CHANGES in the metabolic activity of embryonic chick spinal cords were
examined following alpha-bungarotoxin (alpha-BTX) administration, in
order to investigate a potential mechanism by which this toxin arrests
motoneurone apoptosis during neurogenesis. Chick embryos were injecte
d i.p. with alpha-BTX and after 25 h the metabolic markers 2-deoxygluc
ose and cytochrome oxidase were examined in alternate serial sections
of the brachial and lumbar spinal cord. Glucose uptake and cytochrome
oxidase activity were reduced throughout the spinal cord and pronounce
d in the lateral motor columns. Iodinated alpha-BTX reaches and binds
to neuronal alpha-BTX-sensitive nicotinic cholinoceptors. Binding of a
lpha-BTX to these neuronal receptors and to those at the neuromuscular
junction has now been shown to have a demonstrable effect on neuronal
metabolism. The decreased metabolic activity in spinal cord neurones
as a result of toxin treatment may have an important role in the preve
ntion of motoneurone apoptosis at a critical developmental phase.