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A Glatt

Publications and source records attributed to A Glatt.

13 recordsLinked to original sources
PubMed1992

The time course of sigma activity and slow-wave activity during NREMS in cortical and thalamic EEG of the cat during baseline and after 12 hours of wakefulness.

The extrapolation from recent neurophysiological findings concerning the dependency of spindle and slow-wave oscillations of thalamocortical neurons on membrane potential to macroscopic EEG events, predicts a reciprocal relation between spindle activity and slow-wave activity (SWA) in thalamic and cortical EEG during non-rapid-eye-movement sleep (NREMS). To test this hypothesis, the EEG recorded in 8 cats, from the nucleus centralis lateralis of the thalamus and from the skull during a 12-h baseline dark period and during a 12-h recovery dark period, following a 12-h sleep deprivation, were analyzed. Per 12-s epoch, sleep-wake behaviour was determined and spectral power density was computed in the slow-wave frequency range (0.5-4.0 Hz) and in the spindle frequency region (sigma activity: 11.0-14.5 Hz). To analyze the development of EEG power densities in the course of NREMS and during the transition from NREMS to REMS, the last epoch of wakefulness and the first 15 epochs of NREMS, as well as the last epochs of NREMS and the first epoch of REMS were selected from the NREM-REM cycles. For each animal the values were averaged over 4-h intervals. In the cortical EEG, SWA was minimal at NREMS onset and increased progressively in the course of NREMS. SWA declined sharply prior to REMS. sigma Activity increased gradually towards a uniform level after NREMS onset. During the transition to REMS, sigma activity initially increased and then decreased rapidly. In the thalamic EEG, the time course of SWA paralleled that of the cortex. However, the development of sigma activity during the first part of NREMS differed: in the thalamic EEG, sigma activity was maximal during the beginning of NREMS and slightly decreased thereafter. After sleep deprivation, SWA within NREMS was markedly enhanced in both the cortical and the thalamic EEG. Sigma activity was attenuated in the thalamic EEG, whereas in the cortical EEG it was temporarily elevated. The present data show that, in the thalamic EEG, an inverse relation exists between spindle and slow-wave activity during baseline NREMS. This relation is preserved after sleep deprivation. In the cortical EEG, a reciprocal relation between spindling and SWA is less evident.

Animals↗
PubMed1992

CGS 5649 B, a new compound, reverses age-related cognitive dysfunctions in rats.

CGS 5649 B improves the learning performance of aged rats in a one-way active-avoidance situation. If, under reversed conditions, treated aged rats are also tested for passive avoidance, they show "place learning," which our findings have demonstrated to be typical of young rats. The effects of the substance are not confined to these experimental models nor are they species specific: it also facilitates passive avoidance in mice and social learning in rats. The compound is effective if administered before or immediately after the learning trial.

Aging↗
PubMed1992

Enhanced slow-wave activity within NREM sleep in the cortical and subcortical EEG of the cat after sleep deprivation.

Electroencephalograms (EEGs) of the cortex and of seven subcortical structures were recorded during two baseline days and during a recovery day following a 12-hour period of sleep deprivation (SD) in eight cats. The EEGs were analyzed by visual scoring and by spectral analysis. The following subcortical structures were studied: hippocampus, amygdala, hypothalamus, nucleus centralis lateralis of the thalamus, septum, nucleus caudatus and substantia nigra. The EEGs of all brain structures exhibited sleep state-dependent changes. In general, slow-wave activity (SWA, 0.5-4.0 Hz) during nonrapid eye movement (NREM) sleep exceeded that of REM sleep. The power spectra (0.5-24.5 Hz) in NREM, as well as the relationship between the power spectra of NREM and REM sleep, differed between the recording sites. Moreover, the rate of increase of SWA in the course of an NREM episode and the rate of decrease of SWA at the transition from NREM to REM sleep differed between the brain structures. During the first 12 hours following SD, the duration of NREM increased due to a prolongation of the NREM episodes. REM increased by a rise in the number of REM episodes. During the same period, the NREM EEG power density in the delta and theta frequencies was enhanced in all brain structures. Furthermore, in all structures the enhancement of SWA was most pronounced at the beginning of the recovery period and gradually declined thereafter. SD also induced a rise in the rate of increase of SWA in the NREM episodes in all recording sites. This indicates that the enhancement of EEG power density was not only due to prolongation of the NREM episodes. The EEG activity during REM was barely affected by the SD. It is concluded that, in all brain structures studied, the EEG during NREM is characterized by high levels of SWA. Furthermore, in each brain structure, SWA within NREM sleep is enhanced after a prolonged vigil. These data may indicate that SWA reflects a recovery process in cortical and subcortical structures.

