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R Capek

Publications and source records attributed to R Capek.

At least 37 records · Page 2Linked to original sources
PubMed1985

Effects of ammonium chloride on synaptic transmission in the rat hippocampal slice.

Effects of ammonia on excitatory synaptic transmission were studied in the rat hippocampal slice preparation. Population spikes, elicited by orthodromic or antidromic stimulation, were recorded in the cell body layer of the CA1, CA3 and dentate regions. Perfusion with 5 mM ammonium chloride induced a profound and reversible depression of orthodromically evoked population spikes in all three regions. Antidromic population spikes were not depressed in any of the regions, indicating that neither axonal conduction nor electrical excitability were affected by ammonia. The paired-pulse test revealed a transient disinhibition during the early phase of perfusion. Iontophoretic application of glutamate evoked unit firing even when the synaptically evoked responses were reduced by ammonia, indicating that the postsynaptic sensitivity to the putative transmitter was not depressed. Depression of release of the excitatory transmitter, probably because of depletion following the block of transmitter synthesis, is the likely explanation of these findings. It is suggested that ammonia-induced depression of excitatory transmission may account for coma and other symptoms of central nervous system depression encountered in hyperammonemic states.

Ammonium Chloride↗
PubMed1984

Hippocampal field potential: a microcomputer aided comparison of amplitude and integral.

A microcomputer based system is described for the analysis of various aspects of hippocampal field potential response recorded in vitro, either in the dendritic or somatic region. A comparison is made between the average amplitude and the time integral of synaptically evoked population spike at the cell body layer, following various intensities of stimuli delivered to the stratum radiatum. There was a good correlation between the two measures at low and intermediate intensities of stimulation. With stimulus intensities beyond those eliciting the population spike of maximal integral, the amplitude of the population spike further increased while its duration decreased. It is concluded that the integral provides a more accurate estimate of the extent of neuronal firing than the amplitude.

Animals↗
PubMed1983

Effect of phencyclidine on inhibition in the hippocampal slice.

The effects of phencyclidine (PCP) on synaptic transmission were studied in the hippocampal slice. Population spikes evoked by orthodromic or antidromic stimulation were recorded from CAl pyramidal cells. Bath applied PCP (10(-4) M) reduced moderately both the orthodromic and antidromic population spikes. Lower concentrations, 5 X 10(-6) to 5 X 10(-5) M of PCP, which did not depress the population spikes, reduced inhibition of the orthodromically evoked spike in a dose dependent reversible manner. Diazepam (10(-6) to 10(-5) M) restored the inhibition despite the continued presence of PCP. It is suggested that PCP-induced seizures and other signs of hyperexcitability could be a result of reduced inhibition.

Action Potentials↗
PubMed1983

GABA-mediated responses are not selectively depressed by 3-mercaptopropionic acid in the spinal cord.

The competitive inhibitor of glutamic acid decarboxylase (GAD), 3-mercaptopropionic acid (MPA), causes depletion of gamma-aminobutyric acid and convulsions. We expected it to be a superior GABA depleting agent for in vivo experiments to the frequently used semicarbazide. The dorsal root potentials (DRP) and monosynaptic reflex responses (MSR) evoked by adjacent dorsal root and peripheral nerve stimulation, respectively, were recorded in spinal unanaesthetized cats. MPA (100-200 mg/kg) caused a gradual decrease in DRP, reaching a peak in about 40 min after drug administration. This was usually associated with convulsive activity. Postsynaptic direct inhibition was not substantially affected. However, the MSR was consistently decreased, within 10 min after injection of MPA. It is concluded that MPA is not a suitable tool, at least in the spinal cord, for the selective reduction of GABAergic transmission.

3-Mercaptopropionic Acid↗
PubMed1982

Baclofen-induced decrease of excitability of primary afferents and depression of monosynaptic transmission in cat spinal cord.

The relationship of the depressant effect of baclofen on spinal monosynaptic transmission and its effect on the excitability of primary afferents was examined in spinal unanesthetized cats. Baclofen (1.0 mg/kg, i.v.) produced a deep and long-lasting depression of spinal reflex responses with a concomitant decrease of terminal excitability. Primary afferent depolarization, as indicated by an increase of terminal excitability, evoked by conditioning of an antagonistic muscle nerve, was greatly reduced by this drug. Depression of monosynaptic transmission induced by baclofen was temporarily reversed by posttetanic potentiation. However, the same high frequency orthodromic stimulation further reduced excitability of terminals. It is therefore unlikely that block of terminal invasion is responsible for baclofen-induced depression of spinal monosynaptic transmission. These results are compatible with the suggestion that baclofen causes a reduction of transmitter release. In the spinal cord, this action is probably limited to the excitatory transmitter of primary afferents.

Afferent Pathways↗
PubMed1982

Excitability of primary afferents in feline spinal cord: taurine, homotaurine, and gamma-aminobutyric acid compared.

Effects of taurine and homotaurine (3-aminopropanesulfonic acid), on excitability of primary afferents were compared with effects of gamma-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazide, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.

Afferent Pathways↗
PubMed1979

The anticonvulsant effects of propranolol and beta-adrenergic blockade.

The anticonvulsant activity of racemic and (+)-propranolol was studied in rats. Neither drug changed the current to produce a minimal seizure in 50% of animals. Both drugs were effective in the maximal electroshock seizure test, the (+) isomer being more potent than the racemic form. Since the (+) isomer is practically devoid of beta-adrenergic blocking activity, the anticonvulsant effects of propranolol do not result from beta-adrenergic blockade.

