Biomedical subjects

A Jiménez-Anguiano

Publications and source records attributed to A Jiménez-Anguiano.

10 recordsLinked to original sources

PubMed2003

Masculine sexual activity affects slow wave sleep in Golden hamsters.

The sleep pattern is modified by events occurring during wakefulness. In rats, it has been shown that male sexual behavior has a direct influence on sleeping patterns, increasing slow wave sleep (SWS) duration. On the other hand, the sexual behavior pattern of the male Golden hamster differs from the copulatory pattern of male rats. Male hamsters copulate faster and they do not display the motor inhibition observed in rats after each ejaculation. Moreover, close to exhaustion, hamsters display a behavioral pattern known as Long Intromission, which has been linked to an sexual inhibitory process. The present study was performed to determine the effects of male sexual activity on the sleep pattern in hamsters. Subjects were allowed to copulate for 30 and 60 min. In addition, the effect of locomotor activity was also assessed. The results show that male sexual behavior induced a significant increase of SWS II, with a reduction of wakefulness. No effect was observed on REM sleep. Locomotor activity produced only a slight effect on sleep. The results are discussed in terms of the similarities between the effects observed after sexual behavior on sleep in rats and hamsters, despite the substantial differences in the behavioral pattern.

Animals↗

PubMed2000

Cortistatin modulates memory processes in rats.

Cortistatin (CST) is a recently described neuropeptide with high structural homology with somatostatin. Its mRNA is restricted to gamma amino butyric acid (GABA)-containing cells in the cerebral cortex and hippocampus. CST modulates the electrophysiology of the hippocampus and cerebral cortex of rats; hence, it may be modulating mnemonic processes. In this study, we have evaluated the effect of CST and somatostatin (SS) on short- and long-term memory (STM and LTM, respectively), as well as on the extinction of the behavior by using the footshock passive avoidance behavioral test. In addition, we tested the ability of both neuropeptides to affect the generation of cAMP in hippocampal neurons in culture. Results showed that the administration of either CST or SS into the hippocampal CA1 deteriorates memory consolidation in a dose-response fashion and facilitates the extinction of the learned behavior. CST was more potent than SS. Likewise, CST increases cAMP while SS decreases it. These results strongly support a modulatory role for CST in memory processes.

Animals↗

PubMed2000

HIV- and FIV-derived gp120 alter spatial memory, LTP, and sleep in rats.

Human immunodeficiency virus (HIV)-associated dementia (HAD) has been detected in 20-30% of patients suffering AIDS. The envelope glycoprotein 120 (gp120) derived from HIV seems to play a critical role in the pathophysiology of this dementia. Likewise, the feline immunodeficiency virus (FIV)-derived gp120 causes neurological and electrophysiological abnormalitites in cats. We have studied the effects of gp120 derived from HIV or FIV on learning and memory processing, hippocampal long-term potentiation (LTP), hippocampal neuronal cAMP production, the sleep-waking cycle, and locomotor activity and equilibrium in rats. Results showed that while both HIV- and FIV-gp120 impaired the rat's performance in the Barnes maze task, only HIVgp120 impaired the induction and maintenance of LTP. However, both glycoproteins induced a significant decrease in the posttetanic potentiation. HIVgp120 also caused a significant reduction in cAMP production in the hippocampus. Regarding the sleep-waking cycle, HIV- and FIV-gp120 increased the waking state and slow-wave sleep 1 (SWS1), while decreasing both SWS2 and REM sleep. Locomotor activity and equilibrium were significantly altered by these glycoproteins. These results suggest that HIVgp120 causes neurophysiological abnormalities and therefore may facilitate HAD development in AIDS patients.

AIDS Dementia Complex↗

PubMed1998

Manipulations during forced wakefulness have differential impact on sleep architecture, EEG power spectrum, and Fos induction.

