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J Velazquez-Moctezuma

Publications and source records attributed to J Velazquez-Moctezuma.

At least 19 recordsLinked to original sources
PubMed2002

Monoaminergic and cholinergic stimulation of masculine sexual behavior in neonatally demasculinized male rats.

Sexual behavior during adulthood largely depends upon hormonal events that take place around birth. Administration of the antiestrogen Tamoxifen (Tx) to males immediately after birth induces a marked decrease of masculine sexual behavior during adulthood. On the other hand, it is well known that masculine sexual behavior can be stimulated by the administration of drugs acting specifically on the monoaminergic or the cholinergic systems. This study was performed to analyze if masculine sexual behavior can be pharmacologically stimulated in adult male rats neonatally demasculinized by the administration of Tx. Neonatal administration of Tx induced clear impairments of masculine sexual behavior during adulthood. Administration of oxotremorine (OXO), 8-OH-DPAT (8-hydroxy-2(di-n-propylaminotetraline)), yohimbine (YH), and apomorphine (APO), drugs that normally elicit a stimulation of masculine sexual behavior were unable to fully restore it in demasculinized males. Only slight improvements of some behavioral parameters were observed with 8-OH-DPAT and YH. OXO seems to induce a worsening of sexual behavior impairments. Results obtained with APO were not significantly different from saline controls. Data suggest that neonatal treatment with Tx induces permanent impairments of the neural circuitry regulating masculine sexual behavior not only limited to morphological changes but also functional alterations of the neurotransmitter systems.

Adrenergic alpha-Antagonists↗
PubMed2002

Copulatory activity increases slow-wave sleep in the male rat.

It is believed that sexual activity increases the need to sleep in many species. However, the relationship between copulatory activity and sleep has been poorly studied. Several studies have observed variations in the sleep of female rats and women as a function of their reproductive state. These effects have been correlated with the effects of female steroid hormones, but not with sexual activity. The aim of the present study was to evaluate the sleep-wake pattern of male rats immediately after different conditions of copulatory activity. Sexually experienced male rats were chronically implanted with a standard set of electrodes for sleep recording. After a control sleep recording of 8 h, the males were randomly assigned to one of the following experimental conditions: 30 min in the presence of an ovariectomized (OVX) rat; 30 min in the presence of an intact non-receptive female (NRF); with a receptive female until reaching one ejaculation (1E); and with a receptive female until reaching three ejaculations (3E). In addition, after 10 days, males were randomly exposed to one of the following copulatory conditions during 4 h: to remain in the presence of an OVX rat; to remain in the presence of an NRF female, and with receptive females until reaching sexual satiety (SS). Male sexual behavior was assessed just after the onset of the dark period, and sleep recordings were obtained during 8 h immediately after experimental testing. Both the three ejaculations group (3E) in the first experiment and the sexual satiety group (SS) in the second experiment showed enhanced percentages of time spent in slow wave sleep (SWS) II and a shorter latency to the first SWS II episode than in the control group or under basal conditions. In addition, neither the presence of a non-receptive female or an OVX female, nor sexual behavior until reaching one ejaculation induced any effect on the sleep stages. These findings suggest that the increase in SWS II induced by both 3E and SS may be governed by some specific mechanism that is essentially independent of physical exercise or stress. Copulatory activity might be the source of neurohormonal processes that induce sleep and may involve the participation of gamma-aminobutyric acid, serotonin or other endogenous regulators of sleep and wakefulness. Nevertheless, the precise mechanism by which the sexual behavior increases SWS is still to be determined.

Animals↗
PubMed1998

Lack of effect of corticosterone administration on male sexual behavior of rats.

