PubMed Health⌕ Search

Biomedical subjects

R J Salín-Pascual

Publications and source records attributed to R J Salín-Pascual.

15 recordsLinked to original sources
PubMed1998

A novel effect of nicotine on mood and sleep in major depression.

The role of repeated nicotine administration on sleep and major depression was studied. Six non-smoking normal volunteers (NV) and six non-smoking major depressed patients (MD) with a Hamilton Rating Scale for Depression > 18 served as subjects. All subjects underwent the following sleep procedures: acclimatization, control night, four nicotine nights (17.5 mg, transdermal patches) and one withdrawal night (WN). Nicotine increased REM sleep time in both groups and also on the WN. Hamilton scores showed an average reduction of 43.9% in the depressed patients. These findings suggest that nicotine receptor activation may be important in major depression and shows for the first time that nicotine patches may be useful in the treatment of depression.

Administration, Cutaneous↗
PubMed1998

Decrease in muscarinic M2 receptors from synaptosomes in the pons and hippocampus after REM sleep deprivation in rats.

The effects of both REM sleep deprivation and its recovery on pontine and hippocampus muscarinic M2 receptors were investigated in synaptosomes using [3H]-AF-DX 384 as a ligand. Animals were divided into three groups: REM sleep deprivation group (small platforms 6.5 cm of diameter); stress group (large platforms 14 cm of diameter) and cage control group. In a second experiment REM sleep-deprived animals were allowed 48 h of recovery. REM sleep-deprived rats showed a reduction in M2 receptors compared with both intact and stress groups. Changes in M2 receptors were also observed after 48 h of recovery from REM sleep deprivation only in hippocampus. The enhancement of acetylcholine release during both REM sleep deprivation and recovery could explain the present findings.

Animals↗
PubMed1997

Repeated REM sleep deprivation after chronic haloperidol administration in the rat.

Repeated haloperidol administration produces up-regulation of dopamine (DA) receptors. REM sleep deprivation (REMSD) does also, but in addition, has been shown to produce REM sleep rebound. Should DA receptor up-regulation play a role in REM sleep rebound, haloperidol could conceivably have effects similar to those observed following REMSD. This is the central question investigated in this study. Male Wistar rats were prepared for sleep recordings. They were randomly assigned to the following groups: group 1, REMSD by small platforms (40 h REMSD + 8 h recording); group 2, was the large platform control group (40 h in large platforms + 8 h of recording); group 3, received 2-week daily administration of haloperidol (3 mg/kg, i.p.) plus REMSD (40 h REMSD + 8 h of recording); group 4, 2-week administration of haloperidol (3 mg/kg) without sleep manipulation and at the end 40 h were allowed to elapse, following which 8 h of sleep recordings was carried out. In each group the sleep manipulation and/or sleep recordings were repeated five consecutive times. Repeated REMSD produced increases of REM sleep time after each recovery in group 1. Large platforms did not produce increases of REM sleep during the recovery trials. The 2-week administration of haloperidol plus REMSD prevented REM sleep rebound (group 3). The 2-week administration of haloperidol without sleep manipulation (group 4) produced a REM sleep reduction. Dopamine modulation seems not to be important for REM sleep rebound. Hypersensitivity of DA receptors developed after REMSD may be an epiphenomenon associated with this sleep manipulation, but seems not to participate in REM sleep enhancement after REMSD.

Animals↗
PubMed1997

Sleep changes after 4 consecutive days of venlafaxine administration in normal volunteers.

BACKGROUND: The purpose was to examine the effect of the antidepressant drug venlafaxine on sleep architecture and periodic leg movements of sleep (PLMS) in normal volunteers. METHOD: Eight normal volunteers were studied under laboratory sleep conditions as follows: 1 acclimatization night, 1 baseline night, and 4 consecutive nights of venlafaxine p.o. administration (75 mg during the first 2 nights and 150 mg the last 2 nights). RESULTS: Venlafaxine increased both wake time and sleep stage I. Sleep stages II and III were reduced. REM sleep time was reduced after the first venlafaxine dose, and, by the fourth night, REM sleep was completely suppressed in all volunteers. Six of the eight volunteers showed PLMS at a frequency above 25 per hour. CONCLUSION: Venlafaxine produces several sleep disturbances, which include abnormal leg movements.

Adult↗
PubMed1996

Transdermal nicotine on sleep and PGO spikes.

There is conflicting evidence for the role of nicotine in sleep regulation. This study was undertaken to determine the effects of transdermal nicotine at doses of 17.5, 35 and 52.5 mg on sleep and PGO spike activity. Minor effects were observed on sleep with a general increase in waking. PGO spike activity was abolished by all patches. The results are discussed in terms of the mechanisms involved in the disappearance of PGO spikes as a result of nicotine.

Administration, Cutaneous↗
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

Antidepressant effect of transdermal nicotine patches in nonsmoking patients with major depression.

BACKGROUND: A high frequency of cigarette smoking has been reported among individuals with major depression. In a previous study, transdermal nicotine produced short-term improvement in the mood of depressed patients. This study was undertaken to determine the effects of 4 days' administration of transdermal nicotine on mood in nonsmoking patients with major depression. METHOD: The effects of nicotine patches (17.5 mg) on 12 nonmedicated outpatients with major depression (DSM-III-R) were studied for 4 continuous days. Patients had to score 18 points or more on the Hamilton Rating Scale for Depression (HAM-D) (21 items) for admission into the study. The HAM-D (10 items), a visual analog scale, and a side effects scale were scored daily during the trial (baseline, 4 days of nicotine patches, and 4 days of follow-up). RESULTS: Two patients dropped out of the study owing to nausea and vomiting. Results of the visual analog scale and HAM-D (10 items) showed a significant (p < .01) improvement in depression after the second day of nicotine patches. Patients relapsed 3 or 4 days after the last nicotine dose. The side effects observed were an increase in saliva production, nausea, loss of appetite, and mild insomnia. CONCLUSION: Nicotine patches produced short-term improvement of depression with minor side effects. Because of nicotine's high risk to health, nicotine patches are not recommended for clinical use in depression. Analogue drugs may be developed in the future that may help improve depression without the risk of other major health problems.

