Biology subjects

Muhia, M.

Publications and source records attributed to Muhia, M..

2 recordsLinked to original sources

bioRxiv2026

Adaptive brain rewiring after brain injury via adult neurogenesis

The adult mammalian brain has limited regenerative capacity yet retains substantial potential for functional reorganization after experience, injury or disease1-3. While local plasticity at injury sites has been described4,5, the brain-wide consequences of a focal injury and the biological processes that drive them remain unknown. To address this, we performed an unbiased, whole brain screen of neuronal activity at single cell resolution following a focal injury to the primary visual cortex (V1) in mice. Olfactory processing areas emerged as loci of remote activation. We further show that V1 injury promotes the recruitment of adult born neurons into the olfactory bulb (OB) and potentiates cortical feedback onto bulbar circuits. Combining high-density multielectrode array recordings with two-photon calcium imaging revealed OB circuit refinement characterized by increased synchrony and sharpened tuning of principal output neurons. These circuit-level functional enhancements coincide with improved behavioral performance in odor-guided tasks. Motor cortex lesions do not elicit similar cellular and behavioral responses, suggesting that such distal adaptation only develops when injury is coupled with increased olfactory demand. Together, these data demonstrate that the adult brain can recruit alternative sensory circuits distant from a focal lesion to undergo adaptive, functionally relevant reorganization, and implicate adult neurogenesis as a contributing mechanism. Our findings expose a previously underappreciated degree of remote plasticity and reveal a novel role of adult neurogenesis in sensory compensation.

neuroscience↗

bioRxiv2025

Asymmetrical modulation of fear expression via GABAB receptors in the mouse medial habenula

The medial habenula (MHb) is implicated in regulating emotional responses to aversive events. Studies in zebrafish have identified a remarkable morphological left-right asymmetry in the dorsal habenula (zebrafish equivalent of mammalian MHb)-interpeduncular nucleus (IPN) pathway and its left-sided-specific role in modulating fear responses. However, there is little evidence for structural or functional lateralization in the mammalian MHb-IPN pathway. Here, we investigated the synaptic properties of left- and right-MHb afferents to the IPN and their roles in the expression of conditioned fear in mice. We found that each IPN neuron receives inputs from both left and right MHb, but the left MHb-originating synapses exhibit lower release probability and higher {gamma}-aminobutyric acid type B receptor (GABABR)-mediated potentiation compared to the right MHb-originating synapses. Interestingly, these asymmetrical properties persist in the inversus visceral mutant mice with normal internal organ laterality (situs solitus), but nearly disappear in those with reversed internal organ laterality (situs inversus). Behaviorally, chemogenetic inhibition of cholinergic neurons and conditional deletion of GABABR in the left, but not the right, MHb significantly attenuated cue-dependent fear recall. Our results demonstrate functional asymmetry of the MHb under partial influence of the nodal flow in mice, revealing a predominant role of GABABR-mediated signaling in the left MHb-IPN pathway in modulating fear memories. These findings suggest that lateralized MHb pathways could represent a fundamental principle in the neural regulation of emotion across species, but that they develop differently in zebrafish and mice.

neuroscience↗