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M L Zeise

Publications and source records attributed to M L Zeise.

15 recordsLinked to original sources
PubMed1997

Interleukin-1beta does not increase synaptic inhibition in hippocampal CA3 pyramidal and dentate gyrus granule cells of the rat in vitro.

Effects of interleukin-1beta (bath-applied; 500 pM) on rat hippocampal CA3 pyramidal and dentate granule cells were studied using intracellular microelectrode recording in vitro. In both cell types membrane input resistance, resting membrane potential and action potential amplitude remained stable throughout. No change was seen in postsynaptic potentials in granule cells. After blocking excitatory synaptic transmission in CA3 pyramids interleukin-1beta was found to consistently decrease synaptic inhibition by about 30%.

Animals↗
PubMed1996

Corticosterone-induced decrease of inhibitory postsynaptic potentials in rat hippocampal pyramidal neurons in vitro depends on cytosolic factors.

Previous studies using high-resistance sharp electrodes demonstrated that corticosterone (CORT) reduced GABAergic synaptic inhibition in CA1 neurons of the rat hippocampus in vitro. In the present study we used whole-cell gigaseal recordings to investigate the possible role of cytosolic factors in the transduction mechanism underlying this action. The perturbation of the intracellular milieu that occurs under these recording conditions abolished the CORT-induced decrease in inhibitory postsynaptic conductance. CORT actually increased GABAA receptor-mediated conductances in about 50% of the neurons tested when the whole-cell recording mode was employed. As in the high-resistance microelectrode studies, CORT did not change the resting membrane potential, action potential amplitude or input resistance. The results suggest that the reduction of GABAergic synaptic inhibition in hippocampal CA1 pyramidal neurons induced by CORT critically depends on the presence of cytosolic factors, which wash out during whole-cell gigaseal recordings.

Animals↗
PubMed1995

The neuroactive steroid 5 alpha-tetrahydrodeoxycorticosterone increases GABAergic postsynaptic inhibition in rat neocortical neurons in vitro.

The neuroactive steroid 5 alpha-pregnane-3 alpha, 21-diol-20-one (5 alpha-tetrahydrodeoxycorticosterone; 5 alpha-THDOC) has been shown to potentiate GABA-induced chloride currents in cell cultures and subcellular preparations. In this study, we recorded from pyramidal neurons in an in vitro slice preparation of the adult rat frontal neocortex using intracellular microelectrodes. 5 alpha-THDOC (10 microM) increased and prolonged the inhibitory postsynaptic potential (IPSP). The mean maximal synaptic conductance of the early, GABAA receptor-mediated, IPSP was enhanced to more than 700%, the one at the maximum of the late, partially GABAB receptor-mediated, IPSP to approximately 400%. The progesterone/glucocorticoid receptor antagonist RU 38486 did not prevent the IPSP increase. At a concentration of 1 microM 5 alpha-THDOC increased only the early IPSP to about 125%. Responses to the iontophoretically applied specific GABAA receptor agonist muscimol but not to the specific GABAB receptor agonist L-baclofen were enhanced by 5 alpha-THDOC (10 microM). In the giga-seal whole-cell configuration when the GABAB receptor-mediated IPSP component was absent due to intracellular perfusion, 5 alpha-THDOC (10 microM) increased IPSPs to a similar extent as in the conventional microelectrode recordings. Excitatory postsynaptic potentials, resting membrane potential, input resistance and action potential amplitude were not affected by 5 alpha-THDOC (10 microM). These data demonstrate that in neocortical tissue of the rat 5 alpha-THDOC enhances GABAergic inhibition by interacting with postsynaptic GABAA receptors while synaptic excitation and parameters of electric excitability remain unchanged.

Animals↗
PubMed1994

The 5-HT3 receptor agonist 2-methyl-5-HT reduces postsynaptic potentials in rat CA1 pyramidal neurons of the hippocampus in vitro.

The effects of the serotonin (5-HT)3 receptor agonist, 2-methyl-5-hydroxytryptamine (2-methyl-5-HT), were studied in CA1 pyramidal cells of the rat hippocampus in vitro using the whole cell gigaseal technique. 2-Methyl-5-HT (10 and 50 microM) did not change significantly the electrophysiologic properties of the cells but reversibly reduced excitatory and inhibitory postsynaptic potentials evoked by stimulation of the Schaffer collaterals. The onset and termination of this effect was in the order of minutes and no desensitization was observed. The selective 5-HT3 receptor antagonist, granisetron, when applied as a pretreatment completely prevented but did not reverse this action when given after administration of 2-methyl-5-HT while the non-specific 5-HT1,2 receptor antagonist, metergoline, was ineffective. These results suggest that the activation of 5-HT3 receptors reduces the efficacy of glutamatergic synaptic transmission in this area.

