Dataset Information

A Critical Period for the Rapid Modification of Synaptic Properties at the VPm Relay Synapse.

ABSTRACT: In addition to cortical areas, the thalamus also displays plasticity during a critical period in early life. Since most sensory information is transmitted to the cortex via the thalamus, it will be of significant interest to understand the precise time window and underlying mechanisms of this critical period in the thalamus. By using in vitro whole-cell patch recording in acute brain slices, we found that VPm relay synapses were only sensitive to whisker deprivation from postnatal day 11 (P11) to P14. Whisker deprivation initiated within the P11 to P14 window significantly reduced the amplitude of AMPAR-EPSCs, but not NMDAR-EPSCs when recorded 24 h after whisker removal. From P10 to P11, the timing for entry into the critical period and the kinetics underlying NMDAR-EPSCs function were significantly altered. At P11, NMDAR-EPSCs were less sensitive to ifenprodil, a selective blocker of NR2B-containing NMDAR, and the protein level of NR2A was significantly increased compared to those at P10. At the end of the critical period there were no obvious changes in synaptic properties when compared between P14 and P15. Using calcium imaging, we found that fewer P15 VPm neurons could be excited by the GABAa receptor agonist, muscimol, when compared to P14 VPm neurons; this correlated to an increase in KCC2 expression. Our studies revealed a precise critical period of sensory experience-dependent plasticity in the thalamus featuring distinct molecular mechanisms which occur at the start and end of this critical window.

SUBMITTER: Pan L

PROVIDER: S-EPMC5525376 | biostudies-other | 2017

REPOSITORIES: biostudies-other

ACCESS DATA

Similar Datasets

Project description:Critical periods are postnatal, restricted time windows of heightened plasticity in cortical neural networks, during which experience refines principal neuron wiring configurations. Here, we propose a model with two distinct types of synapses, innate synapses that establish rudimentary networks with innate function, and gestalt synapses that govern the experience-dependent refinement process. Nascent gestalt synapses are constantly formed as AMPA receptor-silent synapses which are the substrates for critical period plasticity. Experience drives the unsilencing and stabilization of gestalt synapses, as well as synapse pruning. This maturation process changes synapse patterning and consequently the functional architecture of cortical excitatory networks. Ocular dominance plasticity (ODP) in the primary visual cortex (V1) is an established experimental model for cortical plasticity. While converging evidence indicates that the start of the critical period for ODP is marked by the maturation of local inhibitory circuits, recent results support our model that critical periods end through the progressive maturation of gestalt synapses. The cooperative yet opposing function of two postsynaptic signaling scaffolds of excitatory synapses, PSD-93 and PSD-95, governs the maturation of gestalt synapses. Without those proteins, networks do not progress far beyond their innate functionality, resulting in rather impaired perception. While cortical networks remain malleable throughout life, the cellular mechanisms and the scope of critical period and adult plasticity differ. Critical period ODP is initiated with the depression of deprived eye responses in V1, whereas adult ODP is characterized by an initial increase in non-deprived eye responses. Our model proposes the gestalt synapse-based mechanism for critical period ODP, and also predicts a different mechanism for adult ODP based on the sparsity of nascent gestalt synapses at that age. Under our model, early life experience shapes the boundaries (the gestalt) for network function, both for its optimal performance as well as for its pathological state. Thus, reintroducing nascent gestalt synapses as plasticity substrates into adults may improve the network gestalt to facilitate functional recovery.

Dataset Information

A Critical Period for the Rapid Modification of Synaptic Properties at the VPm Relay Synapse.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets