We studied the CO(2)/H(+)-chemosensitive responses of individual solitary complex (SC) neurons from adult rats by simultaneously measuring the intracellular pH (pH(i)) and electrical responses to hypercapnic acidosis (HA). SC neurons were recorded using the blind whole cell patch-clamp technique and loading the soma with the pH-sensitive dye pyranine through the patch pipette. We found that SC neurons from adult rats have a lower steady-state pH(i) than SC neurons from neonatal rats. In the presence of chemical and electrical synaptic blockade, adult SC neurons have firing rate responses to HA (percentage of neurons activated or inhibited and the magnitude of response as determined by the chemosensitivity index) that are similar to SC neurons from neonatal rats. They also have a typical response to isohydric hypercapnia, including decreased DeltapH(i), followed by pH(i) recovery, and increased firing rate. Thus, the chemosensitive response of SC neurons from adults is similar to the chemosensitive response of SC neurons from neonatal rats. Because our findings for adults are similar to previously reported values for neurons from neonatal rats, we conclude that intrinsic chemosensitivity is established early in development for SC neurons and is maintained throughout adulthood.
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http://dx.doi.org/10.1152/ajpregu.90769.2008 | DOI Listing |
Toxicology
December 2024
Department of Zoology, IIS (deemed to be University), Jaipur, Rajasthan, India.
In the present study, co-parental exposure to polystyrene nanoplastics (PS-NPs) elicits profound teratological impacts, including skeletal and visceral malformations, post-natal effects on neonatal growth and neurobehavioral development in F1 progeny. A comprehensive investigation was conducted on Swiss albino mice fetuses, neonates (PND 1-21) and adult mice offsprings (PND 60) following parental exposure during spermatogenesis and oogenesis period, as well as continued maternal exposure during gestation and weaning. The parental mice were administered PS-NPs via oral gavage at low dose (0.
View Article and Find Full Text PDFJ Mol Neurosci
December 2024
Department of Neurosurgery, National Children's Medical Center (Shanghai), Children's Hospital of Fudan University, No.399 Wan Yuan Avenue, Minhang District, Shanghai, 201102, China.
Focal cortical dysplasia (FCD) II is a cortical malformation characterized by cortical architectural abnormalities, dysmorphic neurons, with or without balloon cells. Here, we systematically explored the pathophysiological role of the GATOR1 subunit NPRL3 variants including a novel mutation from iPSCs derived from one FCD II patient. Three FCD II children aged 0.
View Article and Find Full Text PDFZhongguo Dang Dai Er Ke Za Zhi
December 2024
Department of Neonatology, First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Objectives: To observe the reparative effects of human umbilical cord mesenchymal stem cell (hUC-MSC) transplantation on white matter injury (WMI) in neonatal rats and explore its mechanism through the nuclear factor-kappa B (NF-κB) signaling pathway mediated by microglial cells.
Methods: Sprague-Dawley rats, aged 2 days, were randomly divided into three groups: sham-operation,WMI, and hUC-MSC (=18 each). Fourteen days after modeling, hematoxylin-eosin staining was used to observe pathological changes in the white matter, and immunofluorescence staining was used to measure the expression level of ionized calcium-binding adapter molecule 1 (Iba1).
Epilepsia
December 2024
Department of Physiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Objective: Hypoxic-ischemic brain damage (HIBD) is a leading cause of neonatal mortality, resulting in brain injury and persistent seizures that can last into the late neonatal period and beyond. Effective treatments and interventions for infants affected by hypoxia-ischemia remain lacking. Clinical investigations have indicated an elevation of nuclear factor of activated T cells 5 (NFAT5) in whole blood from umbilical cords of severely affected HIBD infants with epilepsy.
View Article and Find Full Text PDFHum Gene Ther
December 2024
Laboratoire des Maladies Neurodégénératives, MIRCen Institute, Fontenay-aux-Roses, France.
Worldwide, thousands of male patients who carry ATP Binding Cassette Subfamily D Member 1 () mutations develop adrenomyeloneuropathy (AMN) in mid-adulthood, a debilitating axonopathy of the spinal cord. Today AAV gene therapy brings the most hope for this orphan disease. We previously reported that an AAV9-MAG- vector injected intravenously in the neonatal period prevented the disease in 2-year-old mice, the AMN mouse model.
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