Increased alcohol drinking and seizure susceptibility in female humanized ApoE4 knockin rats.

Drinking microstructure analysis of direct controls of water intake in male and female rats.

Diethyl phthalate-induced oxidative stress, genotoxicity, and thyroid hormone disruption in female Wistar rats.

Chronic (180-day) and sub-chronic (90-Day) oral toxicity studies of a novel polyethyleneglycol (PEG)-carbohydrate-lipid conjugate in Wistar rats and beagle dogs.

Protective effects of polydatin on cyclophosphamide-induced ovarian and uterine damage in rats via modulation of hormonal, oxidative, inflammatory, and histopathological alterations.

Early-life exposure to endocrine-disrupting chemicals (EDCs) can interfere with brain development and contribute to long-term cognitive impairments. This study investigated whether hippocampal metabolite alterations at postnatal day 6 (PND6) are associated with behavioral outcomes in early adulthood following perinatal exposure to four EDCs: bisphenol F (BPF), butyl benzyl phthalate (BBzP), triphenyl phosphate (TPHP), and diisononyl cyclohexane-1,2-dicarboxylate (DINCH). Male and female rats were exposed in utero and during lactation, and hippocampal tissue was collected at PND6 for targeted metabolomics and untargeted lipidomics. Behavioral testing in adulthood using the Morris water maze assessed spatial learning (acquisition) and cognitive flexibility (reversal). BBzP exposure impaired acquisition learning, and BPF disrupted reversal performance in males. In females, both DINCH and TPHP led to increased latency during reversal. A multi-layered analytical framework was applied to explore associations between early metabolite and lipid profiles and later behavioral performance, including group-based comparisons, correlation analyses, and evaluation of biologically informed ratios. Results revealed sex- and domain-specific alterations in steroid and thyroid hormones, neurotransmitters, and PUFA-containing lipid classes, as well as changes in functional ratios and metabolite-metabolite coordination. These early metabolic disruptions were associated with increased escape latency in adulthood, suggesting long-term impacts on hippocampal function.

• No effect of prenatal methadone or buprenorphine on weaning or adult weights • Prenatal methadone increased motivated responding for sucrose in males and females • Methadone-induced, female-specific increase in nucleus accumbens gene expression • Differential effects of methadone and buprenorphine in arcuate nucleus The opioid crisis has resulted in escalating rates of opioid use disorder in women of reproductive age and increased prevalence of fetal drug exposure. While medication for opioid use disorder (MOUD) – e.g., buprenorphine or methadone – improves maternal health outcomes, infants exposed to MOUD show a variety of physical and behavioral consequences. There are, however, few clinical or preclinical studies investigating long-term effects of MOUD exposure. The current work investigates the long-term effects of prenatal MOUD exposure on effort-based responding to a palatable food reward and gene expression in regions of the brain related to reward and feeding, including the nucleus accumbens and hypothalamus. Female Sprague Dawley rats were implanted with osmotic minipumps filled with methadone (10 mg/kg/day) or buprenorphine (1 mg/kg/day) or saline control (2.5 μL/hour for 28 days) and mated four days later. In adulthood, male and female offspring began sucrose pellet self-administration to assess the motivational strength of a food reward in MOUD-exposed animals compared to saline controls, followed by analysis of gene expression via RNAscope in situ hybridization. We observed long-term changes in reward motivation, where adults gestationally exposed to methadone – but not buprenorphine – demonstrated increased motivated responding for sucrose. We observed modest sex-dependent effects of MOUD on gene expression in the nucleus accumbens and arcuate nucleus of the hypothalamus following sucrose self-administration. These data suggest differential effects of methadone and buprenorphine on the brain and behavior, providing insight into the potential neuromolecular underpinnings of MOUD-induced changes in neural modulation of reward-motivated behavior.

Early-life dietary long-chain polyunsaturated fatty acid consumption promotes immune function and reduces systemic and adipose inflammation in a sex-specific manner in obese Wistar rats.

Efficacy of Rhizoma Drynariae (Drynaria roosii Nakaike) extracts in treating osteoporosis in rat models: A systematic review and meta-analysis.

