Modulation of nociceptive-like behavior in zebrafish (Danio rerio) by environmental stressors

Zebrafish have been demonstrated to react consistently to noxious chemical stimuli and present reliable phenotypes of stress, fear, and anxiety. In this article, we describe the modulation of nociceptive-like responses of zebrafish to fear-, stress-, and anxiety-eliciting situations. Animals were exposed to an alarm substance, confinement stress, or a novel environment before being injected with 1% acetic acid in the tail. The alarm substance and confinement stress reduced the display of erratic movements and tail-beating behavior elicited by acetic acid. The novelty of the environment, in contrast, increased the frequency of tail-beating behavior. The results suggest that descending modulatory control of nociception exists in zebrafish, with apparent fear- and stress-induced analgesia and anxiety-induced hyperalgesia.

The effects of diazepam on the elevated T-maze are dependent on the estrous cycle of rats

In order to determine the modulation of anxiolytic and panicolytic-like effects of diazepam by the hormonal cycle of female rats, male and female rats – the latter divided per estrous cycle phase (estrus, diestrus, metaestrus and proestrus) – were tested in the elevated T-maze, a behavioral model of panic and anxiety. Diazepam (0.5, 1.0 and 2.0 mg/kg) or saline solution was injected in individual animals that were submitted to one session in the elevated T-maze 25 min after drug/saline administration. The test consisted of three avoidance trials and one escape trial, separated by a 30 s interval, during which the animals were isolated in individual cages. The avoidance trials began with the animal being placed at the end of the maze's enclosed arm. The time necessary for the animal to leave the central square was considered as the response's latency. The trials that exceeded 300 s were considered as failures. Results demonstrate a decrease in the effects of diazepam in inhibitory avoidance (anxiety) trials in females in diestrus and proestrus, but no relation of gender or estrous cycle on diazepam effects on escape trials (fear). The results support the hypothesis that down-regulation of GABAA receptors by activation of nuclear estrogen receptors and induction of PKC-mediated GABAA receptor phosphorylation by activation of surface estrogen receptors in raphe neurons underlie the modulation of diazepam sensitivity by estrogen.