Sensory detection tasks enhance representations of behaviorally meaningful stimuli in primary auditory cortex (A1). However, it remains unclear how A1 encodes decision-making. Neurons in A1 layer 2/3 (L2/3) show heterogeneous stimulus selectivity and complex anatomical connectivity, and receive input from prefrontal cortex. Thus, task-related modulation of activity in A1 L2/3 might differ across subpopulations. To study the neural coding of decision-making, we used two-photon imaging in A1 L2/3 of mice performing a tone-detection task. Neural responses to targets showed attentional gain and encoded behavioral choice. To characterize network representation of behavioral choice, we analyzed functional connectivity using Granger causality, pairwise noise correlations, and neural decoding. During task performance, small groups of four to five neurons became sparsely linked, locally clustered, and rostro-caudally oriented, while noise correlations both increased and decreased. Our results suggest that sensory-based decision-making involves small neural networks driven by the sum of sensory input, attentional gain, and behavioral choice.

Filter theory indicates that changes in cochlear filter bandwidths are accompanied by changes in cochlear response latencies. Previous reports indicate that otoacoustic emission (OAE) delays are reduced by exciting medial olivocochlear (MOC) efferents with contralateral broad-band noise (CBBN). These delay reductions are consistent with MOC-induced widening of cochlear filters. We quantified the MOC-induced changes in human cochlear-filter-related delays using stimulusfrequency and click-evoked OAEs (SFOAE and CEOAEs), recorded with and without MOC activity elicited by 60 dB SPL CBBN. MOC-induced delay changes were measured from the slopes of SFOAE phase functions and from cross-correlation of 500 Hz-wide CEOAE frequencyband waveform magnitudes. The delay changes measured from CEOAEs and SFOAEs were statistically indistinguishable. Both showed greater delay reductions at lower frequencies (a 5% decrease in the 0.5 -2 kHz frequency region). These data indicate that cochlear filters are widened 5% by the MOC activity from moderate-level CBBN. Psychophysically, the large changes in cochlear response latencies, implied by the 0.5 ms change in OAE delay at low frequencies, would have a profound effect on binaural localization if they were not balanced in the central nervous system, or by the MOC system producing similar changes in both ears.

Opioid use by pregnant women is an understudied consequence associated with the opioid epidemic, resulting in a rise in the incidence of neonatal opioid withdrawal syndrome (NOWS) and lifelong neurobehavioral deficits that result from perinatal opioid exposure. There are few preclinical models that accurately recapitulate human perinatal drug exposure and few focus on fentanyl, a potent synthetic opioid that is a leading driver of the opioid epidemic. To investigate the consequences of perinatal opioid exposure, we administered fentanyl to mouse dams in their drinking water throughout gestation and until litters were weaned at postnatal day (PD) 21. Fentanyl‐exposed dams delivered smaller litters and had higher litter mortality rates compared with controls. Metrics of maternal care behavior were not affected by the treatment, nor were there differences in dams' weight or liquid consumption throughout gestation and 21 days postpartum. Twenty‐four hours after weaning and drug cessation, perinatal fentanyl‐exposed mice exhibited signs of spontaneous somatic withdrawal behavior and sex‐specific weight fluctuations that normalized in adulthood. At adolescence (PD 35), they displayed elevated anxiety‐like behaviors and decreased grooming, assayed in the elevated plus maze and sucrose splash tests. Finally, by adulthood (PD 55), they displayed impaired performance in a two‐tone auditory discrimination task. Collectively, our findings suggest that perinatal fentanyl‐exposed mice exhibit somatic withdrawal behavior and change into early adulthood reminiscent of humans born with NOWS.

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