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At least 451 records · Page 25Linked to original sources
PubMed2006

Early life blockade of 5-hydroxytryptamine 1A receptors normalizes sleep and depression-like behavior in adult knock-out mice lacking the serotonin transporter.

In serotonin transporter knock-out (5-HTT-/-) mice, extracellular serotonin (5-HT) levels are markedly elevated in the brain, and rapid eye movement sleep (REMS) is enhanced compared with wild-type mice. We hypothesized that such sleep impairment at adulthood results from excessive serotonergic tone during early life. Thus, we assessed whether neonatal treatment with drugs capable of limiting the impact of 5-HT on the brain could normalize sleep patterns in 5-HTT-/- mutants. We found that treatments initiated at postnatal day 5 and continued for 2 weeks with the 5-HT synthesis inhibitor para-chlorophenylalanine, or for 4 weeks with the 5-HT(1A) receptor (5-HT(1A)R) antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl) cyclohexane carboxamide (WAY 100635), induced total or partial recovery of REMS, respectively, in 5-HTT-/- mutants. Early life treatment with WAY 100635 also reversed the depression-like behavior otherwise observed in these mutants. Possible adaptive changes in 5-HT(1A)R after neonatal treatment with WAY 100635 were investigated by measuring 5-HT(1A) binding sites and 5-HT(1A) mRNA in various REMS- and/or depression-related brain areas, as well as 5-HT(1A)R-mediated hypothermia and inhibition of neuronal firing in the dorsal raphe nucleus. None of these characteristics were modified in parallel with REMS recovery, suggesting that 5-HT(1A)Rs involved in wild-type phenotype rescue in 5-HTT-/- mutants are located in other brain areas or in 5-HT(1A)R-unrelated circuits where they could be transiently expressed during development. The reversal of sleep alterations and depression-like behavior after early life blockade of 5-HT(1A)R in 5-HTT-/- mutants might open new perspectives regarding preventive care of sleep and mood disorders resulting from serotonin transporter impairments during development.

Animals↗
PubMed1985

Electroencephalographic correlates of cataplectic attacks in narcoleptic canines.

Cataplectic attacks were monitored behaviorally and polygraphically in 4 narcoleptic dogs, of which three inherited the disorder. The recorded EEG signals were evaluated by power spectral analysis. We found 3 distinct stages of cataplexy: an initial stage which resembled wakefulness with tonic suppression of EMG activity, a later stage which was highly similar to REM sleep, and a final transitional stage to wakefulness or NREM sleep. The first stage of cataplexy was characterized by full postural collapse, a waking-like EEG spectrum, visual tracking, and a hypotonic EMG. The second stage of cataplexy differed electrographically from the previous stage by the onset of hypersynchronous hippocampal theta activity, a REM-like EEG spectrum, larger amplitude EEG signals, and a higher peak theta frequency. Glazed eyes, sporadic rapid eye movements and muscle twitches were also present. The final stage of cataplexy was characterized by mixed amplitude, mixed frequency EEG activity, and by the absence of rapid eye movements, visual tracking, directed movements, and muscle twitches. The EEG spectra of two other narcoleptic phenomena, sleep-onset REM periods and NREM sleep onsets from cataplexy, were nearly identical to the spectra of the normally occurring REM and NREM sleep periods.

Alpha Rhythm↗
PubMed1977

A review of psychogenic aspects and treatment of bruxism.

The signs and symptoms of bruxism are detectable, but unfortunately, the hypothesized etiologies and mechanisms of their action have not been satisfactorily substantiated. 2. Researchers emphasize the significance of the oral cavity in expressing emotions and that occlusal adjustments and other mechanical types of treatment may be inadequate. 3. The treatment of bruxism involves the management of psychic tension, signs and symptoms, occlusal irritations, and neuromuscular habit patterns. 4. With the greater sophistication in the social sciences, therapy for bruxism in the future may become largely behavioral in nature, rather than mechanical.

Bruxism↗
PubMedDate not supplied

[Periodic movements of the limbs during sleep in childhood].

INTRODUCTION: Periodic movements of the limbs (PML) whilst sleeping is a disorder included in the group of intrinsic dysomnias which cause problems of insomnia and somnolence during the day. It is usually associated with the restless legs syndrome (it occurs in 80% of the patients with this syndrome) although PML may occasionally be an isolated finding. The prevalence of the disease is of 11%. It usually occurs in patients aged over 50 years, and the frequency increase with age. It is uncommon in persons aged under 30 years. In children it is almost unknown. When it does occur in this age group it is usually associated with the restless legs syndrome. OBJECTIVE: To obtain data regarding this disorder in childhood, in view of the scarcity of information available in the literature and the importance of the neuropsychological problems and difficulty with learning that affected children have. CLINICAL CASES: We report two cases of PML occurring in girls of under 7 years of age. They had severe associated neuropsychological disorders (disorders of behavior and feeding, psychotic episodes, etc.). The effect on performance at school led to complete failure in one case. We describe the clinical course of the two girls, emphasizing the variability, and both diagnostic and therapeutic difficulties. CONCLUSIONS: Although this condition is uncommon in childhood, it should always be borne in mind in cases of children with sleep disorders, since early diagnosis will prevent major behavior and learning problems.