Animals↗
PubMed1978

Assessment of ether anesthesia in normal and spinal cats using gas--liquid chromatographic analysis of blood.

A new gas-liquid chromatographic method was developed for the determination of diethylether in whole blood. Ether was quantitated by peak area ratio analysis with n-propanol as the internal standard using a flame ionization detector. Blood ether concentrations were determined in cats undergoing inhalational anesthesia by ether in oxygen. In normal spontaneously breathing cats, anesthesia began at ether concentrations of about 0.6 g/l, and respiratory arrest occurred at 2.4 g/l and above. Mean arterial blood pressure was well maintained throughout the entire anesthetic range. In spinal artificially respired animals, mean arterial blood pressure correlated inversely with blood ether concentration. The data suggest that decline in blood pressure may be a useful sign of ether toxicity in spinal cats.

Anesthesia↗
PubMed1978

Depression of spinal monosynaptic transmission by diethyl ether: quantal analysis of unitary synaptic potentials.

The site at which diethyl ether impairs transmission in the spinal monosynaptic pathway was studied by intracellular recording from lumbosacral motoneurons. The drug was administered by inhalation to spinal cats, in concentrations which produce surgical anesthesia. Ether had no significant effect on resting potential or input resistance of the cell membrane. It decreased the electrical excitability in some but not all motoneurons. This action may contribute to the depressant effects of ether. Monosynaptic excitatory postsynaptic potentials evoked by impulses in a single Ia afferent fiber (unitary EPSPs) of the triceps surae nerve were recorded from homonymous motoneurons. They were measured and their amplitude distribution was analyzed by a computer-aided procedure. The mean amplitude of the unitary EPSPs was 0.15 to 0.31 mV, and the mean number of transmitter quanta released by each impulse ranged from 1.5 to 4.1 before drug administration. Both values were decreased during inhalation of ether but recovered toward normal after the drug was discontinued. The mean amplitude of the EPSPs produced by one transmitter quantum was 0.08 to 0.15 mV and was not depressed during ether administration. It is concluded that either in anesthetic concentrations depresses synaptic potentials presynaptically by decreasing the amount of excitatory transmitter released, while leaving the chemosensitivity of the postsynaptic membrane unchanged.

Action Potentials↗
PubMed1977

Homosynaptic depression and transmitter turnover in spinal monosynaptic pathway.

1. The transmission in the spinal monosynaptic pathway was studied during repetitive stimulation of a motor nerve by 10 stimuli at 2, 5, or 10 Hz in spinal cats. Initially, the amplitudes of the monosynaptic responses rapidly declined, reaching a plateau after a few stimuli. The level of the plateau was inversely related to the frequency of stimulation. 2. This depression of monosynaptic response was seen only when the same pathway was stimulated; the response elicited from the lateral gastrocnemius was not depressed when preceded by stimulation of the medial gastrocnemius nerve and vice versa. Pretreatment with semicarbazide left the homosynaptic depression unchanged while suppressing the dorsal root reflex. The participation of a depolarization of primary afferents in the described depression is, therefore, unlikely. 3. The decrease of transmitter release by successive volleys, which is the cause of the observed depression, could conceivably be related to the depletion of transmitter stores. 4. A procedure is described, based on this assumption, which allows the calculation of transmitter turnover. The input-output relation in the spinal monosynaptic pathway is used to convert the amplitudes of monosynaptic responses to the amounts of transmitter, both relative to the maximum response. The changes of transmitter release are analyzed under the assumption that each volley releases instantaneously a constant fraction of the transmitter store available for release and that this store is replenished at a constant fraction of the depleted part per second. 5. The values of fractional release per volley were about 0.4, irrespective of frequency of stimulation. 6. The values of fractional replenishment per second ranged from about 1 to 5 on the average, depending directly on the frequency of stimulation. 7. It is suggested that the described procedure might be useful in analyzing drug effects on synaptic transmission.

Animals↗
PubMed1977

Effects of ethosuximide on transmission of repetitive impulses and apparent rates of transmitter turnover in the spinal monosynaptic pathway.

The effects of ethosuximide on spinal monosynaptic transmission were studied in cats. The drug in doses of 200 or 400 mg/kg deepened the decline of monosynaptic response amplitude evoked by trains of 10 stimuli to a motor nerve at 2, 5 or 10 Hz, without affecting the transmission of single isolated impulses. The patterns of decline were analyzed under the assumption that they reflect a partial depletion of the apparent transmitter stores in the presynaptic terminals, each incoming volley releasing a constant fraction of the store while a constant fraction of the instant size of the depleted part is being replenished per second. Ethosuximide increased the fractional release without a consistent effect on the fractional rate of replenishment. It is suggested that the resulting more rapid and more profound depletion of the apparent transmitter store could account for the observed preferential depression of repetitive transmission in the spinal monosynaptic pathway by this drug.

Animals↗
PubMed1976

Quantitative characterization of THC and ethanol interaction.

The anticonvulsant activity of ethanol, delta9-tetrahydrocannabinol and their combinations was measured in the maximal electroshock seizure test. The determined median anticonvulsant doses (ED50) of drug combinations were compared with those calculated on the assumption of additivity of doses. No significant difference was found between the determined and expected values. It is concluded that in this test ethanol and THC may interact additively.

Animals↗