| Signalling between individual nerve terminals and perisynaptic Schwann cells (PSCs) was investigated at the neuromuscular junction. When deprived of neuronal activity in vivo, either by motor nerve transection or injection of the nerve blocker tetrodotoxin, these teloglia rapidly up-regulated glial fibrillary acidic protein (GFAP). Addition of transcription or translation inhibitors to excised muscles prevented increases in GFAP. When neuronal activity was simulated in cut nerves by electrical stimulation, increases in GFAP were prevented. Stimulation of cut nerves prevented GFAP up-regulation even when postsynaptic nicotinic receptors were blocked, but not when transmitter release was blocked with {dollar}omega{dollar} -conotoxin GVIA. This evidence suggests that there is a nerve terminal to glia signalling pathway requiring presynaptic neurotransmitter release, which regulates PSC gene(s). This may be a general phenomenon since many types of glia are sensitive to transmitters applied in vitro or released in situ. |
