Hearing Vocalizations during First Social Experience with Pups Increase Bdnf Transcription in Mouse Auditory Cortex

Author:

Moreno Amielle12ORCID,Rajagopalan Swetha2,Tucker Matthew J.2,Lunsford Parker23,Liu Robert C.24ORCID

Affiliation:

1. Neuroscience Graduate Program, Emory University, Atlanta, Georgia 30332, USA

2. Department of Biology, Emory University, Atlanta, Georgia 30322, USA

3. College of Science Undergraduate Neuroscience Program, Georgia Institute of Technology, Atlanta, Georgia 30332, USA

4. Center for Translational Social Neuroscience, Emory University, Atlanta, Georgia 30322, USA

Abstract

While infant cues are often assumed to innately motivate maternal response, recent research highlights how the neural coding of infant cues is altered through maternal care. Infant vocalizations are important social signals for caregivers, and evidence from mice suggests that experience caring for mouse pups induces inhibitory plasticity in the auditory cortex (AC), though the molecular mediators for such AC plasticity during the initial pup experience are not well delineated. Here, we used the maternal mouse communication model to explore whether transcription in AC of a specific, inhibition-linked, memory-associated gene, brain-derived neurotrophic factor (Bdnf) changes due to the very first pup caring experience hearing vocalizations, while controlling for the systemic influence of the hormone estrogen. Ovariectomized and estradiol or blank-implanted virgin female mice hearing pup calls with pups present had significantly higher AC exon IV Bdnf mRNA compared to females without pups present, suggesting that the social context of vocalizations induces immediate molecular changes at the site of auditory cortical processing. E2 influenced the rate of maternal behavior but did not significantly affect Bdnf mRNA transcription in the AC. To our knowledge, this is the first time Bdnf has been associated with processing social vocalizations in the AC, and our results suggest that it is a potential molecular component responsible for enhancing future recognition of infant cues by contributing to AC plasticity.

Funder

National Institutes of Health

Publisher

Hindawi Limited

Subject

Neurology (clinical),Neurology

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