Biology subjects

Sosa, M. J.

Publications and source records attributed to Sosa, M. J..

3 recordsLinked to original sources

bioRxiv2026

An egocentric map prioritizing peri-personal space in the mouse rostro-lateral visual area

All physical interactions between an organism and its environment occur within the space immediately adjacent to and surrounding its body, its peripersonal space (PPS). This space has been extensively studied behaviorally in humans, and through sparse single-neuron recordings in primates. However, how PPS is represented and organized at cellular and circuit scales remains poorly understood. Here, using dense extracellular recordings in the mouse rostro-lateral visual cortex (VISrl; >19,000 single units), we reveal the cellular and circuit organization of PPS in mice. Visuo-tactile neurons prioritize near-body space while also representing farther space in a direction-selective manner, tracking approaching but not receding objects across the environment. VISrl PPS neurons integrate vision and touch nonlinearly, and their tactile responses are progressively facilitated as visual objects near the body. PPS neurons are embedded in structured networks characterized by "like-to-like" functional connectivity and remap according to recent visuo-tactile statistics. Together, these findings establish VISrl as a circuit-accessible substrate for PPS, and reveal how near-body space is represented by a dynamic, plastic, multisensory cortical network.

neuroscience↗

bioRxiv2024

Impaired drainage through capillary-venous networks contributes to age-related white matter loss

The progressive loss of cerebral white matter during aging contributes to cognitive decline, but whether reduced blood flow is a cause or consequence remains debated. Using deep multi-photon imaging in mice, we examined microvascular networks perfusing myelinated tissues in cortical layer 6 and corpus callosum. We identified sparse, wide-reaching venules, termed principal cortical venules, that exclusively drain deep tissues and resemble vasculature at the human cortex and U-fiber interface. Aging involved selective constriction and rarefaction of capillaries in deep branches of principal cortical venules. This resulted in mild hypoperfusion that was associated with microgliosis, astrogliosis and demyelination in deep tissues, but not upper cortex. Inducing a comparable hypoperfusion in adult mice using carotid artery stenosis triggered a similar tissue pathology specific to layer 6 and corpus callosum. Thus, impaired capillary-venous drainage is a contributor to hypoperfusion and a potential therapeutic target for preserving blood flow to white matter during aging.

neuroscience↗

bioRxiv2023

Capillary regression leads to sustained local hypoperfusion by inducing vasoconstriction in upstream transitional vessels

In the brain, a microvascular sensory web coordinates oxygen delivery to regions of neuronal activity. This involves a dense network of capillaries that send conductive signals upstream to feeding arterioles to promote vasodilation and blood flow. Although this process is critical to the metabolic supply of healthy brain tissue, it may also be a point of vulnerability in disease. Deterioration of capillary networks is a hallmark of many neurological disorders and how this web is engaged during vascular damage remains unknown. We performed in vivo two-photon microscopy on young adult mural cell reporter mice and induced focal capillary injuries using precise two-photon laser irradiation of single capillaries. We found that [~]63% of the injuries resulted in regression of the capillary segment 7-14 days following injury, and the remaining repaired to re-establish blood flow within 7 days. Injuries that resulted in capillary regression induced sustained vasoconstriction in the upstream arteriole-capillary transition (ACT) zone at least 21 days post-injury in both awake and anesthetized mice. This abnormal vasoconstriction involved attenuation of vasomotor dynamics and uncoupling from mural cell calcium signaling following capillary regression. Consequently, blood flow was reduced in the ACT zone and in secondary, uninjured downstream capillaries. These findings demonstrate how capillary injury and regression, as often seen in age-related neurological disease, can impair the microvascular sensory web and contribute to cerebral hypoperfusion. SIGNIFICANCEDeterioration of the capillary network is a characteristic of many neurological diseases and can exacerbate neuronal dysfunction and degeneration due to poor blood perfusion. Here we show that focal capillary injuries can induce vessel regression and elicit sustained vasoconstriction in upstream transitional vessels that branch from cortical penetrating arterioles. This reduces blood flow to broader, uninjured regions of the same microvascular network. These findings suggest that widespread and cumulative damage to brain capillaries in neurological disease may broadly affect blood supply and contribute to hypoperfusion through their remote actions.

neuroscience↗