The increase in plasma levels of corticosteroids as part of the stress response has been associated with failure in the reproductive function in most vertebrate species, both in females and males. Recently, we have shown that male sexual performance in rats is readily affected by different stressors, both acutely and chronically applied. However, there are few reports that directly correlate the increase in corticosteroid levels with the behavioral effects of stress. In this study we investigated whether the administration of corticosterone, either acutely or chronically, could reproduce the effects of stress on male sexual behavior in the male rat. Four doses of corticosterone (0.5, 1, 2, and 4 mg) or the vehicle, were administered during four consecutive days to sexually experienced males. Male sexual behavior was assessed after the first and the fourth injection. After the last test, males were killed and levels of corticosterone and testosterone were measured by HPLC. We observed an increase in corticosterone plasma levels in a dose-dependent manner. None of the sexual behavior parameters, however, was modified. Plasma levels of testosterone were not modified by corticosterone administration. Both steroids were increased in response to sexual activity, though. These data show that, unlike amphibians and female mammals, corticosteroids do not alter sexual behavior in male rats and suggest that the effect of stress on male sexual behavior cannot be explained by increases in corticosterone.

Animals↗
PubMed1998

Pharmacological features of masculine sexual behavior in an animal model of depression.

Neonatal treatment with clomipramine induces behavioral alterations during adulthood that resemble symptoms observed in human depression. Therefore, it has been proposed as an animal model of depression. Impairment of male sexual performance is one of the main effects of this treatment. Using this model of depression, we evaluated the effects of drugs that stimulate sexual performance by acting selectively on the adrenergic, serotonergic, or cholinergic system. Yohimbine, a selective antagonist of the alpha-2 receptors; 8-OH-DPAT, a selective agonist of the 5-HT1A receptors; and oxotremorine, a muscarinic agonist, were administered to male rats neonatally treated with clomipramine that showed sexual behavior impairments. Yohimbine and oxotremorine induced only a slight improvement of sexual deficiencies. 8-OH-DPAT not only restored sexual behavior to normal levels, but induced facilitation in most of the copulatory parameters. These results suggest that neonatal treatment with clomipramine induces sexual deficits acting mainly on the adrenergic and cholinergic systems, while the serotoninergic system seems to be preserved.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Cholinergic-androgenic interaction in the regulation of male sexual behavior in rats.

It is well known that testosterone (T) plays a major role in the adequate expression of male sexual behavior. On the other hand, the stimulation of central muscarinic receptors with oxotremorine (OXO), a specific agonist, facilitates the expression of masculine sexual behavior in rats. In this study, we analyzed the relationship between T and the cholinergic system, recording the effect of OXO administration on masculine sexual behavior in gonadectomized rats, before and after receiving T treatment. Sexually experienced and unexperienced male rats were gonadectomized and periodically tested for sexual behavior. Once this behavior was absent or drastically reduced, males were treated with OXO or saline and sexual behavior was assessed. 112 or 167 days later, animals were treated daily with T during 21 days, recording the response to OXO in days 12 and 21. Sexual behavior decreased more rapidly after gonadectomy in inexperienced males. OXO administration did not improve sexual performance in either group. The administration of T rapidly restored sexual behavior of experienced males: recovery of inexperienced males was slower. In the presence of T, OXO administration exerted a facilitative effect on sexual performance of both groups. These results suggest that the facilitative effect of muscarinic stimulation on sexual behavior requires the presence of testosterone.

Acetylcholine↗
PubMed1996

Effects of short- and long-term REM sleep deprivation on sexual behavior in male rats.

The influence of selective REM sleep deprivation on masculine sexual behavior has been a matter of controversy. In the present study, the sexual behavior of male rats was analyzed in subjects deprived on REM sleep by the island technique for 24 or 16 h daily during 20 days. When compared to control rats, both groups displayed changes in sexual performance since the first day. The effects were: an increase in mount, intromission and ejaculation latencies and in mount frequency as well; a decrease of ejaculation frequency and of the Hit rate. The effects became stronger as REM sleep deprivation progressed. Rats deprived of REM sleep for 24 h were extremely debilitated after 12 days and some of them died, whereas the rats REM deprived for 16 h remained healthy during the 20 days. These data indicate that REM sleep deprivation interferes with the mechanisms that regulate male sexual behavior.

Animals↗
PubMed1996

Effect of acute and chronic stress on masculine sexual behavior in the rat.

