Neuroprotective properties of lifarizine compared with those of other agents in a mouse model of focal cerebral ischaemia

1 Changes in the peripheral type benzodiazepine binding site density following middle cerebral artery occlusion in the mouse, have been used as a marker of neuronal damage. These sites can be identified using the selective ligand [3H]‐PK 11195 located on non neuronal cells, macrophages and astroglia, within the CNS. Glial cell proliferation and macrophage invasion is an unvoidable sequelae to cerebral ischaemic injury, secondary to neuronal loss. Following occlusion of the left middle cerebral artery (left MCA) a reproducible lesion was found in the parietal cortex within 7 days which gave rise to a significant increase in [3H]‐PK 11195 binding. 2 Treatment of animals with the sodium channel blocker, lifarizine, significantly reduced the ischaemia‐induced increase in [3H]‐PK 11195 binding when given either 30 min pre‐ischaemia and three times daily for 7 days at 0.5 mg kg−1, i.p. (P