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C Gottesmann

Publications and source records attributed to C Gottesmann.

At least 37 records · Page 2Linked to original sources
PubMed1991

Anticonvulsant and sleep-waking influences of riluzole in a rat model of absence epilepsy.

Six WAG/Rij rats, an animal model of human absence epilepsy, were injected intraperitoneally with riluzole. At 4 mg/kg, riluzole decreased the number, mean duration and spike-frequency of the spontaneously occurring discharges for 3 h. Riluzole also increased slow wave sleep at the expense of waking. As riluzole at 3 mg/kg decreased the number and spike-frequency of the discharges without inducing a sedative effect, this compound could be of therapeutic interest in human absence epilepsy.

Animals↗
PubMed1991

Riluzole prevents hyperexcitability produced by the mast cell degranulating peptide and dendrotoxin I in the rat.

Using electroencephalographic (EEG) recordings in freely moving rats and extracellular neuronal firing-rate recordings in hippocampal slices, we examined the effects of riluzole (RP 54274), a compound with anti-glutamate properties, against the convulsive seizures and the cellular hyperexcitability produced by the mast-cell degranulating peptide (MCD), dendrotoxin I (DTXi) and 4-aminopyridine (4-AP). I.c.v. administration of riluzole (10 nmol) prevented the seizures induced by MCD, and to a lesser extent those due to DIXi, whilst leaving 4-AP seizures unaffected. This effect was also present after oral administration of the compound (4 mg kg-1) and lasted for approximately 6 h. Electrophysiological recordings in vitro confirmed that riluzole dose dependently and reversibly abolished the sustained increase in firing rate induced by both MCD and DTXi in the hippocampus. These results indicate that the anti-epileptic spectrum of riluzole in this model has similarities with, but is not identical to, that of classical potassium channel openers, and differs from that of calcium channel blockers or other glutamate antagonists such as D(-)-2-amino-5-phosphono-valeric acid. However, since MCD releases glutamate, the preventive effect of riluzole in this model may involve direct or indirect interaction with glutamatergic processes.

4-Aminopyridine↗
PubMed1991

The intermediate stage of sleep in mice.

Seven mice of Balb/C strain were implanted with electrodes to perform sleep-waking recordings. In 100% of the cases, the mice showed, prior to paradoxical sleep, the intermediate stage of sleep characterized by high-amplitude cortical spindles interspersed with slow waves and low-frequency theta rhythm in the dorsal hippocampus. Consequently, the intermediate stage which seems to correspond to a transient functional isolated forebrain does exist in the rat, cat and mouse. in the rat, cat and mouse.

Animals↗
PubMed1991

Hippocampal and cortical EEG activity in rats with transected hypothalamus.

The brain was transected in eight rats: the transection passed through the posterior pole of the superior colliculi and ended down at midhypothalamic level. The EEG activity in the dorsal hippocampus and cortex showed continuously slow, high amplitude waves. Thus the posterior hypothalamus is critical for the previously described hippocampal theta rhythm found in rats transected at the posthypothalamic level.

Animals↗
PubMed1990

Genetically epileptic rats show a pronounced intermediate stage of sleep.

Rats of the genetically epileptic WAG/Rij strain show a more long-lasting intermediate stage of sleep compared to rats of the Wistar strain. Therefore the WAG/Rij strain provides a privileged model for studying this stage of sleep. On the other hand, the percentage of paradoxical sleep in WAG/Rij rats is lower than in Wistar rats, for the reason that the intermediate stage in WAG/Rij rats is less frequently followed by paradoxical sleep and more frequently by slow wave sleep and especially by arousals. It is speculated that the epileptic rats encounter a greater difficulty in entering into paradoxical sleep.

Animals↗
PubMed1989

Analogies and differences in the mode of action and properties of binding sites (localization and mutual interactions) of two K+ channel toxins, MCD peptide and dendrotoxin I.

