Need For Postsynaptic Protein Kinase Activity In Ltp Induction

Experiments using intracellular electrodes to perfuse membrane-impermeant peptides directly and selectively into the postsynaptic cell have been instrumental in clarifying a necessity for postsynaptic events in LTP induction. Based on many studies of this sort, it is clear that LTP induction is blocked by infusion of compounds whose permeation is restricted to the intracellular compartment of the post-synaptic cell. Some of the pioneering studies of this sort utilized injection of protein kinase inhibitors postsynaptically, which not only illustrated a need for postsynaptic events generally but also clarified a need for postsynaptic signal transduction events specifically for the induction of LTP.

In some of the earliest studies, involvement of Ca2+-dependent protein kinases was tested by intracellular injection of peptides that inhibited either PKC or CaMKII (26). As we will discuss later, many second messenger-regulated protein kinases have within their amino acid sequence autoinhibitory domains. Synthetic peptides that inhibit these domains are some of the most selective pharmacologic tools available anywhere. In one early experiment pep-tides corresponding to the protein kinase C autoinhibitory domain were infused post-synaptically and found to block LTP induction (see, for example, reference 26). (See figure.) While a variety of other earlier studies had shown that less-selective kinase inhibitors could block LTP induction, these early studies were landmark findings because of the specificity of the experimental manipulation.

In other early studies, a role for post-synaptic CaMKII was also investigated using a similar approach. Two different

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