Administration, Cutaneous↗
PubMed1995

Effects of transderman nicotine on mood and sleep in nonsmoking major depressed patients.

The role of nicotine as an indirect cholinergic agent in sleep has been studied in normal subjects. There are no studies of its effects on sleep in depressed patients. Nicotine transdermal patches (17.5 mg), were studied in eight depressed patients (DSM-III-R) and eight normal volunteers. Subjects wore placebo and nicotine patches for 24 h. Depressed patients showed increased REM sleep without changes in other sleep variables. They also showed a short term improvement of mood. Normal volunteers had sleep fragmentation, and reduction of REM sleep time. No major side effects were reported in either group.

Adult↗
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↗
PubMed1989

Effects of physostigmine infusion on healthy volunteers deprived of rapid eye movement sleep.

Rapid eye movement sleep (REMS) deprivation is believed to alter the sensitivity of various neurotransmitter systems. In the present article, we studied 20 healthy volunteers divided into three groups. Group A attended the sleep laboratory for three nights: acclimatization, a baseline night, and one night of physostigmine infusion. Group B attended for eight nights; acclimatization, baseline, four nights of REMS deprivation, and two recovery nights. With the exception of the first recovery night, when group C volunteers were administered physostigmine, group C's schedule was identical to group B's. The infusions received by group A and C were composed of 1.0 mg of physostigmine, dissolved in 100 ml of saline solution. These were administered 5 min after sleep onset and thereafter every hour, except when the subjects were either awake or in REMS. All of the subjects receiving the cholinomimetic infusion were given a peripheral anticholinergic. Group A experienced a great number of awakenings with a decrease in REMS percentage. Group B recovery occurred over two nights, with an increase in the average length of REMS. Group C exhibited maximum REMS rebound on the first recovery night with an increased number of REMS episodes, as well as significant reductions in the first REMS latency. Our findings suggest that physostigmine alters REMS rebound following REMS deprivation.

Adolescent↗
PubMed1988

The effect of total sleep deprivation on plasma melatonin and cortisol in healthy human volunteers.

Twelve healthy volunteers were included in this study. Baseline curves for melatonin and cortisol were obtained after one night of adaptation to laboratory conditions. From 10:00 p.m. to 6:00 a.m., blood samples were drawn every hour. On the third night, the subjects were kept awake at the sleep unit. Curves for the two hormones were then obtained after 36 h of total sleep deprivation (SD). The levels of these hormones were evaluated by calculating the area under the curve at each hour in both situations (basal and after sleep deprivation). It was found that the melatonin levels were increased after sleep deprivation, whereas the cortisol levels remained the same. These results suggest a mechanism by which a reset of abnormal rhythms can occur in depression.

Adolescent↗
PubMed1985

[Advances in the psychopharmacological management of the narcoleptic patient].

Sleep attacks, cataplexy, sleep paralysis and hypnagogic hallucinations are the cardinal signs of narcolepsy. However most patients present only with sleep attacks at disease onset. Animal and human studies on the psychopharmacology and neurochemistry of narcolepsy, suggest abnormalities on rapid eye movement (REM) sleep. Thus, most drugs used on its treatment, such as tricyclic antidepressants and psychostimulant agents, are aimed to reduce REM sleep. However, there is growing evidence that some drugs that can alleviate fragmentation of sleep rather than suppress REM sleep can also be clinically effective for this condition. The authors review the subject and comment on their experience with clonidine, an imidazoline derivative marketed as an antihypertensive agent, and suggest that REM suppression is not always necessary for narcoleptics to improve.

Animals↗
PubMedDate not supplied

[Hypocretins and adenosine in the regulation of sleep].

OBJECTIVES: To review the recent discovery of hypocretins (orexins) and their link to the pathophysiology of narcolepsy and the role of adenosine in the integration of brain metabolism and sleep. DEVELOPMENT: The importance of the functions carried out by the hypothalamus in the regulation of sleep and the waking state has been consolidated by the discovery of hypocretins and the role played by cerebral adenosine. Hypocretins are two peptides made up of 33 and 28 amino acids whose neurons are located predominantly in the lateral hypothalamus and surrounding regions. In the Doberman canine narcolepsy model, in which this disease is presented with an autosomal recessive pattern, a mutation was detected in one of the receptors involved in the hypocretin system, namely the hypocretin-2 receptor. Failures in the hypocretin system have been confirmed as a key factor in narcolepsy by other findings in laboratory animals and humans. Adenosine, on the other hand, is accumulated during the waking state as a result of neuronal metabolism and this in turn is related to drowsiness. Sleep episodes lower the levels of this substance in the brain. Adenosine receptor antagonists increase wakefulness (e.g. caffeine), while the agonists promote slow-wave sleep. CONCLUSIONS: Hypocretins and adenosine from the hypothalamus perform functions involving the regulation of sleep and wakefulness. Understanding these two systems can have repercussions on clinical problems such as insomnia, hypersomnia and other neuropsychiatric disorders.

Adenosine↗