Abstract
The roles played by cortical inhibitory neurons in experience-dependent plasticity are not well understood. Here we evaluate the participation of parvalbumin-expressing (PV+) GABAergic neurons in two forms of experience-dependent modification of primary visual cortex (V1) in adult mice: ocular dominance (OD) plasticity resulting from monocular deprivation and stimulus-selective response potentiation (SRP) resulting from enriched visual experience. These two forms of plasticity are triggered by different events but lead to a similar increase in visual cortical response. Both also require the NMDA class of glutamate receptor (NMDAR). However, we find that PV+ inhibitory neurons in V1 play a critical role in the expression of SRP and its behavioral correlate of familiarity recognition, but not in the expression of OD plasticity. Furthermore, NMDARs expressed within PV+ cells, reversibly inhibited by the psychotomimetic drug ketamine, play a critical role in SRP, but not in the induction or expression of adult OD plasticity.
Highlights
Understanding how brain synapses, cells, and circuits are persistently modified by experience to store information represents one of the great challenges in neuroscience
Our experiments reveal a surprising role for PV+ inhibitory neuron activity in the expression of selective response potentiation (SRP) but not of eye dominance or deprivation-enabled potentiation of the non-deprived eye after monocular deprivation (MD) in the adult mouse
The data show that NMDA receptor (NMDAR) in PV+ neurons are critically important for the expression of SRP, and that familiarity recognition and novelty detection measured behaviorally are compromised both by loss of PV+ neuron activity within V1 and loss of NMDAR from PV+ neurons
Summary
Understanding how brain synapses, cells, and circuits are persistently modified by experience to store information represents one of the great challenges in neuroscience. There is evidence that the response potentiation is mediated in part by “Hebbian” strengthening of excitatory synaptic transmission in visual cortex, as induction requires cortical NMDA receptor (NMDAR) activation (Sawtell et al, 2003) (Sato and Stryker, 2008) and acalcium/calmodulin-dependent protein kinase II (aCAMKII) expression in principal cells (Ranson et al, 2012) This form of ocular dominance (OD) plasticity is likely responsible for the increase in visual acuity that occurs through the non-deprived eye following adult monocular deprivation (Iny et al, 2006), and is of particular interest in the context of recovery of brain function after deprivation, disease, or damage (Cho and Bear, 2010)
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