Abstract
AbstractDuring development, retinal axons create broad and imprecise connections in the thalamus. This topology, very different from adults, supplies developing thalamic neurons with locally homogeneous synaptic currents and should cause spike correlation between thalamocortical neurons on a millisecond timescale. Such correlations have not been observedin vivo, at these ages, and would likely be maladaptive. Here, we use a biophysical model of the visual thalamus with the membrane and synaptic properties of 7-10 day-old mice to show that the developmentally appropriate dominance of NMDA-receptor currents and absence of strong recurrent inhibitory and excitatory connections prevents precise correlation and preserves topographic information in thalamic spikes. We illustrate possible reasons for this desynchronization using a phenomenological cortical model, which shows impaired network diversity when driven with precisely correlated inputs. Our results suggest that developing synapses and circuits evolved mechanisms to compensate for detrimental, “parasitic” correlation arising from the unrefined and immature circuit.
Publisher
Cold Spring Harbor Laboratory