Effects of kainate on CA1 hippocampal neurons recorded in vitro.
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Action Potentials↗
Biomedical subjects
C Rovira
Publications and source records attributed to C Rovira.
The excitation of frog motoneurones in vitro by the glutamate analogue, DI-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA), and the effect of amino acid antagonists.
Intracellular recordings were made from motoneurones of the frog spinal cord in vitro and the excitatory effects of the glutamate analogue DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) examined. AMPA (25-100 microM) depolarized motoneurones with an increase in input conductance and an increase in spontaneous cell firing. The time-course of the AMPA response was prolonged compared to L-glutamate. D-Aminophosphonovalerate (1 microM) and D-aminoadipate (100 microM) did not antagonize AMPA-induced excitations while depressing L-glutamate responses. Glutamate diethylester up to 1 mM was not found to be a useful amino acid antagonist since it did not significantly reduce the depolarizations to quisqualate, L-glutamate and AMPA. The results are compatible with an action of AMPA on receptors distinct from those to N-methyl-D-aspartate and shared by quisqualate.
2-Amino-5-phosphonovalerate↗
Spontaneous and evoked release of endogenous Zn2+ in the hippocampal mossy fiber zone of the rat in situ.
In rats anaesthetized with urethane, push pull cannulae were stereotaxically introduced in the hippocampus (bilaterally) and Zn2+ assayed in the perfusate by atomic absorption spectrophotometry. When the cannula was located in the immediate vicinity of the mossy fiber zone, both spontaneous and K+ evoked release of Zn2+ were observed, this release was associated with a reduction in the histologically demonstrable Zn2+ as assessed by means of the Timm's stain. Neither spontaneous nor evoked release of Zn2+ was observed when the cannula was located in the medial part of CA1, the fimbria or the thalamus. These observations suggest that Zn2+ is released in the mossy fiber zone.
Animals↗
Pharmacological characterization of D-aminophosphonovaleric acid antagonism of amino acid and synaptically evoked excitations on frog motoneurones in vitro: an intracellular study.
The effect of D-aminophosphonovaleric acid (D-APV) on the depolarizations induced by N-methyl-D-aspartate (NMDA), glutamate, aspartate or quisqualate was studied with intracellular recordings from frog motoneurones in vitro. D-APV (0.5-10 microM) produced a slight hyperpolarization of the motoneuronal membrane without significant changes in input conductance. In control and tetrodotoxin-containing solutions the depolarizations induced by NMDA were strongly reduced by D-APV while quisqualate depolarizations were unaffected. Responses to glutamate and aspartate were antagonized to an intermediate level. The relatively small conductance increases evoked by excitatory amino acids were unaltered in solutions containing D-APV. The amplitude of monosynaptic excitatory postsynaptic potentials (e.p.s.ps) was strongly depressed by D-APV. The amplitude of polysynaptic e.p.s.ps was little changed but their decay time was reduced. It is suggested that D-APV is a powerful and selective NMDA receptor antagonist and that an endogenous amino acid acting via NMDA receptors may be the transmitter of monosynaptic e.p.s.ps on frog motoneurones.
2-Amino-5-phosphonovalerate↗
Somatic and dendritic actions of gamma-aminobutyric acid agonists and uptake blockers in the hippocampus in vivo.
In rats under urethane anaesthesia gamma-aminobutyric acid agonists and uptake blockers were microiontophoretically applied in the pyramidal layer of CA1 and in the apical dendrites using a twin set of multibarrelled micropipettes. Thus, the somatic and dendritic field potentials elicited by commissural stimulation were recorded simultaneously and the effects of iontophoretic applications at either site studied. Somatic applications of gamma-aminobutyric acid, isoguvacine or muscimol produced an inhibition of the somatic population spike; this showed rapid fade and was followed by an "off" response i.e. an enhancement of the population spike discharge and the occurrence of a second (and occasionally third) spike. The order of potency with regard to the "off" response was muscimol greater than isoguvacine much greater than gamma-aminobutyric acid. In contrast, the inhibition of the population spike produced by 4,5,6,7-tetrahydroisoxazolo(5,4-C) pyridin 3-OL showed little fade and no prominent "off" response. The fade and "off" response were not associated with significant changes in the dendritic field excitatory postsynaptic potential concommittantly recorded and were exclusively restricted to the immediate vicinity of the pyramidal layer. Ejection of gamma-aminobutyric acid and its agonists in the stratum radiatum produced a reduction of the field excitatory postsynaptic potential and the somatic spike, this effect however showed no fade (even during prolonged applications of high doses) and no "off" response. Somatic applications of the uptake blockers nipecotic acid or guvacine consistently produced: an increase in the effectiveness of the inhibition produced by gamma-aminobutyric acid and its analogues: a decrease in the latency to peak of the inhibition and an increase in the time to recovery; a full blockade of the fade and the "off" response. All of these effects were rapid and fully reversible without significant changes in either the field excitatory postsynaptic potential or the (control) somatic spikes. The more specific glial uptake blocker, 4,5,6,7-tetrahydroisoxazolo(4,5-C) pyridin 3-OL occasionally blocked the "off" response, however it was less potent and also tended to reduce the spike amplitude. Dendritic applications of the uptake blockers reduced the excitatory postsynaptic potential and the somatic spike but failed to produce prominent changes in the action of gamma-aminobutyric acid and its analogues.(ABSTRACT TRUNCATED AT 400 WORDS)
Acetylcholine↗
Dual cholinergic modulation of hippocampal somatic and dendritic field potentials by the septo-hippocampal pathway.