Animals↗
PubMed1993

Acamprosate (calciumacetylhomotaurinate) decreases postsynaptic potentials in the rat neocortex: possible involvement of excitatory amino acid receptors.

Acamprosate (calciumacetylhomotaurinate) is used therapeutically against relapse in weaned alcoholics. In the present study, the mechanism of action was investigated by making intracellular in vitro and extracellular in vivo recordings from rat neocortical neurons. Acamprosate (0.1-1 mM) added to the perfusion fluid in vitro reduced excitatory and inhibitory postsynaptic potentials and the depolarizing responses evoked by iontophoretic application of the excitatory amino acids, L-glutamate, L-aspartate, L-homocysteate and N-methyl-D-aspartate, but did not alter the responses to gamma-aminobutyric acid. Acamprosate decreased electrical excitability without apparently changing membrane potential, input resistance, afterhyperpolarization, or threshold and amplitude of the action potential. In vivo iontophoretic application of acamprosate reduced the extracellularly recorded unit activity elicited by iontophoretically applied L-glutamate, whereas spontaneous discharges remained unaffected. These data suggest that acamprosate reduces the postsynaptic efficacy of excitatory amino acid neurotransmitters and lowers neuronal excitability in the neocortex of the rat.

Acamprosate↗
PubMed1992

Interleukin-1 beta increases synaptic inhibition in rat hippocampal pyramidal neurons in vitro.

Interleukin-1 (IL-1), a cytokine with a broad spectrum of biological activity, modulates electrical properties of central neurons in the brain. The effects of IL-1 beta (143 pM) on conductances opened by synaptic stimulation of the Schaffer collaterals were studied by intracellular recording of hippocampal pyramidal cells of the CA1 region. IL-1 beta enhanced and prolonged synaptic inhibition by about 2 to 3-fold. Heat-inactivated IL-1 beta had no effect. This finding implies that IL-1 beta changes interneuronal communication in the hippocampus with a possible impact on neuronal plasticity.

Animals↗
PubMed1991

Valproate suppresses N-methyl-D-aspartate-evoked, transient depolarizations in the rat neocortex in vitro.

Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1-1 mM) in a dose-related manner suppressed the characteristic transient depolarizations induced by N-methyl-D-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5-10 mM) also reduced L-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.

Animals↗
PubMed1988

(+/-)-beta-Parachlorophenylglutamate selectively enhances the depolarizing response to L-homocysteic acid in neocortical neurons of the rat: evidence for a specific uptake system.

The effect of (+/-)-beta-parachlorophenylglutamate (CP) on depolarizations induced by iontophoretically applied L-glutamate, L-aspartate, L-homocysteate (L-HCA) and D-HCA was investigated in neurons of the rat neocortex in vitro. CP, a reported blocker of amino acid uptake, strongly enhanced L-HCA responses whereas responses to the other amino acids remained little affected. This action was observed irrespective of whether CP was administered iontophoretically or pneumatically from micropipettes. CP (5 mM) administered alone had no effect on membrane potential. These findings suggest the existence of a specific uptake system for L-HCA providing further evidence in favour of a possible function of L-HCA as an endogenous ligand for the N-methyl-D-aspartate receptor in the rat neocortex.

Animals↗
PubMed1987

Valproate enhances inhibitory postsynaptic potentials in hippocampal neurons in vitro.

Effects of sodium valproate (0.5-10 mM) on hippocampal cells (CA3 pyramidal cells and granule cells) of the guinea pig in vitro were studied by intra- and extracellular recording. Inhibitory postsynaptic potentials were markedly and reversibly augmented. Their shunting action as well as duration increased by more than 150%. Effects of locally administered gamma-aminobutyric acid (GABA) did not change significantly. Membrane characteristics such as membrane potential, membrane input resistance and action potential did not alter. Valproate suppressed spontaneous spiking and repetitive discharges evoked by GABA antagonists. It is concluded that valproate enhances GABAergic synaptic transmission by a presynaptic mechanism. However, postsynaptic mechanisms might be involved in the limitation of repetitive firing.

Animals↗
PubMed1987

L-homocysteic acid but not L-glutamate is an endogenous N-methyl-D-aspartic acid receptor preferring agonist in rat neocortical neurons in vitro.

