Proceedings of Annual Meeting of the Physiological Society of Japan
Proceedings of Annual Meeting of the Physiological Society of Japan
Session ID : 2P082
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Neurons & synaptic functions
Mechanisms underlying the lidocaine-induced epileptic discharges in the hippocampus.
Eiichiro TanakaYoshinaka MuraiHideho Higashi
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CONFERENCE PROCEEDINGS FREE ACCESS

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Abstract
Extracellular recordings were made from CA1 regions in the rat hippocampal slice tissues. Superfusion of slice preparations with various concentration (1–1000 μM) of lidocaine induced a transient inhibition and subsequent augmentation of the maximal slope of the field excitatory postsynaptic potentials (fEPSPs). High concetrations (300–1000 μM) of lidocaine suppressed the maximal slope of the fEPSPs. The amplitude of presynaptic volleies was simply suppressed by lidocaine in a conaentration-dependent manner. Pretreatment of adenosine 1 (A1) receptor antagonist, DPCPX (1 μM) diminished the transient inhibition of the fEPSPs. Intracellular recordings from CA1 neurons showed that lidocaine suppressed the amplitudes of the evoked fast EPSPs and, of the fast and late IPSPs dose-dependently; the IC50 value for the fast EPSPs was 68 μM and, that for the fast IPSP was 7 μM. Neither exogenous glutamate-induced depolarization nor GABA-induced hyperpolarization was affected by the administration of lidocaine (30 or 300 μM). These results suggest that the lidocaine-induced transient inhibition of the fEPSPs is mediated by activation of A1 receptors. The subsequent augmentation of the fEPSPs is due to the depression of the IPSPs by the low concentrations of lidocaine. [Jpn J Physiol 55 Suppl:S143 (2005)]
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© 2005 The Physiological Society of Japan
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