Beani_1983_Br.J.Pharmacol_79_623

The effect of glycine (Gly) on acetylcholine (ACh) release from superfused, resting or electrically-stimulated slices of guinea-pig caudate nucleus (CN), brain stem (BS) and cerebral cortex (CC) was studied. The amino acid 1 X 10(-4)-6 X 10(-3)mol 1(-1) reduced the electrically-induced release and increased the spontaneous and KCl-evoked transmitter outflow, mostly in CN but also in BS, whereas it was ineffective in CC. Taurine, chosen as a structurally related compound, moderately affected only the spontaneous release in CN. Strychnine 2 X 10(-7) mol 1(-1) was per se ineffective, but prevented most Gly effects. The Gly-induced increase of ACh outflow in resting CN slices, however, could be completely antagonized only by administering strychnine and picrotoxin together. These findings suggest that: (i) the overall pattern of Gly influence on cholinergic function is similar to that previously described for gamma-aminobutyric acid (GABA); (ii) specific receptors seem to be present in BS and, above all, in CN; (iii) a positive cooperation between endogenous GABA and Gly is evident in resting CN slices; (iv) the absence of any apparent endogenous glycinergic control on the cholinergic neurones casts doubt on but does not exclude the existence of glycinergic neurones in CN.