Ia afferent excitation of motoneurones in the in vitro new-born rat spinal cord is selectively antagonized by kynurenate.

Intracellular recordings from motoneurones in in vitro preparations of new-born rat spinal cord were used to study the sensitivity of the Ia excitatory post-synaptic potential (e.p.s.p.) to antagonists of excitatory amino acids, in order to test whether group Ia primary afferents release L-glutamate, or a similar compound, as a neurotransmitter. The Ia e.p.s.p. was isolated for study by using low intensity stimulation of individual muscle nerves and by the addition to the superfusate of high concentrations of divalent cations which suppressed polysynaptic inputs to the motoneurones. The pattern of convergence of group Ia afferents from homonymous, heteronymous and antagonist muscle nerves onto motoneurones in the new-born rat was similar to that reported in the adult cat spinal cord. Homonymous muscle nerve stimulation evoked the largest amplitude Ia e.p.s.p.s while heteronymous muscle nerve stimulation elicited smaller e.p.s.p.s or had no effect. Stimulation of antagonist muscle nerves resulted in inhibitory post-synaptic potentials (i.p.s.p.). Superfusion of the specific N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonovalerate, did not inhibit the Ia e.p.s.p. but did suppress later, polysynaptic components of the response evoked from dorsal roots. Kynurenate was a potent inhibitor of the Ia e.p.s.p. The site of action of kynurenate was examined by observing its effect on synaptic depression and was found to be consistent with a post-synaptic mechanism. Kynurenate selectively blocked the depolarization of motoneurones elicited by L-glutamate and had no effect on the depolarization evoked by carbachol. The selectivity of action of kynurenate was further examined by comparing its effect on the recurrent i.p.s.p. evoked by ventral root stimulation with its effect on the Ia e.p.s.p. The recurrent i.p.s.p. was antagonized by strychnine and dihydro-beta-erythroidine while kynurenate, at a concentration which greatly reduced the Ia e.p.s.p., had no effect. These results suggest that stimulation of group Ia primary afferents evokes the release of L-glutamate, or a similar compound, which activates non-NMDA excitatory amino acid receptors on motoneurones which, in turn, mediate the Ia e.p.s.p.