Abstract
In adult neurogenesis young neurons connect to the existing network via formation of thousands of new synapses. At early developmental stages, glutamatergic synapses are sparse, immature and functionally 'silent', expressing mainly NMDA receptors. Here we show in 2- to 3-week-old young neurons of adult mice, that brief-burst activity in glutamatergic fibers is sufficient to induce postsynaptic AP firing in the absence of AMPA receptors. The enhanced excitability of the young neurons lead to efficient temporal summation of small NMDA currents, dynamic unblocking of silent synapses and NMDA-receptor-dependent AP firing. Therefore, early synaptic inputs are powerfully converted into reliable spiking output. Furthermore, due to high synaptic gain, small dendritic trees and sparse connectivity, neighboring young neurons are activated by different distinct subsets of afferent fibers with minimal overlap. Taken together, synaptic recruitment of young neurons generates sparse and orthogonal AP firing, which may support sparse coding during hippocampal information processing.
Highlights
In the adult hippocampus new neurons are continuously generated throughout life
To examine glutamatergic synaptic signaling in these neurons, we identified 2-week-old neurons in adult mice using retrovirus-mediated green fluorescent protein (GFP) labeling (Figure 1, Figure 1—figure supplement 1, Zhao et al, 2006)
We show that glutamatergic synapses onto newly generated young granule cells are formed as ‘silent’ synapses containing mainly NMDA receptors
Summary
In the adult hippocampus new neurons are continuously generated throughout life. Appropriate control of new synapse formation is critically important for the survival of the young cells and for proper circuit function. The first glutamatergic synapses are mostly silent synapses expressing NMDA receptors but no AMPA-receptors (Chancey et al, 2013) These early NMDA-only synapses are activated during learning and shape dendrite development as early as 1–2 weeks post mitosis (Tronel et al, 2010). Consistent with this notion, the time window between 1–3 weeks after cell division is important for spine formation, it constitutes a critical period for NMDA-dependent survival, as cell death during this period is strongly increased in newborn neurons with a genetic deletion of the NR1 NMDA receptor subunit (Tashiro et al, 2006, 2007; Mu et al, 2015). The functional impact of silent synapses in adult-born granule cells is largely unclear
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