Abstract
Upon electrical stimulation three transmitters are known to be released from the adrenergic nerve terminals of the isolated MVD preparation: two motor transmitters (noradrenaline (NA) and ATP) acting synergistically to provoke twitch contraction, and an inhibitory transmitter, the peptide NPY. The frog alkaloid pumiliotoxin-B (PTX-B) displayed two opposite effects on the electrically stimulated MVD: at low concentrations (0.1-0.3 microM) it caused twitch depression, at higher concentrations (0.5-2 microM) there was a potent twitch stimulation. Transmitters and/or receptors involved in the depressive effect could not be clearly identified, although interference with NPY is possible. On the other hand, the potent twitch stimulation caused by PTX-B may be due to exaggerated release of the same transmitters (NA and ATP) involved in twitch stimulation produced by electrical stimulation. Opening by PTX-B of the Na+ channels on the membrane of the adrenergic nerve terminals causes activation of the amine pump facilitating re-uptake of not only endogenous NA but also of exogenous catecholamines.
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