Animals↗
PubMed1991

Effects of circadian phase and duration of sleep deprivation on sleep and EEG power spectra in the cat.

The electroencephalogram (EEG) of cats was recorded under baseline conditions (LD 12:12) and after 4 and 8 h of sleep deprivation (SD). The EEG was analyzed by visual scoring and by spectral analysis. Under baseline conditions the 24-h distribution of sleep was bimodal: the smallest amounts of sleep occurred at the light-dark and dark-light transitions. EEG slow-wave activity (power density in the delta frequency range: 0.5-4.0 Hz) in non-rapid-eye-movement sleep (NREMS) showed a small variation over the 24-h period. When recovery sleep, following 4 h and 8 h of SD, started at the beginning of the dark period, no significant rebound of NREMS and REMS occurred during the 24-h recovery period. When recovery sleep, after 4 h of SD, started at the fifth hour of the light period, the amount of NREMS was increased. In all experiments the EEG power density in NREMS was enhanced after SD in the entire frequency range studied (0.5-31.5 Hz), but more prominently in the delta and theta (4.5-7.0 Hz) frequency bands. The effects dissipated in the course of the recovery period. The magnitude and duration of the enhancements of EEG power densities were dependent on the duration of SD and on the circadian phase at which SD was scheduled. It is concluded that in the cat sleep is a function of both circadian and homeostatic processes and that especially the EEG power density in NREMS is highly responsive to sleep loss.

Analysis of Variance↗
PubMed1989

Spontaneous motor activity in healthy volunteers after single doses of haloperidol.

Video recordings of the spontaneous motor activity of 6 healthy volunteers after treatment with 0.75 mg haloperidol i.v., or placebo, were transcribed into a time-series protocol of motor behaviour. Characteristic changes seen after the injection of haloperidol consisted in a reduction of the motility of the extremities and prolongation of the phases of both movement and immobility of the head. The tested dose of haloperidol induced a distinct rise in serum prolactin and sedation, but had no effects on the pharmaco-EEG or on the critical flicker-fusion frequency. Analysis of the motor phenomena evoked by neuroleptics in healthy persons and in patients may help, on the other hand, to establish correlations with the motor effects observable in preclinical investigations in animals and might also contribute towards the elucidation of the extrapyramidal side-effects of these drugs.

Adult↗
PubMed1988

Antimicrobial agents.

Explore the source record for details and available documents.

Drug Administration Schedule↗
PubMed1987

Cholinomimetics induce theta rhythm and reduce hippocampal pyramidal cell excitability.

The actions of cholinomimetics and of physostigmine were tested on two parameters reflecting hippocampal activity, namely theta activity and pyramidal cell excitability. In rats pretreated with methylscopolamine and anaesthetized with urethane i.v. administration of the cholinomimetics oxotremorine and arecoline and the cholinesterase blocker physostigmine evoked theta wave activity in the hippocampus, which was blocked by scopolamine. Spectral analysis demonstrated that the frequency of the theta waves induced was dose-related, ranging from about 3 Hz to between 5 and 6 Hz. theta Activity could not be induced by arecoline in animals with large septal lesions. Pyramidal cell excitability is known to be increased by endogenous acetylcholine released from cholinergic fibres. In the present study, however, i.v. injections of oxotremorine, arecoline and physostigmine in doses that induce theta activity diminished the excitability of CA1 pyramidal cells in a dose-dependent manner, as judged by the reduction in the amplitude of the population spike and the dendritic epsp. These depressant effects were attenuated by scopolamine but not by methylscopolamine. The depressant effect of arecoline was attenuated in rats with extensive lesions in the medial septal area. The present findings demonstrate that exogenously administered cholinomimetics only partly mimic the action of endogenous acetylcholine in the hippocampus. The central sites of action of exogenously administered cholinomimetics for mediation of theta activity and alteration of pyramidal cell excitability remain to be elucidated.

Acetylcholinesterase↗
PubMed1986

Behavioral effects and general pharmacology of 4-(5-chloro-benzofuranyl-2)-1-methylpiperidine HC1, an antidepressant inhibiting both monoamine oxidase A and 5-hydroxytryptamine uptake.

