Abstract
Spike timing‐dependent plasticity (STDP) is an attractive candidate to mediate the synaptic changes that support circuit plasticity in sensory cortices during development. STDP is prevalent at excitatory synapses, but it is not known whether the underlying mechanisms are universal, or whether distinct mechanisms underpin STDP at different synapses. Here, we set out to compare and contrast STDP at vertical layer 4 and horizontal layer 2/3 inputs onto postsynaptic layer 2/3 neurons in the mouse barrel cortex. We find that both vertical and horizontal inputs show STDP, but that they display different time windows for induction of timing‐dependent long‐term depression (t‐LTD). Moreover, whereas t‐LTD at vertical inputs requires presynaptic NMDA receptors and is expressed presynaptically, using paired recordings we find that t‐LTD at horizontal inputs requires postsynaptic NMDA receptors and is expressed postsynaptically. These results demonstrate that similar forms of plasticity on the same postsynaptic neuron can be mediated by distinct mechanisms, and suggest that these forms of plasticity may enable these two types of cortical synapses to support different functions.
Highlights
Synapses in the superficial layers of primary somatosensory cortex (S1) provide a good model system in which to study synaptic mechanisms of receptive field plasticity (Feldman and Brecht 2005; Petersen and Crochet 2013)
This study shows that both vertical and horizontal inputs onto layer 2/3 postsynaptic neurons in mouse barrel cortex display NMDA receptor-dependent spike timing-dependent plasticity (STDP); the mechanism underlying the induction and expression of timing-dependent long-term depression (t-LTD) is different in the two pathways
The time window for t-LTD induction at the vertical input is significantly broader than that at the horizontal input, making STDP depression-biased at the vertical input (Feldman 2012)
Summary
Synapses in the superficial layers of primary somatosensory cortex (S1) provide a good model system in which to study synaptic mechanisms of receptive field plasticity (Feldman and Brecht 2005; Petersen and Crochet 2013). In the mouse barrel cortex, this has been ascribed to potentiation of vertical excitatory inputs onto layer 2/3 neurons (Clem et al 2008), which, in turn, can alter synaptic drive onto other layer 2/3 neurons as they are highly reciprocally connected (Lefort et al 2009). An attractive mechanism for experience-dependent synaptic changes is spike timing-dependent plasticity (STDP; Feldman 2012). At barrel cortex layer 4-to-layer 2/3 connections, timing-dependent long-term potentiation (t-LTP) requires postsynaptic NMDA receptors and is expressed postsynaptically (Bender et al 2006; Nevian and Sakmann 2006; Rodriguez-Moreno and Paulsen 2008; Rodriguez-Moreno et al 2011; Itami and Kimura 2012), whereas timing-dependent long-term depression (t-LTD) requires activation of presynaptic NMDA receptors and is expressed presynaptically (Rodriguez-Moreno and Paulsen 2008)
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