Calcium Signaling in Induction of Synaptic Plasticity in Cortical Pyramidal Neurons

Abstract

Pairing of pre‐ and postsynaptic activity in layer 2/3 pyramidal neurons in visual cortex at a fixed temporal delay results in variable plasticity outcomes (long term synaptic potentiation ‐ LTP, long term synaptic depression ‐ LTD or no significant change ‐ NC). In order to understand the role that intracellular calcium signaling may play in the different outcomes, we measured [Ca2+]i transients during pairing while pharmacologically inhibiting different calcium sources. In control experiments, pre‐postsynaptic pairing resulted in a net LTP but individual cells in the sample underwent either LTD or LTP or NC. Selective inhibition of individual intracellular calcium sources such as IP3 receptors or ryanodine receptors changed the plasticity outcome to a net LTD when RyRs were blocked with 200μM ryanodine while inhibition of IP3 receptors with 1.0 uM xestospongin resulted in a net LTP. Individual [Ca2+]i. Controls had peak transients =430±87 nM and an average decay time constant = 323±44 msec. However, ryanodine treatment reduced the calcium transient peaks to 310±56 nM and reduced the decay time constant to 239±38 msec. Inhibition of IP3 receptors with xestospongin c reduced the peak transient level to 380±62 nM and the decay time constant to 417±55). Thus, the specific and selective mobilization of different intracellular calcium signaling pathways may be one source of the variable plasticity outcomes between cells.Supported by NIH grant EY‐12782 to MJF