Masculine sexual behavior in rats can be stimulated by acutely stressing the animals. Nevertheless, little is known about the effect that different stressors could have on sexual behavior. In this work we studied the effect of different stressors applied both acutely and chronically on masculine sexual behavior. Sexually active male Wistar rats were submitted to stress by: immobilization (IMB); immersion in cold water (WIM); and electrical foot shock (EFS). These stressors were applied during 20 consecutive days and masculine sexual behavior was assessed on days 1, 4, 8, 12, 15 and 20. Motivational component, copulatory performance and copulatory potential were drastically altered by WIM. EFS produced significant alterations in almost all sexual parameters recorded but only when it was applied chronically. IMB only altered mount frequency and hit rate, although inconsistently. These results suggest that the effect of stress on sexual behavior depends on the nature and, in some conditions, on the duration of the stressor.

Animals↗
PubMed1993

The relative effects of selective M1 muscarinic antagonists on rapid eye movement sleep.

Three muscarinic antagonists, scopolamine, trihexyphenidyl and biperiden were systemically administered (0, 0.5, 1, 2 and 4 mg/kg) in rats. Scopolamine increased wakefulness and deceased sleep, both slow wave and REM. Trihexyphenidyl increased wakefulness and decreased REM sleep while biperiden decreased REM sleep selectively. The rank order REM-suppressing effect was roughly scopolamine and trihexyphenidyl having a greater suppressing effect than biperiden. These results suggest that the regulation of the sleep-wake cycle is at least partially controlled by the M1 muscarinic receptor.

Animals↗
PubMed1993

The effect of prenatal stress on adult sexual behavior in rats depends on the nature of the stressor.

It is well known that prenatal stress induces behavioral demasculinization and/or feminization in male offspring during adulthood. In this study, four different stressors were prenatally applied to rats. Pregnant rats were subjected to immobilization, unavoidable electric foot shocks, rapid eye movement sleep deprivation (REMd), or immersion in cold water. During adulthood, male offspring were tested for masculine and feminine sexual behavior. The results corroborated the fact that immobilization induced an impairment of masculine sexual behavior and a facilitation of feminine sexual behavior. Electric shocks showed only minor differences in masculine behavior when compared to intact controls, and no signs of lordosis behavior were observed. The REMd group displayed a major impairment of masculine behavior, even greater than that observed within the immobilization group. However, lordosis behavior was only induced with estradiol. On the other hand, water immersion seems to have a facilitatory effect on several parameters of masculine behavior and did not show lordosis behavior even with hormonal treatment. These results strongly suggest that changes in sex behavior induced by prenatal stress are linked to the nature of the stressor.

Animals↗
PubMed1993

Muscarinic and nicotinic influences on masculine sexual behavior in rats: effects of oxotremorine, scopolamine, and nicotine.

In this study, the role of cholinergic systems in the regulation of male sexual behavior was analyzed by different approaches. Both muscarinic agonists and antagonists, as well as a nicotine agonist, were administered to sexually experienced male rats. In Experiment 1, oxotremorine (OXO), a muscarinic agonist, decreased the intromission frequency and ejaculatory latency in a dose-dependent way. Moreover, an increase in ejaculatory frequency was observed. In Experiment 2, the muscarinic antagonist scopolamine (SCO) produced a dose-related impairment of sexual behavior, decreasing the percentage of sexually active males. The smaller doses of SCO delayed the initiation of sexual behavior and decreased ejaculatory frequency. In an attempt to analyze the effect of muscarinic supersensitivity on sexual behavior, in Experiment 3 a long-term blockade of muscarinic receptors (SCO for 17 days) was followed by OXO administration. Animals displayed a significant increase of mount frequency, which results in the decrease of both the hit rate and ejaculatory frequency. In Experiment 4, six doses of nicotine were acutely administered. Only the higher doses (0.4, 0.8, and 1.6 mg/kg) induced a decrease in intromission frequency, although no significant differences were found in any other parameter. These results strongly suggest that cholinergic participation in masculine sexual behavior regulation is mediated mainly through muscarinic system.