Anticonvulsants↗
PubMed2005

State-dependent alterations in hippocampal oscillations in serotonin 1A receptor-deficient mice.

Mice lacking the serotonin 1A receptor (5-HT(1A)R) show increased levels of anxiety-related behavior across multiple tests and background strains. Tissue-specific rescue experiments, lesion studies, and neurophysiological findings all point toward the hippocampus as a potential mediator of the phenotype. Serotonin, acting through 5-HT(1A)Rs, can suppress hippocampal theta-frequency oscillations, suggesting that theta oscillations might be increased in the knock-outs. To test this hypothesis, local field potential recordings were obtained from the hippocampus of awake, behaving knock-outs and wild-type littermates. The magnitude of theta oscillations was increased in the knock-outs, specifically in the anxiety-provoking elevated plus maze and not in a familiar environment or during rapid eye movement sleep. Theta power correlated with the fraction of time spent in the open arms, an anxiety-related behavioral variable. These results suggest a possible role for the hippocampus, and theta oscillations in particular, in the expression of anxiety in 5-HT(1A)R-deficient mice.

Animals↗
PubMed1979

Electroencephalographic and behavioral tolerance to and cross-tolerance between D-Ala2-methionine-enkephalinamide and morphine in the rat.

Rats were given repeated intraventricular (i.vt.) injections of D-enkephalin (20 microgram/4 hr) or morphine (20 microgram/4 hr) for 72 to 96 hr during electroencephalograman(EEG) recording. Initial epileptiform EEG and associated wet-dog shakes occurred following D-enkephalin but not morphine. The epileptoid EEG progressed to a continous high-voltage EEG synchrony similar to morphine and was associated with behavioral stupor. Rapid eye movement sleep was also suppressed. Repeated administration of D-enkephalin or morphine produced tolerance to their effects. When challenged with i.vt. morphine, D-enkephalin-tolerant rats were cross-tolerant to morphine. Likewise, morphine-tolerant rats were cross-tolerant to D-enkephalin. While the morphine-tolerant rats demonstrated a marked abstinence syndrome when challenged with naloxone (10 mg/kg i.p.), no abstinence signs were observed in the D-enkephalin-tolerant rats. The demonstration of tolerance and cross-tolerance between morphine and D-enkephalin suggests a similar mechanism of action, but the differential development of physical dependence may entail different mechanisms or receptor sensitivities for this effect. These findings of similarities and differences in the acute and chronic effects of D-enkephalin and morphine support the contention that heterogenous opiate receptors may mediate their pharmacologic actions.

Animals↗
PubMed1983

Effect of methylmercury chloride on sleep-waking rhythms in rats.

Effects of methylmercury chloride (MMC) on circadian sleep-waking rhythms were examined in rats which had been chronically implanted with EEG and EMG electrodes. Bihourly distributions of wakefulness (W), slow wave sleep (SWS) and paradoxical sleep (PS) and 12-h amounts of W, SWS and PS during light and dark periods were measured before and after MMC administration for 2 successive days at 3 dose levels. A total dose of 10 mg MMC/kg body wt was found to be the threshold for inducing reversible changes in the sleep-waking patterns. A total dose of 30 mg MMC/kg produced an increase in both dark-phase SWS and PS as well as a decrease in light-phase PS at the expense of an increase in light-phase W and a delayed phase of the circadian PS rhythm. The delayed phase of the PS rhythm tended to persist after the increased SWS during the dark period returned to normal. Brain mercury concentrations were measured in order to find the dose-response relationship and the time dependence of the MMC-induced sleep disorder. The sleep-waking disorder was found to appear at lower levels of brain Hg and shorter latency than behavioral disorders of movement and postural maintenance previously reported [5-8].

Animals↗
PubMed1980

Decrease in speech pause times with treatment of endogenous depression.

