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Colonnese, M. T.

Publications and source records attributed to Colonnese, M. T..

3 recordsLinked to original sources

Synaptic and circuit mechanisms prevent detrimentally precise correlation in developing visual system

During 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 observed in 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.

neuroscience↗

Consequences of blindness for neural dynamics in mouse visual cortex

The role of experience in the development and maintenance of emergent network properties such as cortical oscillations and states is poorly understood. To define how early-life experience affects cortical dynamics in adult visual cortex, we examined the effects of two forms of blindness, bilateral loss of retinal input (enucleation) and degradation of visual input (eyelid-suture), on spontaneous activity in awake head-fixed mice of both sexes. Neither form of deprivation fundamentally altered the state-dependent regulation of firing-rates or local field potentials. However, each form of deprivation did cause a unique set of changes in network behavior. Laminar analysis revealed two different generative mechanisms for low-frequency synchronization, one prevalent during movement, the other during quiet-wakefulness. The former was absent in enucleated mice, suggesting a mouse homolog of human alpha oscillations. In addition, neurons in enucleated animals were less correlated and fired more regularly, but showed no change in mean firing-rate. Chronic lid-suture decreased firing rates during quiet-wakefulness, but not during movement, with no effect on neural correlations or regularity. Sutured animals showed a broadband increase in dEEG power and an increased occurrence, but reduced central frequency, of narrowband gamma oscillations. The complementary--rather than additive--effects of lid-suture and enucleation suggest that the development of these emergent network properties does not require vision but is plastic to modified input. Our results suggest a complex interaction of internal set-points and experience determines the expression of mature cortical activity, with low-frequency synchronization being particularly susceptible to early deprivation. SIGNIFICANCE STATEMENTThe developmental rules that guide how cortex balances internal homeostatic set points with external inputs to establish the emergent network level dynamics critical to its function are unclear. Using multiple methods of early deprivation, we show that the development of dynamics in mouse visual cortex is not dependent on the type of input. Rather, specific neural rhythms, firing-rate set points, and neural correlations are differentially modified by experience. Our deprivations identify one specific rhythm as a likely homolog to human alpha and suggest a mechanism for its loss in blindness. Our results advance our understanding of the regulatory mechanism leading to normal cortical processing, which is altered in blindness and multiple neural disorders.

neuroscience↗

Input-independent homeostasis of developing thalamocortical activity

The isocortex of all mammals studied to date shows a progressive increase in the amount and continuity of background activity during early development. In humans the transition from a discontinuous (mostly silent, intermittently bursting) cortex to one that is continuously active is complete soon after birth and is a critical prognostic indicator in newborns. In the visual cortex of rodents this switch from discontinuous to continuous background activity occurs rapidly during the two days before eye-opening, driven by activity changes in relay thalamus. The factors that regulate the timing of continuity development, which enables mature visual processing, are unknown. Here we test the role of the retina, the primary input, in the development of continuous spontaneous activity in the visual system of mice using depth electrode recordings of cortical activity from enucleated mice in vivo. Bilateral enucleation at postnatal day (P)6, one week prior to the onset of continuous activity, acutely silences cortex, yet firing rates and early oscillations return to normal within two days and show a normal developmental trajectory through P12. Enucleated animals showed differences in silent period duration and continuity on P13 that resolved on P16, and an increase in low frequency power that did not. Our results show that the timing of cortical activity development is not determined by the major driving input to the system. Rather, homeostatic mechanisms in thalamocortex regulate firing rates and continuity even across periods of rapid maturation.

neuroscience↗