N. Chub et Mj. Odonovan, BLOCKADE AND RECOVERY OF SPONTANEOUS RHYTHMIC ACTIVITY AFTER APPLICATION OF NEUROTRANSMITTER ANTAGONISTS TO SPINAL NETWORKS OF THE CHICK-EMBRYO, The Journal of neuroscience, 18(1), 1998, pp. 294-306
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
.