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J Velazquez-Moctezuma

Publications and source records attributed to J Velazquez-Moctezuma.

24 records · Page 2Linked to original sources

Differential effects of cholinergic antagonists on REM sleep components.

We examined the effects of cholinergic receptor blockers on changes in rapid eye movement (REM) sleep components. M1 and M2 muscarinic receptor antagonists or atropine were microinfused before an M2 muscarinic receptor agonist, and the effects on individual REM sleep components were assessed. All drugs were microinjected into the same locus within the medial pontine reticular formation in cats, and sleep recordings were made for at least 3 hours postinjection. Results suggest that desynchronized electroencephalogram (EEG) is influenced by the M1 muscarinic receptor, muscle atonia is influenced by the M2 muscarinic receptor, and ponto-geniculo-occipital (PGO) waves are affected by the nicotinic receptor.

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Effect of specific M1, M2 muscarinic receptor agonists on REM sleep generation.

Specific agonists for muscarinic receptor subtypes were infused by microinjection into the medial pontine reticular formation of freely moving cats. The M2 agonists Oxotremorine-M and Cisdioxolane significantly increased REM sleep percentage. The results obtained with microinfusions of carbachol, a mixed muscarinic agonist, were similar to that obtained by the M2 agonists. The M1 agonist McN-A-343 did not elicit any change in sleep or REM sleep percentage. The generation of REM sleep by cholinergic stimulation of the medial pontine reticular formation may be mediated by the M2 muscarinic receptor subtype.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

Facilitation of the effect testosterone on male sexual behavior in rats deprived of REM sleep.

The possibility of rapid eye movement sleep deprivation (REMd) altering the effect of testosterone on masculine sexual behavior was investigated. Adult castrated male Wistar rats with no sexual experience were randomly assigned to the following three groups: REMd (using the water tank technique) for 7 days, large platform control for 7 days, and undisturbed sleep control. All subjects were treated with 1 mg testosterone propionate daily for 14 days. Masculine sexual behavior was assessed 3 consecutive days prior to steroid administration and was evaluated daily during the treatment. Frequencies and latencies of mounts, intromissions, and ejaculations, as well as the postejaculatory refractory period were recorded. One hundred percent of the REMd subjects presented mounts, intromissions, and ejaculations sooner than the control group. In almost all parameters, a clear facilitation of sexual activity was observed in the REMd group.

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REM sleep deprivation facilitates the estrogen effect on heterotypical sexual behavior in male rats.

Gonadectomized male rats were submitted to REM sleep deprivation (REMd) for 120 hr and their hetero and homotypical sexual response to estradiol benzoate (EB) was tested. Subjects (Ss) receiving 20 micrograms EB showed lordosis quotients (LQ) twice as high as those receiving 10 micrograms EB and at the same time the LQs in these groups were higher than in the non-REMd groups. Gonadectomized-adrenalectomized control Ss showed the highest levels of lordosis throughout the experiment. REMd by itself does not produce lordosis response. The results indicate that the brain structures underlying this behavior in males are probably similar to those in females, since REMd increases lordosis in both cases. The lack of homotypical sexual behavior normally observed in gonadectomized male rats does not seem to be affected by this treatment. The issue of adequate controls for REMd experiments is discussed.

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Effects of REM deprivation on the lordosis response induced by gonadal steroids in ovariectomized rats.

Ovariectomized rats were submitted to REM sleep deprivation (REMd) using the water tank technique and their behavioral responsiveness (lordosis) to gonadal steroids was tested. In Experiment 1, animals received 2 micrograms of estradiol benzoate (EB) followed by 2 mg of progesterone (P) 44 hours later. Several REMd periods (12, 72, 96 and 120 hr) were applied, all ending four hr after P. REMd animals showed significantly lower lordosis quotients (LQ) than undisturbed sleep animals regardless of the duration of the deprivation period. In Experiment 2, animals received a single dose of EB (2 micrograms) and were REMd for 120 hours. Animals were tested daily to evaluate their LQ. EB, at this dose level, failed to elicit significant lordosis behavior in undisturbed sleep rats. REMd rats gradually increased their LQ values reaching maximal levels at 72 hours. Adrenalectomized control groups receiving the same hormonal treatment responded similarly to the experimental groups, thus discarding the participation of adrenal steroids in these effects. The present results show that REMd differentially affects the response to E and P in ovariectomized rats, enhancing the former and inhibiting the latter.

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Effect of electric foot shocks, immobilization, and corticosterone administration on the sleep-wake pattern in the rat.

Knowledge concerning the impact of stressful situations on the sleep-wake pattern has been growing rapidly in the last decade. Immobilization (IMB) in rats elicits a significant increase of rapid eye movement (REM) sleep during the following 10 h. Participation of the adrenergic system has been clearly shown in this effect. On the other hand, it is well known that the time of the circadian cycle in which the stressor is applied could influence the results. It is also well known that the activation of the hypothalamic-pituitary-adrenal (HPA) axis, the release of corticosterone (COR), and the activation of the adrenergic and of the opioidergic systems are the most evident effects of stress. In the present study, we analyzed the effects of two stressors, IMB and electric foot shocks (EFS), on 24 h of continuous sleep recordings. These stressors were applied immediately before the onset of the light period. COR was also administered in an attempt to replicate the stressor-induced effects. Adult, male Wistar rats were chronically implanted for sleep recording, and after a recovery period and a 24-h basal sleep recording, they were submitted to EFS, COR, and IMB. A 10-day period elapsed between each treatment, and all of them were applied during the last moments of the dark phase of the light cycle. Results showed that IMB increased the percentage of REM sleep (83.7%) and slow-wave sleep II (SWS II; 17.3%) mainly during the dark phase (i.e., after 12 h), while EFS and COR administration elicited only slight and transient changes in the sleep-wake pattern. These data suggest that IMB applied to rats at the end of the dark cycle is effective in producing a sleep-elevating response, although this effect is enhanced during the dark phase. It seems, however, that not all the stressful situations are capable of eliciting this sleep-promoting effect, and also that COR release does not mediate this response.

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