Szabadi et al. claimed that speech pause time--the silent interval between phonations--was significantly elongated during episodes of unipolar depressions; thus representing an objective measure of psychomotor retardation. Phonation times were said to be unchanged. To replicate and possibly expand these findings, we measured pause and phonation times among four unipolar (UP) and three bipolar (BP) endogenously depressed inpatients. Speech was recorded while patients counted from one to ten at their desired rate, and then converted to paper prints with a voice-operated electrical relay. Among all patients, pause times were substantially longer during base-line medication-free periods than at discharge. Progressive decreases occurred in conjunction with clinical improvement. These data replicated Szabadi's observation on UP patients and extended it to BP depressed patients. Of potential clinical importance, in two cases we documented decreases in pause time of more than 50% within several days after starting treatment. Speech pause times may be pragmatically useful as objective pathophysiologic markers in depression. Significant decreases occur with recovery, and early decreases during treatment may, like changes in REM sleep, be predictive of ultimate clinical response.

Adult↗
PubMed2006

Sleep disorders in psychiatry.

Sleep is an active state that is critical for our physical, mental, and emotional well-being. Sleep is also important for optimal cognitive functioning, and sleep disruption results in functional impairment. Insomnia is the most common sleep disorder in psychiatry. At any given time, 50% of adults are affected with 1 or more sleep problems such as difficulty in falling or staying asleep, in staying awake, or in adhering to a consistent sleep/wake schedule. Narcolepsy affects as many individuals as does multiple sclerosis or Parkinson disease. Sleep problems are especially prevalent in schizophrenia, depression, and other mental illnesses, and every year, sleep disorders, sleep deprivation, and sleepiness add billions to the national health care bill in industrialized countries. Although psychiatrists often treat patients with insomnia secondary to depression, most patients discuss their insomnia with general care physicians, making it important to provide this group with clear guidelines for the diagnosis and management of insomnia. Once the specific medical, behavioral, or psychiatric causes of the sleep problem have been identified, appropriate treatment can be undertaken. Chronic insomnia has multiple causes arising from medical disorders, psychiatric disorders, primary sleep disorders, circadian rhythm disorders, social or therapeutic use of drugs, or maladaptive behaviors. The emerging concepts of sleep neurophysiology are consistent with the cholinergic-aminergic imbalance hypothesis of mood disorders, which proposes that depression is associated with an increased ratio of central cholinergic to aminergic neurotransmission. The characteristic sleep abnormalities of depression may reflect a relative predominance of cholinergic activity. Antidepressant medications presumably reduce rapid eye movement (REM) sleep either by their anticholinergic properties or by enhancing aminergic neurotransmission. Intense and prolonged dreams often accompany abrupt withdrawal from antidepressant drugs, a reflection of an REM rebound after drug-induced REM deprivation. The postulated link between sleep and psychiatric disorders has been reinforced by the findings of modern neurobiology.

Circadian Rhythm↗
PubMed1980

Focusing on dreams. A preparation program for psychotherapy.

Forty-eight patients selected as potential early dropouts from insight-oriented psychotherapy were offered a two-week program to prepare them for treatment. Thirty-two were sleep-monitored for eight nights; half were given access to their dreams by awakening them from rapid eye movement (REM) sleep periods; the other half were awakened as often, but only from non-FEM (NREM) stages. A third group of 16 subjects went directly into treatment. All laboratory subjects were asked each morning to recall and discuss the reports they had given during the night. The effect of these discussions was measured on the drop-out rate during the first ten treatment hours and on the development of treatment-appropriate behaviors. Those who successfully retrieved and discussed dreams as opposed to other content stayed in therapy at a significantly higher rate and used the hours more productively.

Adolescent↗
PubMed2004

Refractory insomnia and sleep-disordered breathing: a pilot study.

OBJECTIVE: To assess an uncontrolled, open-label trial of sleep-disordered breathing (SDB) treatment on two different samples of chronic insomnia patients. METHOD: In Study 1 (Retrospective), data from one diagnostic and one continuous positive airway pressure (CPAP) titration polysomnogram were compiled from 19 chronic insomnia patients with SDB. Objective polysomnogram indicators of sleep and arousal activity and self-reported sleep quality were measured. In Study 2 (Prospective), clinical outcomes were assessed after sequential cognitive-behavioral therapy (CBT) and SDB therapy (CPAP, oral appliances, or bilateral turbinectomy) were provided to 17 chronic insomnia patients with SDB. Repeat measures included the Insomnia Severity Index, Functional Outcomes of Sleep Questionnaire, Pittsburgh Sleep Quality Index, and self-reported insomnia indices and CPAP use. RESULTS: In Study 1, seven objective measures of sleep and arousal demonstrated or approached significant improvement during one night of CPAP titration. Sixteen of 19 patients reported improvement in sleep quality. In Study 2, Insomnia Severity Index, Functional Outcomes of Sleep Questionnaire, and Pittsburgh Sleep Quality Index improved markedly with CBT followed by SDB treatment and achieved an average outcome equivalent to curative status. Improvements were large for each treatment phase; however, of 17 patients, only 8 attained a nonclinical level of insomnia after CBT compared with 15 patients after SDB therapy was added. Self-reported insomnia indices also improved markedly, and self-reported SDB therapy compliance was high. CONCLUSIONS: In one small sample of chronic insomnia patients with SDB, objective measures of insomnia, arousal, and sleep improved during one night of CPAP titration. In a second small sample, validated measures of insomnia, sleep quality, and sleep impairment demonstrated clinical cures or near-cures after combined CBT and SDB therapies. These pilot results suggest a potential value in researching the pathophysiological relationships between SDB and chronic insomnia, which may be particularly relevant to patients with refractory insomnia.

