Blockade of ganglionic transmission during synaptogenesis decreases alpha-bungarotoxin binding in the chick ciliary ganglion and iris.
The role of normal synaptic activity in the biochemical development of the nervous system has been examined in the chick embryo. Chlorisondamine, a ganglionic blocking drug, was administered in ovo during the period of synaptogenesis in the parasympathetic ciliary ganglion. Following treatment with chlorisondamine, nicotinic binding sites (as measured with [125I] alpha-bungarotoxin) were significantly reduced in both the ganglion and its end organ, the striated iris muscle. While the number of [125I] alpha-bungarotoxin binding sites eventually approached control levels in the iris, binding in the ciliary ganglion remained below normal values through hatching.
D000818:Animals; D002038:Bungarotoxins / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects*; D002642:Chick Embryo; D002714:Chlorisondamine / Q000494:pharmacology*; D005726:Ganglia, Parasympathetic / Q000187:drug effects* / Q000378:metabolism; D007498:Iris / Q000294:innervation*; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism; D011978:Receptors, Nicotinic; D013569:Synapses / Q000187:drug effects* / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects*; D064569:alpha7 Nicotinic Acetylcholine Receptor
D002038:Bungarotoxins; D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D064569:alpha7 Nicotinic Acetylcholine Receptor; D002714:Chlorisondamine