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Intranasal Administration of Oxytocin Attenuates Social Recognition Deficits and Increases Prefrontal Cortex Inhibitory Postsynaptic Currents following Traumatic Brain Injury
Journal article   Open access   Peer reviewed

Intranasal Administration of Oxytocin Attenuates Social Recognition Deficits and Increases Prefrontal Cortex Inhibitory Postsynaptic Currents following Traumatic Brain Injury

Avery Runyan, Dana Lengel, Jimmy W. Huh, Jessica R. Barson and Ramesh Raghupathi
eNeuro, v 8(3), pENEURO.0061-21.2021
10 Jun 2021
DOI: https://doi.org/10.1523/ENEURO.0061-21.2021
PMID: 34035071
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1523/eneuro.0061-21.2021View
Published, Version of Record (VoR)CC BY V4.0,  Open
url
https://doi.org/10.1523/ENEURO.0061-21.2021View
Published, Version of Record (VoR) Open

Abstract

excitability GABAergic neurotransmission intranasal administration New Research oxytocin pediatric TBI social behavior
Pediatric traumatic brain injury (TBI) results in heightened risk for social deficits that can emerge during adolescence and adulthood. A moderate TBI in male and female rats on postnatal day 11 (equivalent to children below the age of 4) resulted in impairments in social novelty recognition, defined as the preference for interacting with a novel rat compared with a familiar rat, but not sociability, defined as the preference for interacting with a rat compared with an object in the three-chamber test when tested at four weeks (adolescence) and eight weeks (adulthood) postinjury. The deficits in social recognition were not accompanied by deficits in novel object recognition memory and were associated with a decrease in the frequency of spontaneous inhibitory postsynaptic currents (IPSCs) recorded from pyramidal neurons within Layer II/III of the medial prefrontal cortex (mPFC). Whereas TBI did not affect the expression of oxytocin (OXT) or the OXT receptor (OXTR) mRNAs in the hypothalamus and mPFC, respectively, intranasal administration of OXT before behavioral testing was found to reduce impairments in social novelty recognition and increase IPSC frequency in the mPFC in brain-injured animals. These results suggest that TBI-induced deficits in social behavior may be linked to increased excitability of neurons in the mPFC and suggests that the regulation of GABAergic neurotransmission in this region as a potential mechanism underlying these deficits.

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21 citations in Web of Science
19 citations in Scopus

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Collaboration types
Domestic collaboration
Web of Science research areas
Neurosciences
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