Ryanodine receptor activation induces long- term plasticity of spine calcium dynamics

A key feature of signalling in dendritic spines is the synapse-specific transduction of short electrical signals into biochemical responses. ca2++ is a major upstream effector in this transduction cascade,serving both as a depolarising electrical charge carrier at the membrane and an intracellular second messenger. upon action potential firing,the majority of spines are subject to global back-propagating action potential (bap) ca2++ transients. these transients translate neuronal suprathreshold activation into intracellular biochemical events. using a combination of electrophysiology,two-photon ca2++ imaging,and modelling,we demonstrate that baps are electrochemically coupled to ca2+ release from intracellular stores via ryanodine receptors (ryrs). we describe a new function mediated by spine ryrs: the activity-dependent long-term enhancement of the bap-ca2++ transient. spines regulate bap ca2++ influx independent of each other,as bap-ca2++ transient enhancement is compartmentalized and independent of the dendritic ca2++ transient. furthermore,this functional state change depends exclusively on baps travelling antidromically into dendrites and spines. induction,but not expression,of bap-ca2++ transient enhancement is a spine-specific function of the ryr. we demonstrate that ryrs can form specific ca2++ signalling nanodomains within single spines. functionally,ryr mediated ca2++ release in these nanodomains induces a new form of ca2++ transient plasticity that constitutes a spine specific storage mechanism of neuronal suprathreshold activity patterns. © 2015 johenning et al.