We propose a hypothesis suggesting that the most prominent experiences occurring during wakefulness activate specific clusters of neurons related to such experiences. These neurons could possibly then evoke the release of various types of sleep-inducing molecules, thereby causing different patterns of sleep architecture. In this study, we therefore sought to determine whether manipulations of behavior during wakefulness, such as forced wakefulness induced by gentle handling, forced wakefulness associated with a stressful condition such as immobilization, or forced wakefulness associated with excess intake of palatable food, could result in a variation of Fos immunoreactivity in selective brain structures and could also result in different sleep and EEG power density patterns. The results showed that the sleep-wake cycle of rats after all the experimental manipulations was different not only with respect to the control group but also among themselves. Additionally, power spectrum analysis showed an increase of 0.25-4.0 Hz in all experimental manipulations, whereas the 4.25-8.0 Hz increase occurred only in the situation of forced wakefulness plus stress. The Fos induction showed activation of cell clusters in cortical areas and telencephalic centers, in several hypothalamic nuclei, in monoaminergic cell groups, and in brain stem nuclei. The density of Fos-immunoreactive neurons varied in relation to the different paradigms of forced wakefulness. These results suggest that activation of cell clusters in the brain are related to the type of manipulation imposed on the rat during wakefulness and that such variation in cell activation prior to sleep may be associated with sleep architecture and EEG power.

Animals↗

PubMed1996

Rapid eye movement (REM) sleep deprivation in 6-OHDA nigro-striatal lesioned rats with and without transplants of dissociated chromaffin cells.

Since both REM sleep deprivation and unilateral 6-OHDA lesions induce supersensitivity of DA receptors, the purpose of this study was to determine whether the response of rats with such lesions would be modified by REM sleep deprivation. In addition, the effect of grafts of dissociated chromaffin cells was also tested. Rats with 6-OHDA lesions were subjected to 24 or 72 h of REM sleep deprivation and tested with various doses of apomorphine to determine turning behavior frequencies. At end of those experiments, the animals were transplanted with dissociated chromaffin cells and turning behavior was tested again. The results showed that REM sleep deprivation nearly doubled the turning behavior frequency, that chromaffin cell grafts decreased it, but that REM deprivation in grafted animals still seemed to produce an increase of post-synaptic supersensitivity independent of denervation. The results were discussed in terms of the possible relationship of sleep with Parkinson's disease through the DA system.

Animals↗

PubMed1996

Brain distribution of vasoactive intestinal peptide receptors following REM sleep deprivation.

Vasoactive intestinal peptide (VIP) has been shown to increase rapid eye movement (REM) sleep in normal and insomniac animals, while the administration of anti-VIP antibodies or an antagonist of VIP receptors decreases REM sleep. In addition, recently, it has been suggested that a VIP-like substance accumulates in the CSF during waking and that it may be involved in the production of the REM rebound normally seen following REM sleep deprivation. This evidence suggests that VIP may be important in modulating REM sleep in normal conditions and during REM sleep rebound. To determine whether VIP is involved in REM sleep homeostasis, VIP receptors of discrete brain areas was determined by autoradiography after 24 and 72 h of REM sleep deprivation (REM SD) by the water tank technique. Since this procedure has been suggested to produce some stress, an additional group adapted for 7 days to the sleep deprivation situation was tested. The results showed that REM SD produces an increase in the density of VIP receptors in several brainstem and forebrain structures at 24 h of REM SD and more so at 72 h of REM SD. Interestingly, results showed that habituation to the REM SD procedure decreases the density of VIP receptors in some areas of the brain of the REM sleep-deprived rats. The results are discussed in terms of the possibility that waking induces an increase of VIP receptors in several structures, which in turn are responsible for modulating REM sleep, but that stress contributes in part to VIP receptor changes.

Animals↗

PubMed1994

Administration of auditory stimulation during recovery after REM sleep deprivation.