Animals↗
PubMed1993

Behavioral effects of neonatal treatment with clomipramine, scopolamine, and idazoxan in male rats.

It has been suggested that REM sleep deprivation due to the administration of clomipramine, during early developmental stages, results in dramatic behavioral changes during adulthood. One of the main alterations is the impairment of masculine sexual behavior (MSB). Clomipramine increase monoaminergic availability at the synaptic level and also suppresses REM sleep. This study was performed to compare the effect on masculine sexual behavior of three different neonatal treatments: clomipramine, which increases monoaminergic availability at the synaptic level and suppresses REM sleep; scopolamine, a cholinergic antagonist that suppresses REM sleep; and idaxozan, a selective adrenergic agonist. Subjects (Ss) were treated neonatally and tested for masculine sexual behavior during adulthood with standard techniques. Results obtained with clomipramine administration showed a marked impairment of MSB, mainly reflected by the decrease in the percentage of active Ss and the decrease in the percentage of Ss reaching ejaculation. In contrast, idaxozan and scopolamine produce a facilitation of MSB. The effect of idaxozan was not significantly different when compared to saline control rats. The effect of scopolamine was greater, and the percentage of Ss reaching ejaculation was significantly larger than saline control. These results suggest that the alterations of sexual behavior induced with neonatally administered clomipramine are not due to early REM sleep deprivation. As idaxozan did not replicate clomipramine results, it is also possible that noradrenergic transmission is not involved in the generation of these effects. It remains possible that the serotonin system could be responsible for the impairment of sexual behavior due to neonatal clomipramine treatment.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed1993

Cholinergic receptor subtypes and REM sleep in animals and normal controls.

As reviewed here and elsewhere in this symposium, acetylcholine, in conjunction with other neurotransmitter systems, plays a very important role in the regulation of circadian and sleep-wake states. To briefly recapitulate, several current basic concepts about the regulation of sleep-wake states include: (a) REM sleep, or at least its phasic events (eye movements and PGO spikes), are promoted by cholinergic neurons originating within the peribrachial regions [LDT/PPT] (Mitani et al., 1988; Shiromani et al., 1988; Datta et al., 1991; Shouse and Siegel, 1992); (b) REM sleep may be inhibited by noradrenergic and serotonergic neurons in the locus coeruleus and dorsal raphe, respectively (Siegel, 1989; Steriade and McCarley, 1990; Jones, 1991); (c) stages 3 and 4 (Delta) sleep are inhibited by cholinergic terminals from basal forebrain to cortex (Buzsaki et al., 1988) and from LDT/PPT to thalamus (Steriade and McCarley, 1990; Steriade et al., 1991); (d) Delta sleep is modulated by complex serotonergic mechanisms; for example, it is increased by pharmacological antagonists of 5HT2 receptors (Declerck et al., 1987; Dugovic et al., 1989; Benson et al., 1991), although the mechanism and neuroanatomical site at which this effect occurs is unknown. Given the importance of mACHR mediation of components of REM sleep, it is unfortunate that so little is known about the distribution of the various subtypes of mACHRs in brainstem areas which regulate REM sleep. mACHR subtypes have been identified by molecular, biological and pharmacological methods.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1993

Evidence that the M1 muscarinic receptor subtype mediates the effects of oxotremorine on masculine sexual behavior.

The cholinergic system participates in the regulation of masculine sexual behavior, mainly through the muscarinic system. Recently, muscarinic receptors have been subdivided into at least two subtypes, M1 and M2, according to their differential affinity for pirenzepine. In this study, we analyzed the possible participation of the M1 muscarinic receptor subtype on masculine sexual behavior regulation. In the first experiment, trihexyphenidyl, a specific M1 antagonist, was administered to experienced adult male rats in a wide range of doses (from 0.1 to 6.4 mg/kg). No modification was observed in any of the male sexual behavior parameters recorded, with the exception of the highest dose at which an increase of the intromission frequency and a decrease of the ejaculation frequency were observed. In the second experiment, trihexyphenidyl was administered in several doses (from 0.2 to 1.6 mg/kg), before the administration of oxotremorine, a muscarinic agonist, at a dose that readily facilitates masculine sexual behavior. Trihexyphenidyl completely prevented the facilitatory effects of oxotremorine even at the smallest dose used. These results strongly suggest that the M1 muscarinic receptor subtype participates in the cholinergic facilitation of masculine sexual behavior.

