Abstract
The non competitive NMDA receptor antagonist ketamine is used as an intravenous anaesthetic induction agent [ I ] Whilst a general reduction in excitatory neurotransmission (via NMDA receptor inhibition) may produce anaesthesia a role for direct Ca” channel blockade cannot be excluded. We have reviously reported that ketamine selectively inhibits K’ evoked [-Hlnoradrenaline release from SH-SY5Y cells with an IC,, of 170pM [2]. As K’ evoked release is entirely extracellular Ca” dependent [3] our data infer that ketamine inhibits Ca2’ influx through voltage sensitive Ca” channels in these cells In this study we have examined the effects of ketamine on K’ stimulated increases in [CaZL], in fura-2 loaded cells P
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