Abstract
The frog spinal cord has been used to test the effects of naturally occurring picrotoxane compounds (picrotoxinin, picrotin, tutin and coriamyrtin) and semisynthetic ones (6-acetylpicrotoxinin and anhydropicrotin) on the electrical activities of dorsal and ventral roots and on amino acid-induced depolarizations of primary afferent terminals. Picrotoxinin, tutin and coriamyrtin (10(-5)-3 X 10(-5)M), which have a free hydroxyl group at the 6-position, caused a gradual depolarization in both ventral and dorsal roots. The depolarizations were accompanied by a reduction in the size of the dorsal root potential (DR-DRP), dorsal root reflex (DR-DRR) and ventral root potential (DR-VRP) and by an augmentation of the first spike potential and polysynaptic components in the ventral root reflex (DR-VRR). 6-Acetylpicrotoxinin (10(-5)-3 X 10(-5)M) caused a slight hyperpolarization in both roots, and this hyperpolarization was accompanied by the augmentation of DR-DRP, DR-VRP and DR-VRR. The DR-DRR was reduced or abolished by the compound. Picrotoxinin, tutin and coriamyrtin reduced gamma-aminobutyric acid (GABA)-, beta-alanine- and taurine-induced depolarizations of primary afferent terminals. 6-Acetylpicrotoxinin showed almost the same degree of inhibition of beta-alanine and taurine as did picrotoxinin, but the GABA- antagonizing action of the compound was significantly weaker than was that of picrotoxinin. Picrotoxinin, tutin, coriamyrtin and 6-acetylpicrotoxinin all blocked presynaptic inhibition of the first spike potential caused by antidromic conditioning stimulation. 6 The present results suggest that the hydroxyl group at the 6-position of picrotoxane compounds are important for antagonism of the effects of GABA, but not of beta-alanine and taurine and for the blocking action of the presynaptic inhibition in the frog spinal cord.
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