Charles V. Vorhees

ORCID: 0000-0003-3558-8812
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurotransmitter Receptor Influence on Behavior
  • Prenatal Substance Exposure Effects
  • Memory and Neural Mechanisms
  • Neuroendocrine regulation and behavior
  • Pharmacological Effects and Toxicity Studies
  • Stress Responses and Cortisol
  • Anesthesia and Neurotoxicity Research
  • Birth, Development, and Health
  • Effects and risks of endocrine disrupting chemicals
  • Forensic Toxicology and Drug Analysis
  • Attention Deficit Hyperactivity Disorder
  • Metabolism and Genetic Disorders
  • Receptor Mechanisms and Signaling
  • Maternal Mental Health During Pregnancy and Postpartum
  • Cannabis and Cannabinoid Research
  • Heavy Metal Exposure and Toxicity
  • Pesticide Exposure and Toxicity
  • Neonatal and fetal brain pathology
  • Zebrafish Biomedical Research Applications
  • Pregnancy and Medication Impact
  • Adipose Tissue and Metabolism
  • Neurogenesis and neuroplasticity mechanisms
  • Phosphodiesterase function and regulation
  • Diet and metabolism studies

University of Cincinnati Medical Center
2015-2025

Cincinnati Children's Hospital Medical Center
2016-2025

University of Cincinnati
2016-2025

University of Georgia
2017

Neurology, Inc
2017

United States Army Medical Research and Development Command
2014

Thomas Jefferson National Accelerator Facility
2014

Children's Hospital & Medical Center
2014

Northern Kentucky University
2012

Pediatrics and Genetics
2010

Abstract d ‐Fenfluramine, a serotonin releaser, was administered to neonatal rats on postnatal days 11–20 (a stage of hippocampal development analogous third trimester human ontogeny). As adults, the ‐fenfluramine‐treated offspring exhibited dose‐related impairments sequential and spatial learning reference memory in absence sensorimotor impairments. Procedures minimize stress control for other performance effects prior testing demonstrated that nonspecific factors did not account selective...

10.1046/j.1460-9568.2002.02100.x article EN European Journal of Neuroscience 2002-08-01

Several disorders have been associated with mutations in Na,K-ATPase α isoforms (rapid-onset dystonia parkinsonism, familial hemiplegic migraine type-2), as well reduction content (depression and Alzheimer's disease), thereby raising the issue of whether haploinsufficiency or altered enzymatic function contribute to disease etiology. Three are expressed brain: α1 isoform is found many cell types, α2 predominantly astrocytes, α3 exclusively neurons. Here we show that mice heterozygous for...

10.1523/jneurosci.4464-06.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-01-17

Recent studies suggest that postmitotic neurons can reenter the cell cycle as a prelude to apoptosis after brain injury. However, most dying do not pass G 1 /S-phase checkpoint resume DNA synthesis. The specific factors trigger abortive synthesis are characterized. Here we show combination of hypoxia and ischemia induces adult rodent indicated by incorporation bromodeoxyuridine (BrdU) expression transition markers. After hypoxia-ischemia, majority BrdU- neuronal nuclei (NeuN)-immunoreactive...

10.1523/jneurosci.3883-04.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-11-24

Volatile anesthetics, such as isoflurane, are widely used in infants and neonates. Neurodegeneration neurocognitive impairment after exposure to midazolam, nitrous oxide neonatal rats have raised concerns regarding the safety of pediatric anesthesia. In mice, prolonged isoflurane triggers hypoglycemia, which could be responsible for impairment. We examined effects blood glucose on brain cell viability, spontaneous locomotor activity, well spatial learning memory mice.Seven-day-old mice were...

10.1213/ane.0b013e31818cdb29 article EN Anesthesia & Analgesia 2008-12-16

In most cells, the ubiquitously expressed Na + /H exchanger isoform 1 (NHE1) is thought to be a primary regulator of pH homeostasis, cell volume regulation, and proliferative response growth factor stimulation. To study function NHE1 during embryogenesis when these cellular processes are very active, we targeted Nhe1 gene by replacing sequence encoding transmembrane domains 6 7 with neomycin resistance gene. NHE activity assays on isolated acinar cells indicated that allele functionally...

10.1152/ajpcell.1999.276.4.c788 article EN AJP Cell Physiology 1999-04-01

Three psychotropic drugs were administered to pregnant rats and then evaluated for their behavioral reproductive effects in the offspring. Control received either saline or vitamin A. Prochlorperazine had most disruptive on reproduction growth, but least effect behavior. Propoxyphene no apparent produced a variety of changes. Fenfluramine was intermediate its growth that revealed tests preweaning development. The data suggest systematic behavior add important information evaluations toxicity...

10.1126/science.472738 article EN Science 1979-09-21

Gaucher disease is caused by defective acid β-glucosidase (GCase) function. Saposin C a lysosomal protein needed for optimal GCase activity. To test the in vivo effects of saposin on GCase, deficient mice (C−/−) were backcrossed to point mutated (V394L/V394L) mice. The resultant (4L;C*) began exhibit CNS abnormalities ∼30 days: first as hindlimb paresis, then progressive tremor and ataxia. Death occurred ∼48 days due neurological deficits. Axonal degeneration was evident brain stem, spinal...

10.1093/hmg/ddp580 article EN Human Molecular Genetics 2010-01-04

Mutations in the creatine (Cr) transporter (CrT; Slc6a8) gene lead to absence of brain Cr and intellectual disabilities, loss speech, behavioral abnormalities. To date, no mouse model CrT deficiency exists which understand develop treatments for this condition. The purpose study was generate a human deficiency. We created mice with exons 2–4 Slc6a8 flanked by loxP sites crossed these Cre:CMV create line ubiquitous knockout expressing mice. Mice were tested learning memory deficits assayed...

10.1371/journal.pone.0016187 article EN cc-by PLoS ONE 2011-01-13

Use of 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) has increased dramatically in recent years, yet little is known about its effects on the developing brain. Neonatal rats were administered MDMA days 1-10 or 11-20 (analogous to early and late human third trimester brain development). exposure had no effect survival but did affect body weight gain during treatment. After treatment, largely recovered 90-95% controls. resulted dose-related impairments sequential learning spatial memory,...

10.1523/jneurosci.21-09-03228.2001 article EN cc-by-nc-sa Journal of Neuroscience 2001-05-01

Abstract The teratogenicity and developmental toxicity of valproic acid (VPA) was investigated in Sprague‐Dawley CD rats at doses 0, 150, 200, 300, 400, 600 mg/kg administered by gavage on days 7–18 gestation. VPA‐600 dose maternally toxic, causing death two four dams. This produced 100% embryonic resorption. VPA‐400 toxic as much maternal weight gain reduced, but no deaths occurred. At this five fifteen litters were completely resorbed, 52% all embryos resorbed. Among survivors, 49%...

10.1002/tera.1420350205 article EN Birth Defects Research 1987-04-01

Using homologous recombination, we generated mice lacking phosphodiesterase-mediated (PDE1B) cyclic nucleotide-hydrolyzing activity. PDE1B(-/-) showed exaggerated hyperactivity after acute D-methamphetamine administration. Striatal slices from exhibited increased levels of phospho-Thr34 DARPP-32 and phospho-Ser845 GluR1 dopamine D1 receptor agonist or forskolin stimulation. PDE1B(+/-) demonstrated Morris maze spatial-learning deficits. These results indicate that enhancement nucleotide...

10.1523/jneurosci.22-12-05188.2002 article EN Journal of Neuroscience 2002-06-15
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