Denervation results in reduced bone quality, largely attributed to reduced loading due to concurrent muscle atrophy. However, sensory and sympathetic nerves also directly innervate bone, suggesting additional potential inputs into bone remodeling. A quantitative baseline of bone morphological and functional changes after nerve injury is lacking. We investigated structural, biomechanical, and histological outcomes for time points up to three months following peripheral nerve injury. Our primary objective was to establish timelines over which bone and muscle structure and biomechanical function degraded after denervation. Additionally, we evaluated remodeling of bone innervation and vascularity and alterations in bone homeostatic markers after injury. Using a Lewis rat nerve injury model (n=60 total rats), our findings showed rapid bone deterioration following transection of sciatic nerves of both male and female rats. Biomechanical properties of bone, including three-point bending yield force (P<0.001), ultimate force (P<0.001), and stiffness (P<0.001), were significantly reduced as early as two weeks post-injury. At a slight delay compared to biomechanical changes, micro-CT and MRI revealed that bone mineral density (P<0.0001) and cortical thickness (P<0.001) also declined and porosity increased (P<0.05) within three months. Immunohistochemical analysis revealed marked decreases in sensory (calcitonin gene-related protein; CGRP) and sympathetic (Neuropeptide-Y; NPY) neuropeptides, reduced osteoblast density in periosteal regions, and increased vascular (CD-31) area fraction, accompanied by increased vascular fragmentation. These findings support the possibility that both muscle and neuronal influences underlie denervation-related bone atrophy, setting the stage for evaluation of bone health after nerve repair and targeted rehabilitative or therapeutic interventions.

We investigated whether physiological oscillations detected by noncontrast resting-state magnetic resonance imaging (rsMRI) can be used to measure functional nephron number, nephron density, or estimated single-nephron glomerular filtration rate (eSNGFR) in vivo. We further investigated whether the observed oscillations below 0.05 Hz reflect tubuloglomerular feedback (TGF). First, we compared features of spectral power of oscillations in rsMRI with total nephron number, nephron density, glomerular filtration rate (GFR), and eSNGFR in healthy Sprague-Dawley rats (n = 20). We then compared features of spectral power to total nephron number in Zucker Diabetic Sprague-Dawley (ZDSD) rats (n = 8) with type-2 diabetes. Finally, we tested the hypothesis that spectral features associated with nephron number reflect TGF by comparing spectra before and after furosemide infusion, which blocks the Na-K-2Cl cotransporter required for TGF and attenuates TGF oscillations. In healthy rats, the median power of rsMRI oscillations below 0.05 Hz in the kidney cortex was significantly correlated (P < 0.05) with nephron number in all animals (R2 = 0.68) and within sex groups (R2, males = 0.71; R2, females = 0.73). Median power in this range was inversely correlated with eSNGFR (P < 0.05, R2 = 0.39). No spectral features were correlated with nephron density or GFR. In ZDSD rats with confirmed pathology, total power between 0.015 and 0.045 Hz was significantly correlated with nephron number (R2 = 0.59, P < 0.05). In both male and female rats, furosemide caused a significant attenuation of power in rsMRI spectral peaks below 0.05 Hz throughout the cortex (P < 0.05). This work demonstrates the noninvasive, in vivo measurement of nephron number in healthy and diabetic rats using rsMRI, and the potential application of rsMRI to detect TGF-associated physiological fluctuations.NEW & NOTEWORTHY We previously showed that resting-state magnetic resonance imaging (rsMRI) detects spontaneous physiological oscillations in rat and human kidneys, potentially reflecting autoregulation mechanisms. Here, we apply rsMRI and show that the features of these oscillations can be used to measure nephron number in healthy and diabetic rats, and are associated with the tubuloglomerular feedback mechanism. Because the rsMRI scan is short (∼10 min) and noninvasive, it might be rapidly translated to measure nephron number and function in the clinic.

Descriptive analysis of the celiac ganglia in female rats: an asymmetrical pair with distinct neuronal pathways

Early life energy drink exposure impairs social and cognitive behaviour in female rats before and after pregnancy.

