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Biomedical subjects

Cruz Reyes-Vazquez

Publications and source records attributed to Cruz Reyes-Vazquez.

3 recordsLinked to original sources

Sex differences in tail-flick latency of non-stressed and stressed rats.

The present study was conducted to assess whether there are sex differences between male and female subjects in their response to noxious stimuli under non-stressed and stressed conditions. Tail-flick latency assay was used as an experimental tool on 12 adult male and 12 adult female Sprague-Dawley rats before immobilization (i.e., non-stressed condition) and after 30, 120, 240, and 360 min of continuous immobilization (i.e., stressed conditions). It was found that the non-stressed female rats exhibited significantly longer response latency to noxious thermal stimuli than the non-stressed male rats. Stressed conditions caused by immobilization of the animal inside a ventilated restrainer significantly prolonged the tail-flick latency thresholds of both sexes. Female and male rats did not develop any adaptation after 120, 240, and 360 min of immobilization compared to their 30 min of immobilization, as demonstrated by the tail-flick assay. Moreover, the difference in the tail-flick latency between male and female rats was reduced as the duration of immobilization in the restrainer lengthened. At 30 min of immobilization, the significant difference between the sexes reduced to p < .05 compared to p < .01 before immobilization, and to statistically non-significant differences after 120, 240, and 360 min of immobilization. Results from this study suggested that female rats had longer tail-flick latency than male rats in non-stressed environment, and the difference in tail-flick latency after immobilization between the sexes became less significant with time. In addition, 360 min of immobilization was not enough to adapt to the restrainer, as shown by the tail-flick assay.

Animals↗

Serotonin modulates hypothalamic neuronal activity.

Effects of serotonin (5-HT) on electrophysiological activities of single hypothalamic arcuate neurons in rat brain slices were observed by extracellular recording. The results showed that (1) of 385 arcuate neurons observed, the patterns of spontaneous firing were divided into 3 categories: "slow irregular" (46.0%), "fast continuous" (22.6%), and "bursting" firing (31.4%); (2) of 149 neurons tested for 5-HT, most (55.0%) responded to the drug by decreasing firing rate, 22.2% by increasing firing rate, 11.4% exhibit biphasic pattern, and 11.4% did not respond to 5-HT application; (3) substitution of low Ca2-high Mg2+ artificial cerebrospinal fluid (ACSF) for normal ACSF did not abolish the 5-HT-induced excitatory effect while it did abolish the 5-HT-induced inhibitory effect, suggesting the effect in latter cases was elicited by a Ca2+-dependent release of neuroactive substances; (4) cyproheptadine, a non-selective 5-HT receptor antagonist, antagonized the 5-HT-induced excitatory effect in all neurons tested, while pindolol, a 5-HT1A/1B receptor antagonist, antagonized the 5-HT-induced excitatory effect in 50% of neurons tested; (5) both cyproheptadine and pindolol antagonized the 5-HT-induced inhibitory effect; and (6) bicuculline, a GABAA receptor antagonist, antagonized the 5-HT-induced inhibitory effect. These results suggest that 5-HT may exert its excitatory effects directly through 5-HT1A/1B and other subtypes of 5-HT-receptors located on the surface of the neurons recorded, while its inhibitory effects are mediated indirectly through the activation of a local inhibitory GABAergic interneuron.

Action Potentials↗

ATP-sensitive potassium channels and endogenous adenosine are involved in spinal antinociception produced by locus coeruleus stimulation.

The effects of locus coeruleus stimulation on nociceptive evoked discharges of thalamic parafascicular (PF) neurons were investigated in lightly urethane-anesthetized rats, aiming to study the mechanisms underlying these effects. Intrathecal (i.t.) administration of aminophylline (an adenosine antagonist), glibenclamide (an ATP-sensitive potassium [K+(ATP)] channels blocker), nicrorandil (Nico; an agonist of K+(ATP) channel and a K+(ATP) channel opener), and 5'-N-ethylcarboxamido-adenosine (NECA; an adenosine agonist) were used. The results showed that (1) locus coeruleus stimulation significantly inhibited the nociceptive evoked discharges of parafascicular neurons, (2) locus coeruleus stimulation-produced antinociception in PF neurons was blocked by both it. glibenclamide and i.t. aminophylline, (3) nociceptive discharges of PF neurons were also suppressed by both i.t. NECA and i.t. nicorandil, and (4) i.t. glibenclamide showed no effect on the suppression of nociceptive discharges induced by NECA, whereas aminophylline blocked the suppression of nociceptive discharges induced by nicorandil. These results suggest that (a) K+(ATP) channels and endogenous adenosine may be involved in the mediation of antinociception induced by norepinephrine, which is released in the dorsal horn by descending fibers originating from the locus coeruleus and (b) the opening of K+(ATP) channels may precede the release of endogenous adenosine in the process of suppressing nociceptive transmission at the spinal level.

Action Potentials↗