Fig. 4

A working model for the role of translin/trax RNase complex in hippocampal synaptic plasticity. a During basal synaptic transmission, the inactive translin/trax (TN/TX) RNase complex localizes to the discrete ribonucleoprotein foci called Processing body (P-body) in the postsynaptic dendrites. P-bodies also contain the microRNA-induced silencing complex (miRISC) formed by the microRNAs and other associated protein factors that bind to the mRNA transcripts and repress their translation. b Synaptic activity that induces persistent plasticity leads to NMDAR-mediated Ca²⁺ entry and GPCR activation by modulatory neurotransmitters (e.g. norepinephrine and dopamine). This results in adenylyl cyclase activation, rise in cAMP levels and PKA activation in the postsynaptic compartment. Synaptic activity also leads to dynamic changes in P-bodies causing them to localize in the vicinity of active dendritic spines. Active PKA subsequently results in activation of the translin/trax RNase in the P-bodies, either directly or through other targets. Once active, the translin/trax RNase degrades microRNAs bound to the mRNA transcripts, thus reversing the translational silencing. The released mRNAs are then translated by the polyribosomes leading to the synthesis of key plasticity-related proteins required for long-lasting synaptic plasticity