TCP shortens the latency of onset of isoelectricity in hypoglycaemia and fails to protect striatal neurones and dentate gyrus granule cells from hypoglycaemic injury in rats.

Competitive N-methyl-D-aspartate (NMDA) receptor antagonists are known to protect neurones against hypoglycaemic damage. We tested N-[1-(2-thienyl)cyclohexyl]piperidine (TCP), a non-competitive NMDA antagonist, in a recovery model of hypoglycaemic coma in the rat. Administered concomitantly with insulin, TCP shortened the latency of onset of electrocerebral silence, and failed to prevent striatal and dentate gyrus hypoglycaemia-induced injury. This effect is probably related to an increase in glucose consumption of neurones: TCP enhances energy metabolism in several brain structures, which could facilitate, at low blood glucose levels, the onset of isoelectricity, and hamper a putative neuro-protective effect of the drug.