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Cuarenta, A.

Publications and source records attributed to Cuarenta, A..

2 recordsLinked to original sources

Early life adversity disrupts adult social reward motivation

Early life adversity can produce persistent changes during development that increase vulnerability to neuropsychiatric disorders. Although disruptions in reward processing are widely recognized as a hallmark of these disorders, reward is not a single construct. Distinct forms of reward including social interaction and primary rewards such as food rely on overlapping but dissociable neural circuitry and may be differentially affected by adverse experiences. Here, we used a rodent model of neonatal predator odor exposure (POE) to determine how early life threat influences motivation for social and sucrose reward in adulthood using operant procedures. Neonatal POE reduced adult motivation for a social reinforcer during an operant social self-administration task, whereas motivation for a sucrose reinforcer was unchanged. However, we did find a significant difference in sucrose self-administration with POE females pressing more for sucrose than control females. These findings demonstrate that neonatal threat does not produce a generalized deficit in motivation but rather selectively alters motivation across distinct reward domains. Together, this work identifies social reward as a particularly vulnerable behavioral domain following early life threat and provides new insight into how adverse developmental experiences shape adult reward-related behavior.

animal behavior and cognition↗

Early resource scarcity drives persistent transcriptional changes and vascular remodeling in the female prefrontal cortex

Early childhood poverty is an environmental risk factor for psychiatric and neurodegenerative disorders, yet the cellular mechanisms by which resource scarcity produces persistent brain vulnerability remain poorly understood. The medial prefrontal cortex (mPFC), which regulates executive function and motivated behavior, is sensitive to early environmental conditions. To identify mechanisms linking early resource scarcity to lasting mPFC dysfunction, we used the rat limited bedding and nesting (LBN) model, which recapitulates key features of poverty. Prior work shows LBN disrupts mPFC-mediated behaviors in adulthood, often in a sex-specific manner. Here, we used single-nucleus RNA sequencing (snRNAseq) to identify sex- and cell-type-specific transcriptional alterations in the adult mPFC following brief postnatal LBN exposure or control housing. LBN induced more differentially expressed genes (DEGs) across multiple pyramidal neuron clusters in females than in males. Unexpectedly, the largest transcriptional changes due to LBN occurred in vascular cells in females, whereas male vascular cells exhibited no DEGs. These female-specific vascular genes were enriched for alterations of transcriptional programs regulating angiogenesis and endothelial structure. This molecular profile was orthogonally validated with 3D vascular reconstruction, revealing LBN reduced vascular coverage in the adult female mPFC, driven by decreased vessel volume and shortened vessel length, while males were unaffected. Reduced vascular coverage may constrain metabolic support to this region. The postnatal period is a critical window for vascular maturation, and, taken together, these findings identify persistent, female-specific vascular alterations as a novel and previously unrecognized mechanism through which early resource scarcity may persistently affect brain function and vulnerability.

neuroscience↗