Animals↗
PubMed1992

Neonatal treatment with clomipramine increased immobility in the forced swim test: an attribute of animal models of depression.

The forced swimming test in rats has been identified as a suitable model for detecting antidepressant activity of several drugs regardless of their mode of action. On the other hand, a number of animal models of human endogenous depression have been proposed. Recently, it has been reported that perinatal administration of clomipramine in rats elicits behavioral changes in adulthood that resemble human endogenous depression. In the present study, we showed that in this new animal model of depression immobility was increased when animals were submitted to the forced swimming test. This finding supports the notion that the amount of immobility during the forced swimming test is directly proportional to a depressive state in the rat.

Animals↗
PubMed1991

Cholinergic antagonists and REM sleep generation.

In this study we extended our observations on the role of M1 and M2 muscarinic receptors in mediating the cholinergic induction of REM sleep. Cats were chronically implanted with sleep recording electrodes and microinjections of Ringer's or muscarinic antagonists followed by the relatively specific M2 muscarinic agonist, cis-methyl-dioxolane (cisdioxo), were made into the medial pontine reticular formation (mPRF). The microinjection of Ringer's followed by cisdioxo significantly increased REM sleep percentage. Atropine, a mixed muscarinic receptor antagonist, administered before cisdioxo blocked the REM sleep increase while pirenzepine, a selective M1 muscarinic antagonist, did not block the cisdioxo-induced increase in REM sleep. Gallamine, a nicotinic and a putative M2 antagonist, tended to inhibit the cisdioxo-induced increase in REM sleep. These results support the hypothesis that the cholinergic stimulation-induced REM sleep in the medial pontine reticular formation is mediated by a non-M1 muscarinic receptor subtype.

Animals↗
PubMed1991

Effects of sleep deprivation on sleepiness and increased REM sleep in rats selectively bred for cholinergic hyperactivity.

In this study we employed a modification of the multiple sleep latency test (MSLT) to determine whether rats of a strain with increased cholinergic activity were sleepier compared to randomly bred control rats. Seven rats each from the Flinders sensitive line (FSL, hypercholinergic) and Flinders resistant line (FRL, age-matched controls) were kept awake for 20 min and then allowed to sleep ad libitum for 20 min. The regimen of 20 min of wakefulness followed by 20 min of sleep was repeated 12 times during the day. There were no differences in latency to sleep or to rapid eye movement (REM) sleep or in percent total sleep time, drowsy, or slow-wave sleep between FSL rats and FRL rats. However, FSL rats showed a significant increase in REM sleep compared to FRL rats. This selective increase in REM sleep may be coupled to an increase in brain muscarinic receptors in the FSL rats.

Animals↗
PubMed1990

Microinjections of nicotine in the medial pontine reticular formation elicits REM sleep.

Microinfusion of non-specific cholinergic muscarinic-nicotinic agonists, such as carbachol, into the medial pontine reticular formation readily elicits REM sleep. It has generally been assumed that muscarinic receptors mediate the action of cholinergic agonists in triggering rapid eye movement (REM) sleep. Very little is known, however, about the role of nicotinic mechanisms in REM sleep generation. In this study, we administered nicotine and Ringer's solution into the medial pontine reticular formation of freely moving cats. Compared to control Ringer's injections, nicotine increased REM sleep and decreased wake and slow wave sleep (SWS) I percentage. Nicotine also shortened the time to REM sleep onset. These findings suggest a role of nicotinic mechanisms in REM sleep generation.

Animals↗