Ca2+ store‐dependent potentiation of Ca2+‐activated non‐selective cation channels in rat hippocampal neurones in vitro

1 Potentiation of calcium‐activated non‐selective cation (CAN) channels was studied in rat hippocampal neurones. CAN channels were activated by IP3‐dependent Ca2+ release following metabotropic glutamate receptor (mGluR) stimulation either by Schaffer collateral input to CA1 neurones in brain slices in which ionotropic glutamate and GABAA receptors, K+ channels, and the Na+‐Ca2+ exchanger were blocked or by application of the mGluR antagonist ACPD in cultured hippocampal neurones. 2 The CAN channel‐dependent depolarization (ΔVCAN) was potentiated when [Ca2+]i was increased in neurones impaled with Ca2+‐containing microelectrodes. 3 Fura‐2 measurements revealed a biphasic increase in [Ca2+]i when 200 μm ACPD was bath applied to cultured hippocampal neurones. This increase was greatly attenuated in the presence of Cd2+. 4 Thapsigargin (1 μm) caused marked potentiation of ΔVCAN in CA1 neurones in the slices and of the CAN current (ICAN) measured in whole cell‐clamped cultured hippocampal neurones. 5 Ryanodine (20 μm) also led to a potentiation of ΔVCAN while neurones pretreated with 100 μm dantrolene failed to show potentiation of ΔVCAN when impaled with Ca2+‐containing microelectrodes. 6 The mitochondrial oxidative phosphorylation uncoupler carbonyl cyanide m‐chlorophenyl hydrazone (2 μm) also caused a potentiation of ΔVCAN. 7 CAN channels are subject to considerable potentiation following an increase in [Ca2+]i due to Ca2+ release from IP3‐sensitive, Ca2+‐sensitive, or mitochondrial Ca2+ stores. This ICAN potentiation may play a crucial role in the ‘amplification’ phase of excitotoxicity.

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