DOI: 10.5061/dryad.2ds7p
title: Data from: Sociosexual and communication deficits after traumatic injury to the developing murine brain

description: Despite the life-long implications of social and communication dysfunction
 after pediatric traumatic brain injury, there is a poor understanding of
 these deficits in terms of their developmental trajectory and underlying
 mechanisms. In a well-characterized murine model of pediatric brain
 injury, we recently demonstrated that pronounced deficits in social
 interactions emerge across maturation to adulthood after injury at
 postnatal day (p) 21, approximating a toddler-aged child. Extending these
 findings, we here hypothesized that these social deficits are dependent
 upon brain maturation at the time of injury, and coincide with abnormal
 sociosexual behaviors and communication. Age-dependent vulnerability of
 the developing brain to social deficits was addressed by comparing
 behavioral and neuroanatomical outcomes in mice injured at either a
 pediatric age (p21) or during adolescence (p35). Sociosexual behaviors
 including social investigation and mounting were evaluated in a
 resident-intruder paradigm at adulthood. These outcomes were complemented
 by assays of urine scent marking and ultrasonic vocalizations as indices
 of social communication. We provide evidence of sociosexual deficits after
 brain injury at p21, which manifest as reduced mounting behavior and scent
 marking towards an unfamiliar female at adulthood. In contrast, with the
 exception of the loss of social recognition in a three-chamber social
 approach task, mice that received TBI at adolescence were remarkably
 resilient to social deficits at adulthood. Increased emission of
 ultrasonic vocalizations (USVs) as well as preferential emission of high
 frequency USVs after injury was dependent upon both the stimulus and prior
 social experience. Contrary to the hypothesis that changes in white matter
 volume may underlie social dysfunction, injury at both p21 and p35
 resulted in a similar degree of atrophy of the corpus callosum by
 adulthood. However, loss of hippocampal tissue was greater after p21
 compared to p35 injury, suggesting that a longer period of lesion
 progression or differences in the kinetics of secondary pathogenesis after
 p21 injury may contribute to observed behavioral differences. Together,
 these findings indicate vulnerability of the developing brain to social
 dysfunction, and suggest that a younger age-at-insult results in poorer
 social and sociosexual outcomes.
description: BodyWeights_dataBody weights of mice used in this study, across time post-injury3chamber_test_dataMice injured at adolescence (postnatal day 35) and tested in the three-chamber social approach task at adulthood. Percentage time spent in each chamber was quantified.CC_volume_dataStereological analyses were performed using StereoInvestigator to determine the volume loss of the corpus callosum at adulthood after injury at either p21 or p35.Res-Intr_test_dataSocial investigation of a novel (male or female) stimulus mouse was quantified as duration spent investigating different regions (e.g. anogenital), during the resident-intruder task.Scent_mark_test_dataGrid squares containing scent marks were quantified during the scent marking test towards a novel female mouse, of sham or TBI (traumatic brain injury) mice at adulthood after injury at p21 or p35.USV_dataUltrasonic vocalizations (USVs) were recorded during encounters of the test mouse (sham or brain-injured) with (1) a novel male, (2) a novel female, or (3) soiled bedding from a novel female. Several parameters including total number of calls, high frequency calls (&gt; 75 kHz) and # calls in bursts were quantified.