CALCIUM CALMODULIN-DEPENDENT KINASE-II AND LONG-TERM POTENTIATION ENHANCE SYNAPTIC TRANSMISSION BY THE SAME MECHANISM

Ca2+-sensitive kinases are thought to play a role in long-term potenti ation (LTP), To test the involvement of Ca2+/calmodulin-dependent kina se II (CaM-K II), a truncated, constitutively active form of this kina se was directly injected into CA1 hippocampal pyramidal cells. Inclusi on of CaM-K II in the recording pipette resulted in a gradual increase in the size of excitatory postsynaptic currents (EPSCs). No change in evoked responses occurred when the pipette contained heat-inactivated kinase, The effects of CaM-K II mimicked several features of LTP in t hat it caused a decreased incidence of synaptic failures, an increase in the size of spontaneous EPSCs, and an increase in the amplitude of responses to iontophoretically applied ha-amino-3-hydroxy-5-methyl-4-i soxazolepropionate. To determine whether the CaM-K II-induced enhancem ent and LTP share a common mechanism, occlusion experiments were carri ed out. The enhancing action of CaM-K II was greatly diminished by pri or induction of LTP. In addition, following the increase in synaptic s trength by CaM-K II, tetanic stimulation failed to evoke LTP. These fi ndings indicate that CaM-K II alone is sufficient to augment synaptic strength and that this enhancement shares the same underlying mechanis m as the enhancement observed with LTP. `