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Significance: Light is a good probe for studying the nanoscale-level structural or molecular-specific structural properties of brain cells/tissue due to stress, alcohol, or any other abnormalities. Chronic alcoholism during pregnancy, i.e., fetal alcoholism, being teratogenic, results in fetal alcohol syndrome, and other neurological disorders. Understanding the nano-to-submicron scale spatial structural properties of pup brain cells/tissues using light/photonic probes could provide a plethora of information in understanding the effects of fetal alcoholism.
Aim: Using both light scattering and light localization techniques to probe alterations in nano- to-submicron scale mass density or refractive index fluctuations in brain cells/tissues of mice pups, exposed to fetal alcoholism.
Approach: We use the mesoscopic physics-based dual spectroscopic imaging techniques, partial wave spectroscopy (PWS) and molecular-specific inverse participation ratio (IPR) using confocal imaging, to quantify structural alterations in brain tissues and chromatin/histone in brain cells, respectively, in 60 days postnatal mice pup brain, exposed to fetal alcoholism.
Results: The finer focusing PWS analysis on tissues shows an increase in the degree of structural disorder strength in the pup brain tissues. Furthermore, results of the molecular-specific light localization IPR technique show an increase in the degree of spatial molecular mass density structural disorder in DNA and a decrease in the degree in histone.
Conclusions: In particular, we characterize the spatial pup brain structures from the molecular to tissue levels and address the plausible reasons for such as mass density fluctuations in fetal alcoholism.
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http://dx.doi.org/10.1117/1.JBO.27.7.076002 | DOI Listing |
Nat Commun
August 2025
School of Biomedical Engineering, Southern Medical University, Guangzhou, China.
Maternal defense, a hallmark of motherhood, often involves protecting offspring at personal risk. However, the neural mechanisms underlying the emergence and modulation of this behavior remain not-well understood. Here, we introduce a novel paradigm in which mother mice under threat prioritize offspring protection over self-preservation by approaching, collecting, and retreating pups to safety, a risk-associated behavior that also develops in virgin females following maternal experience.
View Article and Find Full Text PDFNeuropharmacology
November 2025
Faculty of Psychology, Southwest University, Chongqing, 400715, China; Key Laboratory of Cognition and Personality, Ministry of Education, 400715, China. Electronic address:
Maternal behavior during the postpartum period is mediated by various neural mechanisms. While dopamine D receptor activation is known to affect maternal behavior in early postpartum, its role in the late postpartum period remains unclear. This study explores the neural mechanisms governing maternal behavior across the early and late postpartum periods by activating D receptors in different maternal brain regions: the ventral tegmental area (VTA), nucleus accumbens (NAc), and medial prefrontal cortex (mPFC).
View Article and Find Full Text PDFProg Neuropsychopharmacol Biol Psychiatry
August 2025
Philipps-Universität Marburg, Faculty of Psychology, Experimental and Biological Psychology, Social and Affective Neuroscience, D-35032 Marburg, Germany; Philipps-Universität Marburg, Center for Mind, Brain, and Behavior (CMBB), D-35032 Marburg, Germany; KU Leuven, Faculty of Psychology and Educat
Deficiency of tryptophan hydroxylase 2 (TPH2), the rate-limiting enzyme for serotonin (5-hydroxytryptamine, 5-HT) synthesis in the brain, was repeatedly reported to cause impairments in socio-affective communication and maternal affiliation across species, including mice, rats, and monkeys. We recently applied a rescue protocol in the Tph2 knockout rat model and demonstrated that communal nesting ameliorates maternal affiliation impairments. Interestingly, however, this rescue strategy did not lead to improvements in socio-affective communication and was associated with an aggravated growth retardation phenotype in Tph2-deficient offspring.
View Article and Find Full Text PDFFront Syst Biol
July 2025
Lawrence D. Longo, MD Center for Perinatal Biology, Department of Basic Science, Loma Linda University, Loma Linda, CA, United States.
Introduction: Preterm hypoxic-ischemic encephalopathy (pHIE) is a complex brain injury that contributes to chronic neural inflammation and neurological disorders. The signs and symptoms of in utero pHIE can often be overlooked, untreated or lumped into more generic conditions such as encephalopathy of prematurity (EOP). Clinical interventions like hypothermia and erythropoietin do not improve pHIE.
View Article and Find Full Text PDFCommun Biol
August 2025
Department of Biology, University of Maryland, College Park, MD, USA.
In mammals, measurable changes in brain and behavior accompany the transition to parenthood. In the biparental California mouse, Peromyscus californicus, fathers experience enhanced neuroplasticity, including increased hippocampal dendritic spine density, reduced anxiety, and improved memory. Here, we first investigate whether siring offspring or pup interaction drives structural neuroplasticity in fathers and find that hippocampal spine density is positively associated with caregiving experience, even in the absence of reproduction.
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