Modulatory effects of amino acids on neuromuscular transmission on the crayfish fast flexor muscle

The modulatory effects of amino acids on neuromuscular transmission from an identified giant motor neuron (MoG) and abdominal fast flexor muscles of t he crayfish were examined using electrophysiological and pharmacological te chniques. The distribution of amino acids in the cell body and axon of a si ngle MoG was revealed using high-performance liquid chromatography with ele ctrochemical detection. Eight different amino acids-aspartate, glutamate, g lutamine, arginine, glycine, taurine, alanaine and gamma-aminobutyric acid- were simultaneously detected in either the cell body or the axon of MoG. As partate, glutamate, alanine and arginine were present at relatively high co ncentration. Local pressure ejection of glutamate caused a depolarization of the abdomin al fast flexor muscle fibers. On the other hand, aspartate, alanine and arg inine had no clear effects on the same muscle fibers. Aspartate and arginin e, however, had modulatory effects on neuromuscular transmission. Alanine h ad no significant effect on the neuromuscular transmission. Aspartate at a concentration of 200 mu M decreased the amplitude of EJPs in the fast flexo r muscle mediated by stimulation of both the MoG and non-giant fast flexor motor neurons. Arginine at a concentration of 200 mu M reduced the EJP ampl itude of the muscle fibers in response to MoG stimulation but enhanced the EJP amplitude of the same muscle fibers by stimulation of non-giant fast fl exor motor neurons. Although rather high concentration (1 mM) were required , aspartate increased and arginine decreased the depolarization of the musc le fibers induced by local ejection of glutamate. The opposite effect of ar ginine on the fast flexor muscles in response to the stimulation of differe nt motor neurons suggested its modulatory role in the different effects of these motor neurons (depression and facilitation) in the fast flexor muscle s. J. Exp. Zool. 283:531-540, 1999. (C) 1999 Wiley-Liss, Inc.