Abstract
Effects of taurine(TAU) on the frog spinal cord was examined and compared with those of GABA. TAU(0.001 - 1 mM) caused concentration-dependent inhibitory actions on the ventral root potentials induced by stimulation of the dorsal root (DR-VRP). GABA also inhibited the potentials, but it needed about a hundred times higher concentrations than TAU did. Membrane conductance of the motoneuron was increased by both TAU and GABA to the same degree, and the hyperpolarization of motoneuron induced by both amino acids was accompanied by the same level of increase in the extracellular K-activity. Picrotoxinin and anisatin (10 μM) reduced GABA-induced depolarizations in the primary afferent terminal, while these agents also caused significant inhibition of TAU-induced depolarization. Strychnine (10 μM) and dendrobine (30 μM) showed no GABA-antagonizing action, but markedly antagonized the action of TAU. The presynaptic inhibition on the first spike potential in the DR-VRR was markedly blocked by these antagonists. The blocking actions of latter two agents were stronger than those of former two. Strychnine and dendrobine abolished the early components of the DR-DRP, while rather augmented the later components. On the other hand picrotoxinin and anisatin reduced the size of DR-DRP. These results suggest that the postsynaptic actions of GABA and TAU are almost equipotent, but the presynaptic action of TAU is more effective than that of GABA. The effects of antagonists indicate that early component of the DR-DRP may be mediated by TAU or its related compound, and the later component may be caused by GABAergic synapses. Thus the major neurotransmitter for the presynaptic inhibition in the frog spinal cord may not be GABA.
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