Articles by Jessie R. Maxwell in JoVE
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats Lauren L. Jantzie1,2, Jesse L. Winer3, Jessie R. Maxwell1, Lindsay A.S. Chan3, Shenandoah Robinson3,4 1Department of Pediatrics, University of New Mexico, 2Department of Neurosciences, University of New Mexico, 3Department of Neurosurgery, Boston Children's Hospital, 4Department of Neurology, Harvard Medical School Encephalopathy of prematurity encompasses the central nervous system abnormalities associated with injury from preterm birth. This report describes a clinically relevant rat model of in utero transient systemic hypoxia-ischemia and intra-amniotic lipopolysaccharide administration (LPS) that mimics chorioamnionitis, and the related impact of infectious stimuli and placental underperfusion on CNS development.
Other articles by Jessie R. Maxwell on PubMed
Interventions Using Electronic Medical Records Improve Follow Up of Infants Born to Hepatitis C Virus Infected Mothers The Pediatric Infectious Disease Journal. Apr, 2014 | Pubmed ID: 24401869 The American Academy of Pediatrics recommends hepatitis C virus (HCV) antibody testing for all HCV- exposed infants at age ≥ 18 months. However, many of these infants are not appropriately tested. In 2006, the pediatric infectious disease service (PIDS) at our institution implemented interventions using electronic medical records (EMR) to improve appropriate HCV testing for HCV-exposed infants.
Chloride Cotransporter NKCC1 Inhibitor Bumetanide Protects Against White Matter Injury in a Rodent Model of Periventricular Leukomalacia Pediatric Research. Apr, 2015 | Pubmed ID: 25585037 Periventricular leukomalacia (PVL) is a major form of preterm brain injury. Na(+)-K(+)-Cl(-) 1 cotransporter (NKCC1) expression on neurons and astrocytes is developmentally regulated and mediates Cl(-) reversal potential. We hypothesized that NKCC1 is highly expressed on oligodendrocytes (OLs) and increases vulnerability to hypoxia-ischemia (HI) mediated white matter injury, and that the NKCC1 inhibitor bumetanide would be protective in a rodent PVL model.
Prenatal Hypoxia-Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone Frontiers in Cellular Neuroscience. 2015 | Pubmed ID: 26388734 Infants who suffer perinatal brain injury, including those with encephalopathy of prematurity, are prone to chronic neurological deficits, including epilepsy, cognitive impairment, and behavioral problems, such as anxiety, inattention, and poor social interaction. These deficits, especially in combination, pose the greatest hindrance to these children becoming independent adults. Cerebral function depends on adequate development of essential inhibitory neural circuits and the appropriate amount of excitation and inhibition at specific stages of maturation. Early neuronal synaptic responses to γ-amino butyric acid (GABA) are initially excitatory. During the early postnatal period, GABAAR responses switch to inhibitory with the upregulation of potassium-chloride co-transporter KCC2. With extrusion of chloride by KCC2, the Cl(-) reversal potential shifts and GABA and glycine responses become inhibitory. We hypothesized that prenatal hypoxic-ischemic brain injury chronically impairs the developmental upregulation of KCC2 that is essential for cerebral circuit formation. Following late gestation hypoxia-ischemia (HI), diffusion tensor imaging in juvenile rats shows poor microstructural integrity in the hippocampal CA3 subfield, with reduced fractional anisotropy and elevated radial diffusivity. The loss of microstructure correlates with early reduced KCC2 expression on NeuN-positive pyramidal neurons, and decreased monomeric and oligomeric KCC2 protein expression in the CA3 subfield. Together with decreased inhibitory post-synaptic currents during a critical window of development, we document for the first time that prenatal transient systemic HI in rats impairs hippocampal CA3 inhibitory tone. Failure of timely development of inhibitory tone likely contributes to a lower seizure threshold and impaired cognitive function in children who suffer perinatal brain injury.