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  • Title: Exogenously administered alpha-bungarotoxin binds to embryonic chick spinal cord: implications for the toxin-induced arrest of naturally occurring motoneuron death.
    Author: Renshaw G, Rigby P, Self G, Lamb A, Goldie R.
    Journal: Neuroscience; 1993 Apr; 53(4):1163-72. PubMed ID: 8506023.
    Abstract:
    Administration of alpha-bungarotoxin and other curare-like drugs during embryogenesis arrests motoneuron death which normally occurs in the spinal cord from day 6 to day 10 of embryogenesis. The accepted explanation is that such motoneuron rescue is mediated by inhibition of neuromuscular transmission following the blockade of nicotinic cholinoceptors at the neuromuscular junction. In this study we investigated a further possibility, namely that motoneuron rescue might also involve the blockade of alpha-bungarotoxin-sensitive sites within the spinal cord. The kinetic profile of [125I]alpha-bungarotoxin binding was examined in the brachial and lumbar regions of chick spinal cord at embryonic day 15. Binding was specific and apparently saturable within the range 1-34 nM reaching a maximum after 45 min. Specific binding involved a single class of non-interacting sites with a KD of 8.0 nM and a Bmax of 106 +/- 12 fmol/mg of protein. Nicotine displaced specific [125I]alpha-bungarotoxin binding in a concentration-dependent manner. Furthermore, specific binding dissociated slowly in the absence of nicotine. Autoradiographs localizing [125I]alpha-bungarotoxin binding in embryonic spinal cord revealed that, at embryonic day 15, specific toxin binding sites could be detected throughout the gray matter. In contrast, at embryonic day 6, the ventral horn contained the majority of specific binding sites. Exogenously administered [125I]alpha-bungarotoxin reached and bound to nicotine-sensitive sites in the spinal cord at embryonic day 7. To conclude, these data demonstrate that central nicotine-sensitive sites which bind [125I]alpha-bungarotoxin in a saturable and specific manner were present at the beginning of the critical motoneuron death phase of neurogenesis and that they were accessible to exogenously administered toxin. It is proposed that the [125I]alpha-bungarotoxin binding characterized here is to a class of putative alpha-bungarotoxin-sensitive nicotinic cholinoceptors. These studies raise the possibility that alpha-bungarotoxin blockade of such putative nicotinic cholinoceptors within the spinal cord may contribute to toxin-induced arrest of naturally occurring motoneuron death.
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