The effects of ionophoretically applied L-homocysteate (L-HCA), L-glutamate (L-Glu) and N-methyl-D-aspartate (NMDA) were compared in rat neocortical neurons recorded intracellularly in vitro. The firing pattern and the time course of membrane depolarization induced by L-HCA resembled those of NMDA responses. Action potentials evoked by NMDA and L-HCA were superimposed upon slow depolarizations in a burst-like pattern, while L-Glu elicited single spike discharges. Ionophoretically applied D-2-amino-5-phosphonovalerate (2-APV) at doses sufficient to abolish NMDA responses, markedly reduced the L-HCA induced depolarizations but had no detectable effect on the L-Glu responses. The present findings are consistent with a possible role of L-HCA as an NMDA receptor preferring neurotransmitter in the rat frontal cortex.

Animals↗
PubMed1985

Melatonin lowers excitability of guinea pig hippocampal neurons in vitro.

Action of melatonin (N-acetyl-5-methoxytryptamine; MEL) on guinea pig hippocampal cells (CA3 neurons and dentate granule cells) were studied in vitro using both extra- and intracellular recording. MEL (1-10 mmol/1) had the following effects: Response to repetitive synaptic stimulation was changed drastically: Double shock facilitation (20 ms interval) turned into depression and stimulus trains of a frequency as low as 1 Hz led to a drastic reduction of the response. Membrane potential was hyperpolarized. Duration of action potential was strongly increased. Threshold for the triggering of action potentials was shifted to more positive levels. IPSPs were prolonged and their shunting power enhanced. Repetitive spiking elicited by the application of bicuculline was reversibly abolished. All these effects had in common that cell excitability was lowered. It is concluded that MEL might influence epileptic seizure activity and should be further investigated as potential anticonvulsant.

Action Potentials↗
PubMed1984

Differences in baclofen-sensitivity between CA3 neurons and granule cells of the guinea pig hippocampus in vitro.

In the slice preparation of the guinea pig hippocampus, the effects of (+/-) baclofen added to the Krebs-Ringer solution on dentate granule cells and CA3 pyramidal cells were investigated by means of intracellular recording techniques. In a 10-25 microM concentration, baclofen reduces the inhibitory postsynaptic potentials of the granule cells evoked by electrical stimulation of the perforant path and hyperpolarizes the granule cell membrane slightly. The reduction of both, the excitatory and inhibitory postsynaptic potentials of CA3 pyramidal cells evoked by mossy fiber stimulation, however, is accompanied by a strong hyperpolarization and conductance increase. Further, repetitive discharges of granule cells elicited in the presence of the convulsant bicuculline (25 microM) are hardly affected by baclofen (50 microM), whereas those of CA3 neurons are blocked.

Animals↗
PubMed1983

Two late response components in on-off ganglion cells of the frog retina: the delayed response-generated by red rods; the second off-response-generated by green rods.

Frog on-off retinal ganglion cells react to diffuse, large-sized stimuli not only with an "early response" and a "delayed response" but also with a "second off-response". The intensity at which the delayed response becomes visible coincides with the quantum amount necessary for saturating the red rod response. The spectral sensitivity of the delayed response fits the nomogram for the 502 nm pigment. Unlike the delayed response, the second off-response appears earlier with increasing stimulus intensity and follows the 433 nm nomogram. Therefore, it is most probably generated by the green rods.

Animals↗
PubMedDate not supplied

Serotonin3 receptor agonists attenuate glutamate-induced firing in rat hippocampal CA1 pyramidal cells.

The techniques of extracellular single cell recording and microiontophoresis were used to study the effect of 5-HT3 receptor agonists on glutamate-activated firing of CA1 hippocampal pyramidal cells. Iontophoretic application of 5-HT3 receptor agonists 2-methyl-5-HT and SR 57227A produced a current (dose)-dependent suppression of the firing of CA1 pyramidal cells; SR 57227A was more effective than 2-methyl-5-HT. The suppressant action of 2-methyl-5-HT and SR 57227A had a slow onset and showed little or no desensitization. This effect was markedly attenuated or completely blocked by the 5-HT3 receptor antagonist BRL 46470A but not by the nonspecific 5-HT1 and 5-HT2 receptor antagonist metergoline or by the 5-HT1A antagonist WAY 100478. Intravenous administration of SR 57227A was effective in reducing the firing rate of CA1 pyramidal cells and this effect was prevented by BRL 46470A administered either i.v. or iontophoretically. Iontophoresis of 2-methyl-5-HT also diminished CA1 postsynaptic field potentials evoked by electrical stimulation of the Schaffer collaterals. Again, BRL 46470A but not metergoline prevented the suppressant action of 2-methyl-5-HT. Taken together, our results indicate that activation of 5-HT3-like receptors in the hippocampal CA1 region effectively reduces the efficacy of glutamatergic neurotransmission.

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