In rats under urethane anaesthesia, brief tetanic stimulation of the medial septum produces a dual effect upon the field potentials elicited in the ammon's horn by commissural stimulation: a facilitation of the population spike recorded in the pyramidal layer and a depression of the field EPSP recorded in the apical dendrites. Both effects, which are also produced by local application of muscarinic agents, are antagonized by local administration of muscarinic antagonists.
Acetylcholine↗
Opposite actions of muscarinic and nicotinic agents on hippocampal dendritic negative fields recorded in rats.
In rats under urethane anaesthesia, microiontophoretic application of muscarinic or nicotinic agents, in the pyramidal layer of the hippocampus, enhanced the population spike (s) evoked by fimbrial stimulation. In contrast, muscarinic and nicotinic agents had an opposite action on on the dendritic field potentials, they respectively reduced and enhanced the negative fields (field EPSP) recorded in the apical dendrites. These effects were antagonized by muscarinic and nicotinic antagonists, respectively.
Acetylcholine↗
Pharmacology of the dendritic action of acetylcholine and further observations on the somatic disinhibition in the rat hippocampus in situ.
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Acetylcholine↗
Intra-amygdaloid injections of kainic acid: regional metabolic changes and their relation to the pathological alterations.
Kainic acid was injected unilaterally in the amygdala of the rat. Following various delays, 2-deoxy-D-[14C]glucose was given intravenously. Autoradiographs of frontal brain sections showed increased glucose uptake in a number of cerebral structures as compared with controls. Most of these structures belong to, or are closely related to, what is traditionally called the 'limbic system'. The structures that show an increased glucose consumption subsequent to kainic acid injections are, with few exceptions, identical to those that are sensitive to the toxic effect that kainic acid exerts on structures distant to the site of injection. The findings are discussed in relation to the hypothesis that the latter effect is secondary to the epileptogenic properties of kainic acid.
Amygdala↗
Simultaneous recording of somatic and dendritic field potentials and combined microiontophoresis in the rat Ammon's horn in situ: effects of GABA and acetylcholine.
In rats under urethane anesthesia, a twin set of multibarreled micropipettes was used to record simultaneously in situ the somatic population spike, the positive field and the dendritic negative field (EPSP) evoked by commissural stimulation, and to apply microiontophoretically GABAergic and cholinergic agents at each level. Relying on the typical somatic responses evoked by local application of GABA and acetylcholine (ACh), an electrode can be positioned in the pyramidal layer with good accuracy (in the range of 50 microns) and the pharmacology of the excitatory drive impinging upon the apical dendrite concomitantly investigated.
Acetylcholine↗
Opposite actions of muscarinic and nicotinic agents on hippocampal dendritic negative fields recorded in rats.
In rats under urethane anaesthesia, microiontophoretic application of muscarinic or nicotinic agents, in the pyramidal layer of the hippocampus, enhanced the population spike (s) evoked by fimbrial stimulation. In contrast, muscarinic and nicotinic agents had an opposite action on on the dendritic field potentials, they respectively reduced and enhanced the negative fields (field EPSP) recorded in the apical dendrites. These effects were antagonized by muscarinic and nicotinic antagonists, respectively.
Acetylcholine↗
Effects of kainate on the excitability of rat hippocampal neurones.
Intracellular recordings from CA1 pyramidal neurones of the rat hippocampal slice preparation were used to study changes in neuronal excitability induced by the excitatory amino acid analogues kainate (KA) and N-methyl-D-aspartate (NMDA). Low concentrations of bath-applied KA (50-200 nM) or NMDA (1-3 microM) elicited a relatively small membrane depolarization and increased the number of spikes fired by a constant current pulse. The spike after-hyperpolarization (AHP) was depressed by KA but enhanced by NMDA. After blockade of the voltage-sensitive Na+ conductances with tetrodotoxin, intracellularly applied current pulses elicited Ca2+ spikes. Whereas NMDA always increased the duration (and number) of Ca2+ spikes and of their AHP, KA conversely reduced these spikes and (in almost half of the cells tested) the late phase of their AHP. When Ba2+ was used to replace extracellular Ca2+, prolonged plateau potentials developed and were also blocked by KA. NMDA had no effect on Ba2(+)-dependent responses. These results suggest that low concentrations of KA profoundly modified the electroresponsiveness of CA1 neurones perhaps by depressing a Ca2(+)-dependent K+ conductance mechanism responsible for dampening the excitability of these cells.
Action Potentials↗