In psychopharmacological tests in rats and mice, 4-(5-chloro-benzofuranyl-2)-1-methylpiperidine HC1 (CGP 4718 A) was found to exert behavioral effects typical of both monoamine oxidase (MAO)-A and 5-hydroxytryptamine (5-HT) uptake inhibitors (reserpine antagonism, L-5-HTP potentiation, antiaggressive activity in isolated mice). The potential antidepressant activity of the drug was indicated in rats by antagonism of reserpine and its effect in the social-conflict test. CGP 4718 A did not impair motor coordination and had no influence on locomotor activity up to high doses in mice and rats. In monkeys, it increased directed individual activities, including sex-related behaviors and diminished locomotor activity and passivity. Electroencephalographic studies in cats revealed a significant decrease in paradoxical sleep after treatment with CGP 4718 A. In isolated organs, no significant antagonism of norepinephrine, 5-HT, acetylcholine or histamine was found. Cardiovascular studies in cats showed only transient effects on blood pressure and no effect on heart rate. In conscious dogs no cardiovascular effects were found. No potentiation of the pressor effect of tyramine in rats was detectable after repeated doses of up to 300 mg/kg p.o. A weak cardiodepressant effect was seen in isolated guinea pig atria. In conclusion, in animal experiments CGP 4718 A combines an interesting spectrum of antidepressant, activating and antiaggressive properties with a lack of cardiovascular and tyramine-potentiating effects.

Animals↗
PubMed1979

Epileptic phenomena induced in the cat by the antidepressants maprotiline, imipramine, clomipramine, and amitriptyline.

The epileptogenic properties of four tricyclic antidepressant drugs: maprotiline, imipramine, clomipramine, amitriptyline, were investigated in locally anesthetized cats immobilized with gallamine and supplied with neocortical, hippocampal, and reticular recording electrodes. The drugs were infused intravenously at a constant rate (0.5 or, in some cases, 0.25 mg/kg per min) up to a final dose of 45 mg/kg. Already in small doses (1 to 5 mg/kg) all four antidepressants produced local signs of epileptiform pathology. Generalized sustained discharges occurred, on the average, at between 20 and 25 mg/kg with all four drugs. Imipramine and amitriptyline, after the first or first few generalized discharges, led to a pattern of repeated short generalized seizures alternating with silent periods. Maprotiline invariably produced this later alternating pattern only after a 10- to 30-min period of a seminormal high amplitude pattern. Clomipramine assumed a position between maprotiline on the one hand and imipramine and amitriptyline on the other. Starting at doses of 2-4 mg/kg, imipramine, clomipramine and amitriptyline, all three being norepinephrine and serotonin uptake inhibitors, induced a high amplitude "sleep" pattern. Maprotiline, a norepinephrine uptake inhibitor, which is thought devoid of serotonin-uptake inhibiting properties, led to high amplitude slow waves only with doses of at least 12.5 to 15 mg/kg.

Amitriptyline↗
PubMed1978

EEG effects of the ventricular cerebrospinal fluid of rabbits submitted to thalamic stimulation.

Electrical stimulation of the "somnogenic" thalamic area of Hess in chronic rabbit donors significantly increases the EEG delta activity against controls (41%; p less than or equal to 0.05). In recipient rabbits infused with cerebrospinal fluid (csf) from these donors, the delta increase against control rabbits (26%) suggests a sedative activity of the infused csf, able to counteract the waking tendency in chronic recipients.

Animals↗
PubMed1978

Influence of vincamine and piracetam on sleep--waking pattern of the cat.

The effect of Vincamine and Piracetam, two geriatric drugs, on sleep behavior of the laboratory cat was studied. The animals were chronically prepared for recording of the EEG of the cerebral cortex, the lateral geniculate body, and the hippocampus, and for recording of eye movements, the muscular tonus and respiration. During the experiment, sleep and waking behavior were monitored by the above mentioned telemetrically transmitted indicators and also through observation via closed-circuit television. Both Vincamine and Piracetam in doses of 1 and 300 mg/kg p.o., respectively, enhance absolute and relative amounts of paradoxical sleep (PS). Smaller doses have a lesser or no effect on PS. Larger doses again have little effect or else, in the first few hours after application, reduce PS and total amount of sleep. Both drugs have little effect on slow wave and total sleep. Piracetam, but not Vincamine, reduces the prominent frequency of the theta band in hippocampus during PS. The PS-enhancing effect of the two geriatric drugs may be related to their memory-improving influence.

Animals↗