Abstract
Visual deprivation during the critical period induces long-lasting changes in cortical circuitry by adaptively modifying neuro-transmission and synaptic connectivity at synapses. Spike timing-dependent plasticity (STDP) is considered a strong candidate for experience-dependent changes. However, the visual deprivation forms that affect timing-dependent long-term potentiation(LTP) and long-term depression(LTD) remain unclear. Here, we demonstrated the temporal window changes of tLTP and tLTD, elicited by coincidental pre- and post-synaptic firing, following different modes of 6-day visual deprivation. Markedly broader temporal windows were found in robust tLTP and tLTD in the V1M of the deprived visual cortex in mice after 6-day MD and DE. The underlying mechanism for the changes seen with visual deprivation in juvenile mice using 6 days of dark exposure or monocular lid suture involves an increased fraction of NR2b-containing NMDAR and the consequent prolongation of NMDAR-mediated response duration. Moreover, a decrease in NR2A protein expression at the synapse is attributable to the reduction of the NR2A/2B ratio in the deprived cortex.
Highlights
It is known that visual experience modifies cortical circuits in the primary visual cortex through synaptic plasticity during a critical period[1,2]
We investigated whether the effects of deprivation on timing-dependent LTP and LTD are different based on visual experience
It is worth noting that the increased fraction of NR2B-containing NMDA receptors (NMDARs) played a principal role in these changes, which was concurrent with a prolonged NMDAR-mediated response duration
Summary
It is known that visual experience modifies cortical circuits in the primary visual cortex through synaptic plasticity during a critical period[1,2]. Visual cortical plasticity has conventionally been ascribed to Hebbian or correlation-based mechanisms such as NMDAR-dependent LTP and LTD[3,4,5,6,7,8]. Spike timing-dependent plasticity (STDP)[9,10,11,12], in which the temporal order of pre- and postsynaptic neuronal activity is critical for the direction of change in synaptic weights, has emerged as a potential mechanism for experience-dependent changes in the neural circuit, including map plasticity of the visual cortex[13,14,15]. For STDP models at excitatory synapses, the induction of timing-dependent LTP (tLTP) in V1 requires the glutamate binding of NMDA receptors (NMDARs) with the concomitant arrival
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