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

The arrest of axonal transport by colchicine administration has been extens ively used in immunocytochemical studies to increase the levels of neuroact ive compounds in neuronal somata. In order to study the accumulation rates of a variety of proteins with location and physiological action at the syna ptic terminal, we analysed, by immunocytochemical methods, the neuronal cel l body content of these synaptic proteins in colchicine-injected rats. In s ham-injected animals, all synaptic proteins tested were essentially observe d in nerve fibres and terminal boutons. After colchicine administration, in tense SNAP-25 immunoreactivity was found in many neuronal cell bodies throu ghout the CNS. In contrast, immunostaining for the rest of the synaptic pro teins analysed (syntaxin 1A and 1B, synaptobrevin I and II, Rab3A, synaptop hysin, synapsin I, synaptotagmin I and GAP-43) was virtually absent in neur onal cell bodies in treated animals. Furthermore, northern blot and in situ hybridization analysis revealed an increase in SNAP-25a and SNAP-25b messe nger RNA isoforms in the brains of adult colchicine-administered animals. I n addition, colchicine administration in five-day-old rat pups induced a no table increase in both SNAP-25 transcript isoforms. The present results ind icate that in vivo colchicine administration, under conditions known to inh ibit axoplasmic transport, upregulates SNAP-25 expression in the rat brain. (C) 1999 IBRO. Published by Elsevier Science Ltd.