Biology subjects

Ribic, A.

Publications and source records attributed to Ribic, A..

6 recordsLinked to original sources

bioRxiv2026

Persistent sensory processing and behavioral atypicalities in a mouse model of neonatal encephalopathy

Neonatal hypoxia-ischemia (HI) injury is a major risk factor for lifelong cognitive impairments. Given its systemic impact, the neural mechanisms of impairments associated with HI injury remain unclear. In this study, we used a mouse model of neonatal HI injury to study its impact on goal-directed behavior and neural activity in adulthood using a head-fixed visual discrimination task. While neonatal HI injury did not impair discriminability or learning, it was associated with increased motor output in form of licking, faster reaction times and liberal decision bias, indicating an impulsive-like phenotype. These behavioral changes were accompanied by suppressed neuronal activity in the primary visual cortex (V1) and elevated cue-driven fluctuations in trial-to-trial firing variability in the prefrontal cortex (PFC), the latter of which was predictive of decision bias in HI mice. Our findings identify the long term impact of neonatal HI injury on goal-directed behavior, describe in detail the task-related patterns of neural activity in HI mice, and implicate abnormal neural variability in the PFC as a driver of impulsive-like behavior in adults that suffered neonatal HI injury.

neuroscience↗

bioRxiv2026

Robust learning-driven structural and functional plasticity of spines in the mature mouse cortex

Spines in the adult cortex are thought to be highly stable, and that their capacity for modest remodeling supports learning. Using a visual association task and a multilevel imaging approach in adult mice, we found a robust learning-driven increase in the complexity of spine nanostructure, as well as a rapid and persistent increase in spine formation during task acquisition that were accompanied by an overall reduction in spine size of layer 2/3 neurons in the primary visual cortex (V1). Trained animals further had an increased fraction of spines tuned to the task-relevant orientations, and the discriminability of spine responses in naive mice was predictive of their subsequent performance. Our results demonstrate that learning drives an increase in spine preferences for task-relevant information and point to reconfiguration of spine nanostructure and spine inputs as the structural drivers of these changes.

neuroscience↗

bioRxiv2025

Critical Period Plasticity is Associated withResilience to Short Unpredictable Stress

Low resilience to stressful events can increase the risk of anxiety and depression. Resilience decreases with age, parallel to drastic changes in the quality of brain plasticity from juvenile to old age, suggesting that the type of plasticity found in the maturing brain promotes resilience. To indirectly test this, we administered short unpredictable stress to adult male and female wild type (WT) C57BL/6 mice, as well as to two groups of mice characterized by heightened cortical plasticity: adolescent C57BL/6 WT mice and adult mice that lack SynCAM 1 (Synaptic Cell Adhesion Molecule 1), a critical plasticity brake in the mature brain. We found that short unpredictable stress robustly increased core body temperature in all groups of mice, indicative of stress-induced hyperthermia (SIH) and confirming the efficacy of the stress paradigm. However, depressive-like behavior as measured though tail suspension test was increased in adult WT mice only, supporting that the type of plasticity found in the immature brains of adolescent WT and adult SynCAM 1 knockout (KO) mice promotes resilience to stress. All three groups of mice showed a mild increase in locomotor activity after stress, suggesting that the quality of plasticity does not correlate with resilience to anxiety-like phenotypes. Our study hence provides indirect evidence for the protective role of developmental plasticity during stress and points to new mechanisms that promote resilience to stress-induced depression.

neuroscience↗

bioRxiv2024

Adolescent-like Processing of Behaviorally Salient Cues in Sensory and Prefrontal Cortices of Adult Preterm-Born Mice

