Abstract: The ability of tetrandrine (Tet), an alkaloid isolated from Radix Stephaniae Tetrandrae, to reduce cortical neuronal injury in cortical cultures derived from fetal rats was quantitatively assessed by examination of morphological changes and measurement of lactate dehydrogenase (LDH) released to the extracellular bathing media. Cell cultures exposed to the excitatory amino acids (EAA)-50 μmol·L^-1 glutamate (Glu), 20 μmol·L^-1 N-methyl-D-aspartate (NMDA), 300 μmol·L^-1 β-N-oxalylamino-L-alanine (BMAA, NMDA receptor agonist) or 20 μmol·L^-1 β-N-oxaly-lamino-L-alanine (BOAA, non-NMDA receptor agonist)for 24 h at 37 ºC showed widespread neuronal injury. Tet had little effect on the injury induced by 20 μmol·L^-1 NMDA but 10^-7 and 10^-6 μmol·L^-1 Tet did partially attenuate the neuronal degeneration, neuronal loss and LDH efflux resulting from prolonged exposures to 100 μmol·L^-1 Glu, 300 μmol·L^-1 BMAA and 20 μmol·L^-1 BOAA respectively. The ability of Tet to reduce the neuronal injury induced by prolonged exposure to EAA may contribute, at least in part, to the reduction of Ca²⁺ influx through inhibiting the opening of voltagegated Ca²⁺ channels. Another mechanism that Tet might have a little inhibitory effect on NMDA receptor on neuronal membrane cannot be excluded, as BMAA has been considered to act as a weak NMDA receptor agonist.

Key words: Tetrandrine, Cortical neuronal culture, Intracellular Ca2+, Excitatory amino acids