α-BTX lowers neuronal metabolism during the arrest of motoneurone apoptosis

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 injected i.p. with alpha-BTX and after 25 h the metabolic markers 2-deoxyglucose 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 pronounced in the lateral motor columns. Iodinated alpha-BTX reaches and binds to neuronal alpha-BTX-sensitive nicotinic cholinoceptors. Binding of alpha-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 prevention of motoneurone apoptosis at a critical developmental phase.