Race and Ethnicity and Exclusive Breastfeeding Success.

Introduction: Breast milk is the ideal food for infants. However, at 6 months of age, <25% of infants in the United States are exclusively breastfed. While racial disparities in breastfeeding have been documented, questions remain about the contributions of paternal race and ethnicity to breastfeeding. Materials and Methods: This single-site, prospective study investigated the association of parental characteristics and exclusive breastfeeding (EBF). EBF and non-EBF (N-EBF) infants who were >35 weeks gestational age were compared at nursery discharge and ∼30 days of age. Results: At nursery discharge (n = 499), mean birth weight (±standard deviation [SD]) was greater in the EBF versus N-EBF cohort (3.4 ± 0.4 versus 3.3 ± 0.5 kg, p = 0.01). When compared to the N-EBF cohort, infants in the EBF cohort were significantly more likely to have the following characteristics: (1) vaginal birth; (2) non-Hispanic parents; (3) parents with higher socioeconomic status, and (4) parents who are English-speaking (p < 0.01 for all). Similar findings persisted at 30 days. Non-Hispanic parents were 2 (95% confidence interval [CI]: 1.4-3.3) and 3.5 (95% CI: 1.5-7.9) times more likely to exclusively breastfeed than Hispanic parents at nursery discharge and 30 days, respectively. At nursery discharge, families with a Hispanic mother and non-Hispanic father were more likely to EBF than families with a Hispanic mother and father (odds ratio 2.9, 95% CI: 1.1-7.6). In multivariate model, parental ethnicity was associated with EBF at discharge (p = 0.03) and 30 days (p = 0.02). Conclusion: Paternal ethnicity may influence EBF. Addressing disparities in EBF may warrant investigations into culturally inclusive and family-centered interventions.

Major Contribution of Somatostatin-Expressing Interneurons and Cannabinoid Receptors to Increased GABA Synaptic Activity in the Striatum of Huntington's Disease Mice.

Huntington's disease (HD) is a heritable neurological disorder that affects cognitive and motor performance in patients carrying the mutated huntingtin (HTT) gene. In mouse models of HD, previous reports showed a significant increase in spontaneous GABAA receptor-mediated synaptic activity in striatal spiny projection neurons (SPNs). In this study, using optogenetics and slice electrophysiology, we examined the contribution of γ-aminobutyric acid (GABA)-ergic parvalbumin (PV)- and somatostatin (SOM)-expressing interneurons to the increase in GABA neurotransmission using the Q175 (heterozygote) mouse model of HD. Patch clamp recordings in voltage-clamp mode were performed on SPNs from brain slices of presymptomatic (2 months) and symptomatic (8 and 12 months) Q175 mice and wildtype (WT) littermates. While inhibitory postsynaptic currents (IPSCs) evoked in SPNs following optical activation of PV- and SOM-expressing interneurons differed in amplitude, no genotype-dependent differences were observed at all ages from both interneuron types; however, responses evoked by either type were found to have faster kinetics in symptomatic mice. Since SOM-expressing interneurons are constitutively active in striatal brain slices, we then examined the effects of acutely silencing these neurons in symptomatic mice with enhanced Natronomonas pharaonis halorhodopsin (eNpHR). Optically silencing SOM-expressing interneurons resulted in a greater decrease in the frequency of spontaneous IPSCs (sIPSCs) in a subset of SPNs from Q175 mice compared to WTs, suggesting that SOM-expressing interneurons are the main contributors to the overall increased GABA synaptic activity in HD SPNs. Additionally, the effects of activating GABAB and cannabinoid (CB1) receptors were investigated to determine whether these receptors were involved in modulating interneuron-specific GABA synaptic transmission and if this modulation differed in HD mice. When selectively activating PV- and SOM-expressing interneurons in the presence of the CB1 receptor agonist WIN-55,212, the magnitudes of the evoked IPSCs in SPNs decreased for both interneuron types although this change was less prominent in symptomatic Q175 SPNs during SOM-expressing interneuron activation. Overall, these findings show that dysfunction of SOM-expressing interneurons contributes to the increased GABA synaptic activity found in HD mouse models and that dysregulation of the endocannabinoid system may contribute to this effect.