NEUROSC M101C Lecture Notes - Lecture 11: Rate Project, Anisomycin, Basolateral Amygdala
Document Summary
Ltp is induced by a train of stimulation. Phosphatases are now active and oppose the effects of pka. If we block phosphatase while blocking pka, ltp should be restored! Camkii autophoshorylation is responsible for persistence of ltp. Can perfuse reagents into cytoplasm of postsynaptic cell. Begin intracellular infusion of camkii inhibitory peptide. Attempt to induce ltp at these synapses. Camkii is only activated for ~60 sec following ltp induction. Modi ed camkii with 2 uorophores (amino and carboxy terminal ends) Can look at how uorescence changes as a result of activation. As soon as glutamate is not uncaged, activation dies down. Doesn"t seem to account for persistent activity, however. Pkc can become persistently active following proteolytic cleavage: the atypical pkcs. Pkc is activated by diacyl glycerol --activated in response to gpcr pathways. Pkm-zeta and pkm-iota-lambda -- atypical, persistent forms of pkc. Ca2+ activated proteases - ca2+ turns on these proteins, and they clip regulatory domain.
