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Assessing Dominant-Submissive Behavior in Adult Rats Following Traumatic Brain Injury
Published on: December 16, 2022
Sociosexual and communication deficits after traumatic injury to the developing murine brain
Bridgette D Semple1, Linda J Noble-Haeusslein2, Yong Jun Kwon3
1Department of Neurological Surgery, University of California San Francisco, San Francisco, California, United States of America; Department of Medicine (Royal Melbourne Hospital), Melbourne Brain Centre, University of Melbourne, Parkville, Victoria, Australia.
Insights
Pediatric traumatic brain injury (TBI) impairs social function, with younger injury ages leading to worse outcomes. Brain maturation at the time of injury significantly impacts social and communication deficits later in life.
Area of Science:
- Neuroscience
- Developmental Biology
- Behavioral Science
Background:
- Social and communication deficits persist after pediatric traumatic brain injury (TBI), but their developmental course and mechanisms remain poorly understood.
- Previous research showed significant social interaction deficits emerge in adulthood after pediatric TBI at postnatal day 21 (p21).
Purpose of the Study:
- To investigate if social deficits after pediatric TBI depend on brain maturation at the time of injury.
- To examine sociosexual behaviors and communication in mice with TBI at different developmental stages (pediatric vs. adolescent).
Main Methods:
- Compared behavioral and neuroanatomical outcomes in mice injured at p21 (pediatric) versus p35 (adolescent).
- Assessed sociosexual behaviors (investigation, mounting) and communication (scent marking, ultrasonic vocalizations) in adulthood.
- Analyzed neuroanatomical changes, including corpus callosum and hippocampal tissue volume.
Main Results:
- TBI at p21 caused significant sociosexual deficits in adulthood, including reduced mounting and scent marking.
- Mice injured at p35 showed resilience to social deficits, except for impaired social recognition.
- Ultrasonic vocalization patterns were altered post-injury, influenced by stimulus and social experience.
- Both injury ages caused similar corpus callosum atrophy, but p21 injury led to greater hippocampal tissue loss.
Conclusions:
- The developing brain is vulnerable to social dysfunction following TBI, with younger injury ages resulting in poorer long-term social and sociosexual outcomes.
- Greater hippocampal damage after p21 TBI may contribute to more severe and lasting social deficits compared to adolescent injury.
Abstract:
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.
