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A Konnerth

Publications and source records attributed to A Konnerth.

81 records · Page 5Linked to original sources
PubMed1983

Presynaptic involvement in frequency facilitation in the hippocampal slice.

Orthodromic stimulation with frequencies from 1 to 30 Hz causes facilitation of extracellularly recorded population spikes and a decrease of extracellular Ca2+ concentration ( [Ca2+]o ) monitored with ion selective microelectrodes at the cell body layer of area CA1 of the hippocampal slice. Reducing the Ca2+ content of the perfusion medium impairs synaptic transmission. However, even under these conditions, weak stimulation evokes a significant decrease of [Ca2+]o, which is ascribed to a presynaptic Ca2+ entry. Stimulation with high intensities and/or frequencies initially induces an accelerated decrease in [Ca2+]o followed by the re-establishment of synaptic transmission, indicating a contribution of the presynaptic site to frequency facilitation.

Animals↗
PubMed1983

Effects of GABA on presumed presynaptic Ca2+ entry in hippocampal slices.

Evoked field potentials and changes in [Ca2+]o were measured in the 'in vitro' hippocampal slice of the rat. When [Ca] in the perfusion medium was lowered to 0.2 mM synaptic transmission from Schaffer collateral/commissural fibers was blocked. Nevertheless, repetitive stimulation of afferent fibers still resulted in detectable decreases of [Ca2+]o. In contrast to findings in normal medium these decreases in [Ca2+]o could be larger in stratum radiatum than in stratum pyramidale, so mimicking the spatial distribution of activated afferent fibers. These findings suggest, that the loss of extracellular Ca2+ in low Ca2+ media is predominantly due to entry into presynaptic terminals. This permits to study effects of drugs on presynaptic endings. We found that iontophoretic application of GABA is capable to block this presumed presynaptic Ca2+ entry without affecting the electrical activity of the afferent fibers. This suggests, that presynaptic GABA receptors occur also in the Schaffer collateral/commissural fiber system.

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PubMed1983

Spontaneous epileptiform activity of CA1 hippocampal neurons in low extracellular calcium solutions.

Lowering extracellular [Ca2+] in rat hippocampal slices induces spontaneous epileptiform activity in area CA1, which is characterized by rhythmic burst firing of CA1 neurons and by prolonged negative potential shifts at the pyramidal cell body layer. This activity is accompanied by transient decreases of [Na+] and increases of [K+] in the extracellular space. In spite of the complete blockade of synaptic transmission, the wave of epileptiform activity propagates across area CA1. These findings suggest, that non-synaptic mechanisms may play a role in the generation and spread of epileptiform activity in the mammalian CNS.

Animals↗
PubMed1981

Stimulation induced changes in extracellular free calcium in normal cortex and chronic alumina cream foci of cats.

Changes in extracellular [Ca2+]0 (delta Ca) were measured with ion selective microelectrodes in the sensorimotor cortex of cats, surrounding alumina cream lesions and in the contralateral homotopic cortex. The lesions were produced by topical application of alumina cream 6 months-6 years prior to experiments. In normal cortex, stimulus induced reactions of [Ca2+]0 were found to be maximal (up to 0.45 mM) in depths of 200-300 micrometers below the cortical surface. At depths of 600 micrometers and more below the cortical surface, [Ca+2]0 usually rose by up to 0.2 mM above baseline. In the vicinity of the chronic lesion as well as in contralateral cortex [Ca2+]0 fell initially during stimulation in all depths. Close to the lesion delta Ca was as high as 0.8 mM and sites of maximal delta Ca were found to be located deeper in the cortex. About 5 mm from the scar as well as in the contralateral homotopic cortex, maximum delta Ca levels were found in a depth of 200-300 micrometers. It is suggested that Ca2+ dependent mechanisms are involved in epileptogenesis in chronic epileptic foci.

Aluminum↗
PubMedDate not supplied

A new class of synaptic response involving calcium release in dendritic spines.

In the classical view, transmission of signals across synapses in the mammalian brain involves changes in the membrane potential of the postsynaptic cell. The use of high-resolution cellular imaging has revealed excitatory synapses at which postsynaptic, transient alterations in calcium ion concentration are tightly associated with electrical responses. Here, by investigating the synapse between parallel glutamatergic fibres and Purkinje cells in the mouse cerebellum, we identify a class of postsynaptic responses that consist of transient increases in dendritic Ca2+ concentration but not changes in somatic membrane potential. Our results indicate that these synaptic Ca2+ transients are mediated by activation of metabotropic glutamate-responsive mGluR1-type receptors and require inositol-1,4,5-trisphosphate-mediated Ca2+ release from intradendritic stores. The new type of synaptic response is restricted to postsynaptic microdomains, which range, depending on the frequency of stimulation, from individual spines to small spinodendritic compartments. Thus, the synaptic Ca2+-release signal may be one of the critical cues that determine the input specificity of long-term depression, a well-established form of activity-dependent plasticity at these synapses.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMedDate not supplied

Histamine and noradrenaline decrease calcium-activated potassium conductance in hippocampal pyramidal cells.

Ample evidence exists for histaminergic and noradrenergic projections to the hippocampus. Both amines exert neurotransmitter or modulator actions on principal neurones in the CA 1 and in the dentate area. A number of mechanisms have been proposed for these actions, including increased potassium conductance, increased chloride conductance and electrogenic pump stimulation, and reduction of the anomalous inward rectification. Action potentials, and particularly bursts of spikes, in CA 1 pyramidal cells, are followed by an afterhyperpolarization (AHP) which consists of two components. The late AHP depends on a calcium-activated potassium conductance gK+ (Ca2+), and has recently been shown to be increased by dopamine. We report here a rapid and reversible decrease of the late AHP component following a burst of sodium spikes or a calcium spike, during perfusion with micromolar concentrations of histamine and noradrenaline. This effect is mediated by H2 receptors and beta-receptors, respectively, and occurred in the absence of changes in the calcium spike. By such a mechanism histamine and noradrenaline can profoundly potentiate the excitatory impact of depolarizing signals.

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PubMedDate not supplied

Slow transmission of neural activity in hippocampal area CA1 in absence of active chemical synapses.

Transmission of neural activity in the mammalian cortex involves the operation of chemical synapses. Here we report that activity of hippocampal pyramidal cells (HPC) in vitro can spread through the neural aggregate even when chemical synaptic transmission is blocked by lowering the external Ca2+ concentration ( [Ca2+]0). In these conditions focal stimulation of the HPC body layer (stratum pyramidale) at area CA1 evokes a localized repetitive neural response which, when large enough, spreads along this layer in both transverse directions. It was recently reported for similar conditions that the activated HPC often discharge in synchrony. However, the spread of the neural response does not depend upon the occurrence of synchronized HPC activity, and therefore represents a distinct phenomenon.

Animals↗
PubMedDate not supplied

Local dendritic Ca2+ signaling induces cerebellar long-term depression.

The coordinated activity of large numbers of adjacent parallel fiber synapses elevate calcium concentration locally in small regions of Purkinje cell dendrites. Such activity has also been reported to produce long-term depression of parallel fiber synaptic transmission. We have examined the relationship between these two events by combining patch clamp measurements of parallel fiber synaptic transmission with confocal microscopic imaging of the local calcium signals. We find that patterns of parallel fiber activity capable of evoking long-term depression invariably cause increases in Purkinje cell calcium concentration that are very spatially restricted. These results suggest that one function of the local dendritic calcium signals is to induce long-term depression of parallel fiber synapses.

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