Ionic mechanisms involved in the nodal swelling of myelinated axons caused by marine toxins

This review describes the ionic mechanisms involved in the nodal swelling of frog myelinated axons caused by specific marine neurotoxins (ciguatoxins, brevetoxins, Conus consors toxin and equinatoxin-II), analysed using confocal laser scanning microscopy. We have focussed on toxins that either target neuronal voltage-dependent Na+ channels, or that form cation-selective pores and indirectly affect the functioning of the Na(+)-Ca(++)exchanger

Ionic mechanisms involved in the nodal swelling of myelinated axons caused by marine toxins

This review describes the ionic mechanisms involved in the nodal swelling of frog myelinated axons caused by specific marine neurotoxins (ciguatoxins, brevetoxins, Conus consors toxin and equinatoxin-II), analysed using confocal laser scanning microscopy. We have focussed on toxins that either target neuronal voltage-dependent Na+ channels, or that form cation-selective pores and indirectly affect the functioning of the Na(+)-Ca(++)exchanger

Ionic mechanisms involved in the nodal swelling of myelinated axons caused by marine toxins

This review describes the ionic mechanisms involved in the nodal swelling of frog myelinated axons caused by specific marine neurotoxins (ciguatoxins, brevetoxins, Conus consors toxin and equinatoxin-II), analysed using confocal laser scanning microscopy. We have focussed on toxins that either target neuronal voltage-dependent Na+ channels, or that form cation-selective pores and indirectly affect the functioning of the Na+-Ca++ exchanger

The contribution of intracellular calcium stores to mEPSCs recorded in layer II neurones of rat barrel cortex

Loading slices of rat barrel cortex with 50 μm BAPTA-AM while recording from pyramidal cells in layer II induces a marked reduction in both the frequency and amplitudes of mEPSCs. These changes are due to a presynaptic action. Blocking the refilling of Ca2+ stores with 20 μm cyclopiazonic acid (CPA), a SERCA pump inhibitor, in conjunction with neuronal depolarisation to activate Ca2+ stores, results in a similar reduction of mEPSCs to that observed with BAPTA-AM, indicating that the source for intracellular Ca2+ is the endoplasmic reticulum. Block or activation of ryanodine receptors by 20 μm ryanodine or 10 mm caffeine, respectively, shows that a significant proportion of mEPSCs are caused by Ca2+ release from ryanodine stores. Blocking IP3 receptors with 14 μm 2-aminoethoxydiphenylborane (2APB) also reduces the frequency and amplitude of mEPSCs, indicating the involvement of IP3 stores in the generation of mEPSCs. Activation of group I metabotropic receptors with 20 μm (RS)-3,5-dihydroxyphenylglycine (DHPG) results in a significant increase in the frequency of mEPSCs, further supporting the role of IP3 receptors and indicating a role of group I metabotropic receptors in causing transmitter release. Statistical evidence is presented for Ca2+-induced Ca2+ release (CICR) from ryanodine stores after the spontaneous opening of IP3 stores

A fundamental oscillatory state of isolated rodent hippocampus

Population neuronal rhythms of various frequencies are observed in the rodent hippocampus during distinct behavioural states. However, the question of whether the hippocampus exhibits properties of spontaneous rhythms and population synchrony in isolation has not been definitively answered. To address this, we developed a novel preparation for studying neuronal rhythms in a relatively large hippocampal tissue in vitro. We isolated the whole hippocampus from mice up to 28 days postnatal age, removing the dentate gyrus while preserving the functional CA3-to-CA1 connections. Placing the hippocampal isolate in a perfusion chamber for electrophysiological assessment extracellular recordings from the CA1 revealed rhythmic field potential of 0.5 to ≤ 4 Hz that occurred spontaneously and propagated along the ventro-dorsal hippocampal axis. We provide convergent evidence, via measurements of extracellular pH and K+, recordings of synaptic and intracellular activities and morphological assessments, verifying that these rhythms were not the consequence of hypoxia. Data obtained via simultaneous extracellular and patch clamp recordings suggest that the spontaneous rhythms represent a summation of GABAergic IPSPs originating from pyramidal neurons, which result from synchronous discharges of GABAergic inhibitory interneurons. Similar spontaneous field rhythms were also observed in the hippocampal isolate prepared from young gerbils and rats. Based on these data, we postulate that the spontaneous rhythms represent a fundamental oscillatory state of the hippocampal circuitry isolated from extra-hippocampal inputs