Elizabeth Tang
Research Mentor: Jun Kim
Mentor Department: Kresge Hearing Research Insitutue, Medicine
Author(s): Elizabeth Tang, Sungryeong Yoon, Jun Hee Kim
Session: Session 7 (4:00 PM – 4:50 PM)
Presentation Type: Poster 97
Abstract
Maternal smoking during pregnancy leads to auditory processing disruption. Our previous studies revealed that exposure to nicotine during the critical period of auditory development, starting from the hearing onset (postnatal day(P) 12), results in disturbed synapse development and neurotransmission in the auditory brainstem. In this study, we hypothesize that perinatal nicotine exposure (PNE) causes auditory processing dysfunction in the mice. To develop a PNE mouse model, we injected 1.4 mg/kg of nicotine from P8 to P17 to C57BL/6 mice (both sexes). The sham group receives sterile saline to control for the stress injections may induce. To test the effect of PNE on behaviors during both the juvenile and young adult periods, we conducted behavioral assessments at two time frames (P21-P22 and P28-29). First, we performed an Open Field Test (OFT) to confirm anxiety or hyperactivity. Then, Acoustic Startle Response (ASR), Pre-pulse Inhibition (PPI), and Gap-Prepulse Inhibition of the Acoustic Startle Reflex (GPIAS) were measured to detect auditory deficits and sensorimotor gating in nicotine and sham mice (P22 and P29). The results of our OFT showed no significant differences between the nicotine and sham groups for the percentage of time spent in the middle and edge during P21 (Middle: Sham: 11.18 ± 1.722%, Nicotine: 11.05 ± 2.350%, n = 4, Sham vs n = 5, Nicotine, p = 0.9680, Two-tailed T-test; Edge: Sham: 55.49 ± 1.722%, Nicotine: 58.04 ± 3.379%, p = 0.5548) and P28 (Middle: Sham: 13.10 ± 2.797%, Nicotine: 7.214 ± 1.775%, p = 0.1065; Edge: Sham: 55.09 ± 3.121%, Nicotine: 61.88 ± 3.231%, p = 0.1812). However, there was a significant decrease in locomotor activity for nicotine mice on P21 (Average speed: Sham: 39.53 ± 3.800 mm/s, Nicotine: 38.60 ± 2.398 mm/s, p = 0.0388; Total distance: Sham: 21925 ± 1630 mm, Nicotine: 17076 ± 1011 mm, p = 0.0332). These significant differences were not present during P28 (Average speed: Sham: 49.71 ± 6.883 mm/s, Nicotine: 45.76 ± 5.349 mm/s, p = 0.6751; Total distance: Sham: 21890 ± 2934 mm, Nicotine: 20062 ± 2290, p = 0.6568). Our results of ASR, PPI, and GPIAS showed no significant difference between the PNE and sham groups at P22. However, there is a trend for a decrease in PPI/GPIAS values and an increase in ASR values within male PNE mice at P29 (ASR: n = 2, Sham vs n = 2, Nicotine, p = 0.0173, Two-way ANOVA; PPI: p = 0.0430; GPIAS: p = 0.0246). Our findings from ASR, PPI, and GPIAS suggest that PNE may have lasting, delayed ramifications and cause auditory deficits more prominently in adult male mice. In the future, we want to investigate how sex differences affect behavioral outcomes of auditory processing disruptions caused by PNE. Overall, our study identifies PNE as a potential source for delayed auditory processing deficits in mice, showcasing the importance of chronic PNE exposure at the systemic level.
