Experience Dependence of Alpha Rhythms and Neural Dynamics in the 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 the visual cortex of adult, head-fixed mice, we examined the effects of two forms of blindness initiated before eye opening and continuing through recording: (1) bilateral loss of retinal input (enucleation) and (2) degradation of visual input (eyelid suture). Neither form of deprivation fundamentally altered the state-dependent regulation of firing rates or local field potentials.

A new role for visual experience in top-down cortical development.

In this issue of Neuron, Ibrahim et al. (2021) examine the rules by which top-down connections are made on visual cortical layer 1 interneurons, discovering activity-dependent cooperative interactions with visual input that are specific to neurogliaform cells and anterior cingulate cortex.

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 the visual cortex of rodents this switch from discontinuous to continuous background activity occurs during the 2 d before eye-opening, driven by activity changes in relay thalamus.

Thalamocortical function in developing sensory circuits.

Thalamocortical activity patterns, both spontaneous and evoked, undergo a dramatic shift in preparation for the onset of rich sensory experience (e.g. birth in humans; eye-opening in rodents).

Sensory hypo-excitability in a rat model of fetal development in Fragile X Syndrome.

Fragile X syndrome (FXS) is characterized by sensory hyper-sensitivity, and animal models suggest that neuronal hyper-excitability contributes to this phenotype. To understand how sensory dysfunction develops in FXS, we used the rat model (FMR-KO) to quantify the maturation of cortical visual responses from the onset of responsiveness prior to eye-opening, through age equivalents of human juveniles. Rather than hyper-excitability, visual responses before eye-opening had reduced spike rates and an absence of early gamma oscillations, a marker for normal thalamic function at this age.

Disrupted Cortical State Regulation in a Rat Model of Fragile X Syndrome.

Children with Fragile X syndrome (FXS) have deficits of attention and arousal. To begin to identify the neural causes of these deficits, we examined juvenile rats lacking the Fragile X mental retardation protein (FMR-KO) for disruption of cortical activity related to attention and arousal. Specifically, we examined the switching of visual cortex between activated and inactivated states that normally occurs during movement and quiet rest, respectively.

Homocysteine reduces NMDAR desensitization and differentially modulates peak amplitude of NMDAR currents, depending on GluN2 subunit composition.

N-methyl-d-aspartate receptors (NMDARs) have been linked to schizophrenia because agents that bind the receptor, like ketamine and phencyclidine, are capable of inducing schizophrenia-like symptoms. Here we show that the amino acid homocysteine (HCY), which is increased in the blood of schizophrenia patients, reduces desensitization of NMDARs in cultured mouse neurons, human embryonic kidney cells transfected with GluN1 + GluN2A, GluN2B, or GluN2D subunits, and hippocampal slices. HCY also alters the peak amplitude of NMDAR currents, depending on the GluN2 subunit the receptor contains; GluN1 + GluN2A-containing NMDARs show an increase in peak amplitude when exposed to HCY, while GluN1 + GluN2B-containing NMDARs show a decrease in peak amplitude.

A synaptic strategy for consolidation of convergent visuotopic maps.

The mechanisms by which experience guides refinement of converging afferent pathways are poorly understood. We describe a vision-driven refinement of corticocollicular inputs that determines the consolidation of retinal and visual cortical (VC) synapses on individual neurons in the superficial superior colliculus (sSC). Highly refined corticocollicular terminals form 1-2 days after eye-opening (EO), accompanied by VC-dependent filopodia sprouting on proximal dendrites, and PSD-95 and VC-dependent quadrupling of functional synapses.

cpg15 and cpg15-2 constitute a family of activity-regulated ligands expressed differentially in the nervous system to promote neurite growth and neuronal survival.

Many ligands that affect nervous system development are members of gene families that function together to coordinate the assembly of complex neural circuits. cpg15/neuritin encodes an extracellular ligand that promotes neurite growth, neuronal survival, and synaptic maturation. Here we identify cpg15-2 as the only paralogue of cpg15 in the mouse and human genome.

Development of hemodynamic responses and functional connectivity in rat somatosensory cortex.

Functional magnetic resonance imaging (fMRI) is a valuable method for probing postnatal circuit refinement and plasticity. However, its use during early development has been hindered by uncertainty as to the nature of neurovascular coupling in young individuals. Here we used somatosensory stimulation in rats to determine age-related parameters of the blood oxygenation level-dependent (BOLD) signal from its apparent inception on postnatal day 13 to adulthood.

Long-term potentiation in the juvenile superior colliculus requires simultaneous activation of NMDA receptors and L-type Ca2+ channels and reflects addition of newly functional synapses.

The visual layers of the rodent superficial superior colliculus (sSC) have been the focus of many development studies of the molecular bases of retinotopic map formation, the role of early retinal waves in this process, and the development of glutamate synapses. Previous studies have documented long-term potentiation (LTP), believed to be critical to developmental synapse refinement, in the rodent sSC. However, the means of induction and the preparations used have varied widely, and thus cellular changes underlying this LTP remain ambiguous.