Both the bee venom toxin, mast cell degranulating (MCD) peptide, and the snake toxin, dendrotoxin 1 (DTX1) induce epileptiform activity and paroxystic seizures after intracerebroventricular (i.c.v.) injection to rats. Although many of the properties of the two toxins, which are blockers of the same K+ channel, appear to be very similar, a number of differences have been found. (1) Induced seizures have an hippocampal origin for MCD and two different origins, situated in the cortex and in the limbic system, for DTX1. (2) A first i.c.v. administration of DTXI desensitizes against a second ipsilateral injection of the same peptide as we had previously observed for MCD. However no cross-desensitization was observed between the two different toxins. (3) The number of high affinity (Kd = 41 pM) binding sites for 125I-DTXI in synaptic membranes is about 5 times higher than the number of high affinity (Kd = 158 pM) binding sites for 125I-MCD. (4) Autoradiographic analysis of the distribution of high affinity 125I-DTX1 binding sites has been compared to our previous analysis of high affinity 125I-MCD binding sites. High levels of high affinity binding sites for both toxins seem to be localized in synapse-rich areas. However high affinity binding sites for the two toxins are not always co-localized. Analysis of the mutual interactions between DTXI and MCD binding sites has revealed the presence of classes of low affinity binding sites for MCD. In most areas of the brain, a large proportion of high affinity binding sites for DTXI is allosterically related to low affinity binding for MCD.

Animals↗
PubMed1989

Subtypes of K+ channels differentiated by the effect of K+ channel openers upon K+ channel blocker-induced seizures.

Intracerebroventricular injection of mast-cell degranulating peptide (MCD), dendrotoxin I (DTXI) and 4-aminopyridine (4-AP), 3 blockers of a subclass of K+ channel, produces seizures and convulsions. Three different K+ channel openers are potent blockers of MCD-induced hyperexicitatory effects when they are administered preventively but they are unable to inhibit the epileptogenic effects induced by DTXI and 4-AP which were thought to block the same K+ channel which is blocked by MCD.

4-Aminopyridine↗
PubMed1989

Ca2+ channel blockers prevent seizures induced by a class of K+ channel inhibitors.

Intracerebroventricular injection into rats of mast-cell degranulating peptide (MCD), dendrotoxin I (DTXI) and 4-aminopyridine (4-AP), three blockers of a subclass of K+ channels, elicited epileptiform wave bursts and convulsions. Three different types of L-type Ca2+ channel inhibitors (+)PN 200-110, a 1,4-dihydropyridine, (-)D888, a phenylalkylamine, and fluspirilene, a diphenylbutylpiperidine, were potent blockers of the convulsant-induced hyperexcitatory effects when they were administered preventively. D-AP5, a N-methyl-D-aspartate antagonist, was active on the 4-AP-induced seizures but was without effect on the MCD- and dendrotoxin-induced seizures.

4-Aminopyridine↗
PubMed1989

Hippocampal theta activity in the acute precollicular rat.

In eleven acute precollicular rats, cortical and hippocampal EEG activity was recorded. Hippocampal theta activity of low frequency (mean 4.5 c/sec) was found in nine rats and in four occupied above 50% of the recording time. In contrast, in the cortex the synchronized EEG activity dominated. The electrical stimulation of the posterior hypothalamus induced the theta rhythm, or increased its frequency. The large amounts of theta activity in some rats suggests that the forebrain theta pacemakers, partly modulated by the posterior hypothalamus, are released from brain stem inhibitory influences.

Animals↗
PubMed1989

Influence of instructions in multi-discrimination experiments on event related potentials.

