Colchicine administration in the rat central nervous system induces SNAP-25 expression.

he arrest of axonal transport by colchicine administration has been extensively used in immunocytochemical studies to increase the levels of neuroactive compounds in neuronal somata. In order to study the accumulation rates of a variety of proteins with location and physiological action at the synaptic terminal, we analysed, by immunocytochemical methods, the neuronal cell body content of these synaptic proteins in colchicine-injected rats. In sham-injected animals, all synaptic proteins tested were essentially observed in nerve fibres and terminal boutons. After colchicine administration, intense SNAP-25 immunoreactivity was found in many neuronal cell bodies throughout the CNS. In contrast, immunostaining for the rest of the synaptic proteins analysed (syntaxin 1A and 1B, synaptobrevin I and II, Rab3A, synaptophysin, synapsin I, synaptotagmin I and GAP-43) was virtually absent in neuronal cell bodies in treated animals. Furthermore, northern blot and in situ hybridization analysis revealed an increase in SNAP-25a and SNAP-25b messenger RNA isoforms in the brains of adult colchicine-administered animals. In addition, colchicine administration in five-day-old rat pups induced a notable increase in both SNAP-25 transcript isoforms. The present results indicate that in vivo colchicine administration, under conditions known to inhibit axoplasmic transport, upregulates SNAP-25 expression in the rat brain.