|Title||Receptive field formation and erasure in somatosensory cortex|
|Publication Type||Conference Paper|
|Year of Publication||2013|
|Authors||Kerr, C., Von Kraus L., Iordanou J., Neymotin S. A., Francis J., & Lytton WW.|
|Conference Name||Society for Neuroscience 2013 (SFN '13)|
|Keywords||SFN, Society for Neuroscience|
We used in vivo electrophysiology and a large-scale biomimetic computer model of the ventral posterolateral nucleus (VPL) and primary somatosensory cortex (S1) to investigate the formation of receptive fields (RFs), as well as their subsequent erasure using zeta inhibitory peptide (ZIP). The model consisted of 4950 event-driven integrate-and-fire neurons, divided into three cell types (pyramidal cells, fast-spiking interneurons, and low-threshold interneurons), representing the thalamus and the six layers of the cortex, for 15 neuronal populations in total. Cutaneous stimuli were modeled as inputs every 0.3 s to a contiguous subset of the thalamocortical relay cells of the VPL. Spike-timing-dependent plasticity (STDP) was modeled using a symmetric exponential decay with a time constant of 40 ms, and was present at all excitatory synapses. ZIP was modeled as an erasure of synaptic long-term potentiation (LTP), but not depression, back to baseline values. Results were validated against in vivo electrode array recordings from rat and macaque S1. STDP-induced LTP increased the amplitude of the RF near the center of the stimulus and decreased its amplitude laterally, thereby increasing its contrast; ZIP reversed this effect. The amplitude and spatial extent of this effect was quantitatively similar between the model and experiment (e.g., 0.6$\pm$0.1 and 0.7$\pm$0.2 Hz reductions in peak firing rate following ZIP in experiment and model, respectively). In addition, in both the experiment and the model, ZIP was found to have negligible effects on spontaneous firing rate. The changes in firing between the naive, trained, and ZIP conditions were mediated by changes in synaptic weights. In the model, ZIP resulted in a 27% reduction in the weight of excitatory synapses. However, since this reduction occurred roughly equally at both excitatory-to-excitatory and excitatory-to-inhibitory synapses, the network remained balanced, which explains why there was little overall effect on spontaneous firing rates. To explore the functional correlates of these structural changes, we measured the interlaminar spectral Granger causality before and after applying ZIP. LTP enhanced feedforward information flow. The predominant effect of ZIP was to reduce intracortical causality, including a factor of 3 reduction in causality from layer 2/3 to layer 5. Surprisingly, this change was mediated entirely by enhanced excitatory-to-inhibitory connections, rather than a reduction in excitatory connection strengths from layer 2/3 to layer 5. These results demonstrate several cellular and network-level aspects of ZIP at a level of detail that cannot be directly accessed experimentally.