Pre-ischaemic administration of procaine suppresses ischaemic glutamate release and reduces neuronal damage in the gerbil hippocampus

The effects of intracerebroventricular administration of procaine 2 mu mol on ischaemic release of neurotransmitter amino acids in the gerbil hippocampal CAI region were investigated using a microdialysis-high-performance liquid chromatography procedure. Histological outcome was examined by comparing delayed neuronal death between animals treated with procaine before ischaemia and animals treated after ischaemia. Transient forebrain ischaemia for 3 min produced increases in dialysate amino acid concentrations. Aspartate, glutamate and glycine reached 331%, 394% and 233% of pre-ischaemic values. Basal concentrations were restored immediately by reperfusion. Pre-ischaemic administration of procaine suppressed peak release and improved histological outcome. However, post-ischaemic administration did not protect against ischaemic neuronal death. Improvement in ischaemic neuronal damage by pre-ischaemic administration of procaine may be related to suppression of excitatory amino acid release.