Chronic Disease↗
PubMed2001

Hypocretin-2-saporin lesions of the lateral hypothalamus produce narcoleptic-like sleep behavior in the rat.

Hypocretins (Hcrts) are recently discovered peptides linked to the human sleep disorder narcolepsy. Humans with narcolepsy have decreased numbers of Hcrt neurons and Hcrt-null mice also have narcoleptic symptoms. Hcrt neurons are located only in the lateral hypothalamus (LH) but neither electrolytic nor pharmacological lesions of this or any other brain region have produced narcoleptic-like sleep, suggesting that specific neurons need to be destroyed. Hcrt neurons express the Hcrt receptor, and to facilitate lesioning these neurons, the endogenous ligand hypocretin-2/orexin B (Hcrt2) was conjugated to the ribosome-inactivating protein saporin (SAP). In vitro binding studies indicated specificity of the Hcrt2-SAP because it preferentially bound to Chinese hamster ovary cells containing the Hcrt/orexin receptor 2 (HcrtR2/OX(2)R) or the Hcrt/orexin receptor 1 (HcrtR1/OX(1)R) but not to Kirsten murine sarcoma virus transformed rat kidney epithelial (KNRK) cells stably transfected with the substance P (neurokinin-1) receptor. Administration of the toxin to the LH, in which the receptor is known to be present, eliminated some neurons (Hcrt, melanin-concentrating hormone, and adenosine deaminase-containing neurons) but not others (a-melanocyte-stimulating hormone), indicating specificity of the toxin in vivo. When the toxin was administered to the LH, rats had increased slow-wave sleep, rapid-eye movement (REM) sleep, and sleep-onset REM sleep periods. These behavioral changes were negatively correlated with the loss of Hcrt-containing neurons but not with the loss of adenosine deaminase-immunoreactive neurons. These findings indicate that damage to the LH that also causes a substantial loss of Hcrt neurons is likely to produce the multiple sleep disturbances that occur in narcolepsy.

Adenosine Deaminase↗
PubMed1984

A mechanism of mania and the chemistry of dreams: a hypothesis.

A suggested cause of mania is asynchrony of two biologic clocks that are involved with the sleep-waking mechanism. Increased norepinephrine in the synaptic clefts of the locus ceruleus could quicken the pace of one clock. That same increase in norepinephrine is a possible inducer of euphoria and hyperactivity in mania. The action of melatonin and/or vasotocin on the dorsal raphe nucleus may induce the hallucinatory behavior in mania. Lithium corrects the psychosis by inhibiting adenylate cyclase and slowing the circadian rhythm.

Biological Clocks↗
PubMed1990

[Parasomnia associated with abnormal REM sleep in the aged].

Three aged patients (age 63-78 years) had 3-15-year histories of abnormal behaviors during nocturnal sleep. These three patients presented no other psychiatric problems. Polysomnographic recordings were carried out from 1-3 nights after adaptation. The patients were simultaneously monitored via a video system during the recording period. Various nocturnal behaviors, including laughing, weeping, the shaking of arms and getting up were detected during these recordings. These behaviors appeared exclusively during REM periods which were associated with a large amount of abnormal REM sleep lacking muscle atonia (d-STREM with EMG). NREM sleep architecture was intact and %SWS was within the normal limits per age for all the patients. The patients, manifesting such abnormal behaviors during sleep, could be aroused completely with awakening stimuli, and could recall in detail their unpleasant dreams. Two of the three were treated with clonazepam (0.5-1 mg/day) which immediately decreased the abnormal behaviors during sleep. Polysomnographic studies after the treatment showed a marked decrease in the d-STREM with EMG. The above results indicate that these abnormal behavior during nocturnal sleep were closely linked to d-STREM with EMG. And the administration of clonazepam not only led to an amelioration in the abnormal behaviors but also in the polysomnographic pathology. It is concluded that parasomnia in the aged is characterized by behavioral manifestations of the dreaming due to dysfunctions of the muscle atonia system.

Aged↗