Long Term Potentiation of Inhibition (LTPi)
Visual deprivation during an early “critical period” (CP) leads to loss of visual responsiveness to the deprived eye. Despite decades of research it is still unclear which cellular plasticity mechanism(s) contribute to this loss of visual responsiveness, and by extension are required for the normal development of visual function.

In previous years we found that monocular deprivation (MD) during the rodent CP dramatically potentiates inhibitory transmission at a specific synaptic connection between fast-spiking inhibitory cells, and excitatory star pyramidal neurons within layer 4 of visual cortex (Maffei et al., 2004, 2006). Here we found that the strength of these inhibitory synapses following MD are decreased at pre-critical period ages, yet these same connections increase in strength during the CP. Moreover, we described a novel form of long-term potentiation of inhibition (LTPi) at this synapse.

Currently, we are investigating whether the classical CP is triggered by the maturation of plasticity at fast-spiking interneuron synapses, and if LTPi plays a central role in the loss of visual responsiveness induced by visual deprivation.We are employing an array of techniques to uncover the mechanisms underlying both the induction and expression of these phenomena, including paired neuronal whole-cell recordings, fluorescent microscopy, immuno-electron microscopy and three-dimensional neuronal reconstructions.
Maffei et al., 2006.