Preterm birth is a leading risk factor for atypicalities in cognitive and sensory processing, but it is unclear how prematurity impacts circuits that support these functions. To address this, we trained adult male and female mice born a day early (preterm mice) on a visual discrimination task and found that they fail to achieve high levels of performance due to increased responding to the non-rewarded cue (false alarms). While the representation of task cues measured with in vivo electrophysiology is intact in the primary visual cortex (V1) of trained preterm mice, the representation of the non-rewarded cue is significantly weaker in regular spiking, putative pyramidal neurons in the prefrontal cortex (PFC), a brain area that mediates response inhibition. Responses to both task cues are blunted in electrophysiologically and optogenetically identified fast-spiking Parvalbumin interneurons in preterm mice, indicating impaired processing of task cues in their PFC. Indeed, single trial neuronal responses evoked by the non-rewarded cue predict the behavioral outcome more accurately in term than in preterm mice. Similar cue representation and processing is present in the PFC of adolescent term-born mice, suggesting that preterm birth impedes prefrontal maturation. Surprisingly, environmental enrichment, a well-established paradigm that promotes sensory maturation, fails to improve the performance of preterm mice. Altogether, our study describes the long-term impact of preterm birth on prefrontal and visual circuits and suggests a limited capacity of early interventions for reducing the risk of cognitive deficits after preterm birth.

neuroscience↗

bioRxiv2023

Preterm birth accelerates the maturation of spontaneous and resting activity in the visual cortex

Prematurity is among the leading risks for poor neurocognitive outcomes. The brains of preterm infants show alterations in structure and electrical activity, but the underlying circuit mechanisms are unclear. To address this, we performed a cross-species study of the electrophysiological activity in the visual cortices of prematurely born infants and mice. Using electroencephalography (EEG) in a sample of healthy preterm (N=29) and term (N=28) infants, we found that the maturation of the aperiodic EEG component was accelerated in the preterm cohort, with a significantly flatter 1/f slope when compared to the term infants. The flatter slope was a result of decreased spectral power in the theta and alpha bands and was correlated with the degree of prematurity. To determine the circuit and cellular changes that potentially mediate the changes in 1/f slope after preterm birth, we used in vivo electrophysiology in preterm mice and found that, similar to infants, preterm birth results in a flattened 1/f slope. We analyzed neuronal activity in the visual cortex of preterm mice (N=6 preterm and 9 term mice) and found suppressed spontaneous firing of neurons. Using immunohistochemistry, we further found an accelerated maturation of inhibitory circuits. In both preterm mice and infants, the functional maturation of the cortex was accelerated, underscoring birth as a critical checkpoint in cortical maturation. Our study points to a potential mechanism of preterm birth-related changes in resting neural activity, highlighting the utility of a cross-species approach in studying the neural circuit mechanisms of preterm birth-related neurodevelopmental conditions.

neuroscience↗

bioRxiv2018

Synapse-selective control of cortical maturation and plasticity engages an interneuron-autonomous synaptic switch

HighlightsO_LIThe synaptogenic molecule SynCAM 1 is selectively regulated by visual experience\nC_LIO_LISynCAM 1 controls thalamic input onto cortical Parvalbumin (PV+) interneurons\nC_LIO_LIPV+-specific knockdown of SynCAM 1 arrests maturation of cortical inhibition\nC_LIO_LIThalamic excitation onto PV+ interneurons is essential for critical period closure\nC_LI\n\neTOC BlurbRibic et al. show that network plasticity in both young and adult cortex is restricted by the synapse organizing molecule SynCAM 1. On a cellular level, it functions in Parvalbumin-positive interneurons to recruit thalamocortical terminals. This controls the maturation of inhibitory drive and restricts plasticity in the cortex. These results reveal the synaptic locus of cortical plasticity and identify the first cell-autonomous synaptic factor for closure of cortical critical periods.\n\nSummaryBrain plasticity peaks early in life and tapers in adulthood. This is exemplified in the primary visual cortex, where brief loss of vision to one eye abrogates cortical responses to inputs from that eye during the critical period, but not in adulthood. The synaptic locus of critical period plasticity and the cell-autonomous synaptic factors timing these periods remain unclear. We here demonstrate that the immunoglobulin protein Synaptic Cell Adhesion Molecule 1 (SynCAM 1/Cadm1) is regulated by visual experience and limits visual cortex plasticity. SynCAM 1 selectively controls the number of excitatory thalamocortical (TC) inputs onto Parvalbumin (PV+) interneurons and loss of SynCAM 1 in turn impairs the maturation of TC-driven feed-forward inhibition. SynCAM 1 acts in cortical PV+ interneurons to perform these functions and its PV+-specific knockdown prevents the age-related plasticity decline. These results identify a synapse type-specific, cell-autonomous mechanism that governs circuit maturation and closes the visual critical period.

neuroscience↗