Colchicine affects protein kinase C-induced modulation of synaptic transmission in cultured hippocampal pyramidal cells

Spontaneous excitatory postsynaptic currents (sEPSC) through AMPA-type channels were recorded on cultured hippocampal pyramidal neurons by means of the whole-cell patch-clamp technique. The protein kinase C (PKC) agonist 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA) produced a long-lasting increase in sEPSC frequency not mimicked by the inactive analogue 4 alpha-PM and blocked by the protein kinase inhibitor staurosporine. The 4 beta-PMA-induced change in sEPSC frequency occurred without detectable change in [Ca2+](i). After treatment with the microtubule-disrupting agent colchicine, 4 beta-PMA caused a small and transient increase in sEPSC frequency. It is concluded that colchicine affects the PKC-induced functional plasticity of nerve cells most likely by disturbing the axonal transport. (C) 1997 Federation of European Biochemical Societies.