Rapid eye movement (REM) sleep deprivation and auditory stimulation (ADS), separately, increase REM sleep in rats, cats and humans. The main goal of the present study was to test whether administration of ADS during REM sleep rebound has a synergistic effect on REM sleep elicitation. Male Wistar rats were implanted with standard sleep recording electrodes. Following the recovery period, animals were randomly assigned to the following conditions: undeprived (i.e. control) and 24, 48, 96 and 120 hours of REM sleep deprivation by the platform method. Undeprived and REM sleep-deprived animals were divided into two groups, with and without ADS. ADS was a "beep" of 80 dB and 2,000 Hz, lasting 20 msec every 10 seconds. This stimulus was applied for the first 4 hours of sleep recordings after deprivation. After that, animals were recorded for another 4 hours. In the undeprived situation, the group that received ADS increased REM sleep approximately 70% above the group that did not receive ADS, as has been reported previously (REM sleep without ADS: 38.1 +/- 13.84 vs. with ADS: 64.6 +/- 11.8, p < 0.005). No synergistic effect was observed between REM sleep deprivation and ADS for any REM sleep-deprivation schedule. This result may be explained as an increase in the excitability pattern of pontine neurons and/or changes in the cholinergic system due to REM sleep deprivation that could not be further increased by ADS.

Acetylcholine↗

PubMed1993

Cerebrospinal fluid (CSF) extracted immediately after REM sleep deprivation prevents REM rebound and contains vasoactive intestinal peptide (VIP).

Intraventricular administration of cerebrospinal fluid (CSF) obtained from sleep deprived (SD) animals and vasoactive intestinal peptide (VIP) have been shown to increase rapid eye movement (REM) sleep. It has thus been suggested that VIP may accumulate in the CSF as a consequence of waking, and might thus be partly responsible for the subsequent rebound of REM sleep which follows prolonged wakefulness. To this data there are no studies testing this hypothesis. The purpose of this study, therefore, was to determine REM rebound following the extraction of CSF immediately after REMSD and to quantify by radioimmunoassay (RIA) the concentration of VIP in the CSF of progressively increasing REMSD periods. The results showed that REM rebound normally seen following REMSD is reduced by extraction of CSF, and that VIP concentration in such CSF is augmented. The results are discussed in terms of the possibility that waking induces an accumulation of VIP in the CSF, which is in turn involved in the production of REM sleep.

Animals↗

PubMed1993

Chloramphenicol prevents carbachol-induced REM sleep in cats.

Twenty-four cats were implanted for chronic sleep recordings. One week after the surgery, cats were divided into four groups. Two groups were treated with three i.p. injections of 150 mg/kg chloramphenicol (CAP) separated by 12 h. Carbachol (8 micrograms/1 microliter) or saline (1 microliter) was injected into the pontine reticular formation (PRF) 1 h after the last injection of CAP. The other two groups received saline or carbachol into the PRF without CAP pre-treatment. Polygraphic recordings were started immediately after the microinjection and lasted 11 h. Carbachol increased REM sleep (P < 0.001) and reduced SWS2 (P < 0.05). In contrast, chloramphenicol reduced REM sleep (P < 0.001) and increased SWS2 (P < 0.01). The combination of these drugs increased wakefulness (P < 0.01) and reduced both SWS2 and REM sleep (P < 0.001). This data shows that chloramphenicol prevents carbachol induced REM sleep. Results are discussed in terms of an interaction between brain proteins and the cholinergic system to induce REM.

Animals↗

PubMed1993

The combination of VIP and atropine induces REM sleep in cats rendered insomniac by PCPA.

Twenty-four cats were implanted with electrodes for chronic sleep recordings. One week after the surgery, cats were treated with two intraperitoneal injections of parachlorophenylalanine (PCPA), an inhibitor of serotonin synthesis, to induce insomnia. Twenty-four hours after the second injection of PCPA, cats were at the peak of insomnia (strong reduction of both slow wave sleep 2 and rapid-eye movement [REM] sleep). During this period cats were divided into four groups (n = 6) and were injected with either atropine (0.5 mg/kg, IM [3.5 mmol/kg]), vasoactive intestinal peptide (VIP) (200 ng, ICV [60 pmol]) or atropine plus VIP (same doses and routes of administration). The control group received saline intramuscularly (IM) intracerebroventricularly and (ICV). Results showed that VIP and atropine injected alone and in combination increased mean total time of REM sleep in PCPA-treated animals. These findings are discussed in terms of a serotonin-acetylcholine interaction.

Animals↗