In order to investigate the pharmacodynamic basis of the previously-establi
shed anticonvulsant properties of linalool, we examined the effects of this
compound on behavioral and neurochemical aspects of glutamate expression i
n experimental seizure models. Specifically, linalool effects were investig
ated to determine its inhibition of (i) L-[H-3]glutamate binding at CNS (ce
ntral nervous system membranes), (ii) N-methyl-D-aspartate (NMDA)-induced c
onvulsions, (iii) quinolinic acid (QUIN)-induced convulsions, and the behav
ioral and neurochemical correlates of PTZ-kindling. The data indicate that
linalool modulates glutamate activation expression in vitro (competitive an
tagonism of L-[H-3]glutamate binding) and in vivo (delayed NMDA convulsions
and blockage of QUIN convulsions). Linalool partially inhibited and signif
icantly delayed the behavioral expression of PTZ-kindling, but did not modi
fy the PTZ-kindling-induced increase in L-[H-3]glutamate binding.