BLOCKADE AND RECOVERY OF SPONTANEOUS RHYTHMIC ACTIVITY AFTER APPLICATION OF NEUROTRANSMITTER ANTAGONISTS TO SPINAL NETWORKS OF THE CHICK-EMBRYO

We studied the regulation of spontaneous activity in the embryonic (da y 10-11) chick spinal cord. After bath application of either an excita tory amino acid (AP-5 or CNQX) and a nicotinic cholinergic (DH beta E or mecamylamine) antagonist, or glycine and GABA receptor (bicuculline , 2-hydroxysaclofen, and strychnine) antagonists, spontaneous activity was blocked for a period (30-90 min) but then reappeared in the prese nce of the drugs. The efficacy of the antagonists was assessed by thei r continued ability to block spinal reflex pathways during the reappea rance of spontaneous activity. Spontaneous activity ceased over the 4- 5 hour monitoring period when both sets of antagonists were applied to gether. After application of glycine and GABA receptor antagonists, th e frequency of occurrence of spontaneous episodes slowed and became hi ghly variable. By contrast, during glutamatergic and nicotinic choline rgic blockade, the frequency of occurrence of spontaneous episodes ini tially slowed and then recovered to stabilize near the predrug level o f activity. Whole-cell recordings made from ventral spinal neurons rev ealed that this recovery was accompanied by an increase in the amplitu de of spontaneously occurring synaptic events. We also measured change s in the apparent equilibrium potential of the rhythmic, synaptic driv e of ventral spinal neurons using voltage or discontinuous current cla mp, After excitatory blockade, the apparent equilibrium potential of t he rhythmic synaptic drive shifted similar to 10 mV more negative to a pproximately -30 mV. In the presence of bicuculline, the apparent equi librium potential of the synaptic drive shifted toward the glutamate e quilibrium potential. Considered with other evidence, these findings s uggest that spontaneous rhythmic output is a general property of devel oping spinal networks, and that GABA and glycinergic networks alter th eir function to compensate for the blockade of excitatory transmission .