Cross-comparison of anesthetic regimens for auditory brainstem response recordings in rats.

In vivo biocompatibility of poly-N-isopropylacrylamide (PNIPAM) hydrogels in Wistar rats: Hematological, biochemical, and histopathological assessments.

Sensitive windows, sensitive outcomes: Early or late-postnatal maternal separation differentially impacts puberty and behavior.

Surgical menopause impact on vaginal mechanical properties.

Hydrolyzed pearl improves mitochondrial function in rats with diminished ovarian reserve via modulation of the AMPK/SIRT1/PGC-1α axis

Obstructive sleep apnea (OSA), marked by intermittent hypoxia, is associated with obesity, type 2 diabetes and metabolic associated fatty liver disease. In pregnancy, it remains underdiagnosed despite links to gestational diabetes, hypertension, and foetal growth restriction. Intermittent hypoxia may alter foetal programming and increase the risk of long-term metabolic issues in offspring. This study evaluates the effects of gestational OSA on offspring metabolic function, focusing on weight gain, glucose homeostasis, insulin sensitivity, hepatic glucose metabolism, inflammation and oxidative stress. Experiments were performed on pregnant female Wistar rats submitted to a chronic intermittent hypoxia (CIH) protocol during the last 2 weeks of pregnancy. Offspring were evaluated for body weight, glucose tolerance and insulin sensitivity at 1, 3, and 12 months of age. Liver western blot analysis was performed to assess markers of glucose metabolism (glucokinase, pyruvate kinase and glucose-6-phosphatase), inflammation (NF-kB, IL-1R, IL-6R, TNF-ɑR and NRLP3) and antioxidant enzymes (catalase, SOD-1 and iNOS). CIH did not modify body weight, glucose tolerance and insulin sensitivity at 1, 3 and 12 months of age, except for a transient increase in glucose intolerance observed in 3-month-old females, which was attenuated by 12 months. Moreover, no evidence was found of modifications caused by gestational CIH on markers of hepatic glucose metabolism, inflammation or antioxidant defence. However, there was a gradual increase in inflammation with age. No sexual dimorphism was observed. Overall, these findings suggest that gestational CIH does not predispose offspring to long-term metabolic dysfunction later in life and does not affect biological ageing, regardless of sex.

The cytochrome P450 (CYP) 1A subfamily, regulated by the aryl hydrocarbon receptor (AhR), is central to the bioactivation or deactivation of xenobiotics, endogenous substrates, and carcinogens. Music can alter hormonal and neurotransmitter concentrations, which are partly regulated by CYP-dependent pathways. This study investigated whether defined musical elements modulate hepatic CYP1A in male and female Sprague-Dawley rats. Animals were exposed for 24h to music containing variations of rhythm, tempo, and harmony. Of all conditions tested, fast-tempo, irregular-rhythm, and atonal-harmony (FT-IR-AH) produced the greatest increases in hepatic CYP1A1 (7-ethoxyresorufin O-deethylase) and CYP1A2 (7-methoxyresorufin O-demethylase) activities. In the combined-sex cohort, FT-IR-AH music increased CYP1A1 maximum velocity (Vmax) and intrinsic clearance (CLint) by 3.2- and 3.1-fold, respectively, and increased CYP1A2 Vmax and CLint by 1.9- and 1.8-fold, respectively, without altering enzyme affinities. FT-IR-AH also increased CYP1A1 protein expression by 1.9-fold in females and 2.6-fold in males, and CYP1A2 by 1.6-fold and 1.7-fold, respectively, with concordant elevations in mRNA levels. Replication of the same music elements across different music composers yielded consistent findings, with variations in effects potentially attributed to percentages of gaps (i.e., staccato) and frequency patterns. Selective induction of AhR-regulated genes in the absence of nuclear factor erythroid 2-related factor 2-dependent antioxidant gene activation suggests that FT-IR-AH music selectively engages AhR signaling without a generalized oxidative stress response. These data identify specific music features as an external stimulus capable of modulating CYP1A expression and function, with potential implications for therapeutic responses, toxicological effects, and drug interactions.