NICOTINIC AND MUSCARINIC ACH RECEPTORS IN RHYTHMICALLY ACTIVE SPINAL NEURONS IN THE XENOPUS-LAEVIS EMBRYO

1. Intracellular recordings were made from presumed motoneurones in the Xenopus embryo spinal cord, and their response to cholinergic agents was investigated. Nicotine and 1,1-dimethyl-4-phenylpiperazinium (DMPP; both 1-10 mu M) strongly depolarized, and muscarine and oxotremorine (2-20 mu M) weakly hyperpolarized, these neurones. Tetrodotoxin (1 mu M) which blocks action potentials in Xenopus neurones, did not affect either of these responses. 2. The extrapolated reversal potential of the nicotinic depolarization was -12.1 +/- 8.3 mV (mean +/- S.E.M.) suggesting the opening of a mixed conductance. The nicotinic response was antagonized by dihydro-beta-erythroidine, d-tubocurarine and mecamylamine (10-20 mu M) but not by alpha-bungarotoxin (10 mu M). 3. The muscarinic response was not reversed when recorded with electrodes filled with potassium chloride but was antagonized by atropine (0.1 mu M). 4. Acetylcholine (ACh, 10 mu M) caused a strong depolarization of the neurones which was blocked by d-tubocurarine and dihydro-beta-erythroidine, suggesting that its effects are mediated predominantly by nicotinic ACh receptors. 5. ACh and nicotinic agonists applied to the spinal cord produced a barrage of TPSPs that were blocked by TTX and strychnine.