP (2.5 and 5.0 mg/kg) increased SI in unfamiliar, but not familiar (cagemate) pairings. In rats isolated throughout, SI was markedly increased and this was unaffected by CDP. Isolated rats also exhibited increased motor activity (MA) during SI tests, and the MA of both isolates and PHFIs was reduced by CDP. Finally, levels of aggression were very low except in isolates, where a relatively modest increase in aggression was reversed by either pairing or CDP. To summarise, isolation-induced increases in SI and aggression were reversed by pairing, but pairing only attenuated isolation-induced increases in MA. Although CDP reduced the elevated aggression and MA of isolated rats, it had no effect on their elevated SI scores. These data question the permanence of anxiety-related, isolation-induced behavioural changes and stand in contrast to the irreversible anxiogenic profile reported for isolation-reared rats in the elevated X-test.
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