The purpose of the experiment was to study the effects of psychological factors on slow brain potentials in relation to information processing and strategy establishment. Subjects were subjected to paired stimuli: A) two identical tone bursts (50 ms, 5000 Hz); B) two different stimuli the second (unconditioned) was a low pitched tone burst (50 ms, 500 Hz); C) only the warning stimulus was delivered to the subjects. In a first experiment, subjects (N = 10) were asked to detect and signal by a motor act the low pitched click (B); in a second experiment, subjects (N = 8) were to detect and signal in the same way the unconditioned tone burst omission (C). Results showed that the auditory event-related potentials (ERP) obtained in the two experiments presented two components: a negative wave (N150) followed by a positive one (P270). Solely, the late positive component differed in topography during the two situations. A fronto-central Contingent Negative Variation (CNV) appeared in all the conditions for the two experiments while a Post Imperative Negative Variation was often obvious in the first experiment.

Adult↗
PubMed1988

Fetal serotoninergic transplants in the fourth ventricle of adult rodents reverse sleep disturbances induced by neonatal administration of 5,7-dihydroxytryptamine.

Rats received a neonatal (at 4 days of age) intracisternal injection of 5,7-dihydroxytryptamine which eliminates serotonin (5-HT) throughout adulthood. Sleep recordings, performed on these rats at adult age, demonstrated significant decreases in paradoxical sleep. Dissociated fetal 5-HT cell suspensions transplanted in the IVth ventricle of these rats restored paradoxical sleep. However, fetal neuronal noradrenergic or cholinergic transplants did not restore paradoxical sleep. These results suggest that paradoxical sleep is directly or indirectly mediated through serotoninergic mechanisms.

5,7-Dihydroxytryptamine↗
PubMed1988

What the cerveau isolé preparation tells us nowadays about sleep-wake mechanisms?

The intercollicular transected preparation opened a rich field for investigations of sleep-wake mechanisms. Initial results showed that brain stem ascending influences are essential for maintaining an activated cortex. It was subsequently shown that the forebrain also develops activating influences, since EEG desynchronization of the cortex reappears in the chronic cerveau isolé preparation, and continuous or almost continuous theta rhythm is able to occur in the acute cerveau isolé preparation. A brief "intermediate stage" of sleep occurs during natural sleep just prior to and after paradoxical sleep. It is characterized by cortical spindle bursts, hippocampal low frequency theta activity (two patterns of the acute cerveau isolé preparation) and is accompanied by a very low thalamic transmission level, suggesting a cerveau isolé-like state. The chronic cerveau isolé preparation also demonstrates that the executive processes of paradoxical sleep are located in the lower brain stem, while the occurrence of this sleep stage seems to be modulated by forebrain structures.

Animals↗
PubMed1987

The brain response to the bee venom peptide MCD. Activation and desensitization of a hippocampal target.

The mast cell-degranulating peptide (MCD) isolated from bee venom has been found previously to have receptor sites in rat brain. Behavioral and electrocorticographic responses following intracerebroventricular injections of various doses of MCD have been analyzed. MCD produced a quasi-permanent hippocampal theta rhythm in the motionless animal alternating with epileptiform spike waves and paroxystic seizures. At a dose of 70 pmol seizures occurred for half of the treated rats. At a dose of 100 pmol generalized paroxystic crises were observed for all the rats. These effects were not antagonized by naloxone, morphine, diazepam and progabide. Rats recovered 24 h after a 100 pmol injection of MCD. A second ipsilateral injection to these rats showed the occurrence of a desensitization phenomenon. Desensitization was not observed when the second injection was contralateral. These physiological responses were studied in relation with a biochemical approach on membrane sites of action of MCD using [125I]MCD and their behavior in the desensitization process. The target of [125I]MCD is the ipsilateral hippocampus. Recovery from MCD effects was not due to MCD degradation. Desensitization was not due to down-regulation of the MCD receptor level.

Animals↗
PubMed1987

Sleep deprivation decreases the beard-hair growth in man.

Ten young men underwent a sleep deprivation of 48 h which resulted in a 19 percent decrease of beard-hair growth. This effect, reflecting the lowering of protein synthesis during sleep deprivation, was presumably related to hormonal disturbance, namely depression of growth hormone release, decrease of dihydroxytestosterone availability or increase of sympathetic tone and/or corticoids.

Hair↗