New to MyHealth?
Manage Your Care From Anywhere.
Access your health information from any device with MyHealth. You can message your clinic, view lab results, schedule an appointment, and pay your bill.
ALREADY HAVE AN ACCESS CODE?
DON'T HAVE AN ACCESS CODE?
NEED MORE DETAILS?
MyHealth for Mobile
ALTERING CENTRAL-NERVOUS-SYSTEM PHYSIOLOGY WITH A DEFECTIVE HERPES-SIMPLEX VIRUS VECTOR EXPRESSING THE GLUCOSE TRANSPORTER GENE
ALTERING CENTRAL-NERVOUS-SYSTEM PHYSIOLOGY WITH A DEFECTIVE HERPES-SIMPLEX VIRUS VECTOR EXPRESSING THE GLUCOSE TRANSPORTER GENE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Ho, D. Y., Mocarski, E. S., Sapolsky, R. M. 1993; 90 (8): 3655-3659Abstract
Because of their postmitotic nature, neurons are difficult subjects for gene transfer. To circumvent this, we have used a defective herpes simplex virus vector to overexpress the rat brain glucose transporter (GT) gene under the control of the human cytomegalovirus ie1 promoter. This vector, designated vIE1GT, was propagated using a herpes simplex virus type 1 temperature-sensitive mutant, ts756. GT expressed from vIE1GT was readily immunoprecipitated from membrane fractions of vIE1GT-infected Vero cells. By using indirect double immunofluorescence techniques, vIE1GT was shown to be capable of enhancing GT expression in cultured hippocampal neurons and glia. Glucose transport in such vIE1GT-infected cultures was increased approximately 2-fold relative to controls. The efficacy of this system in vivo was then tested by microinjection of vIE1GT into adult rat hippocampus. When examined 2 days later, GT expression from vIE1GT was demonstrated in hippocampal neurons by in situ hybridization; a small but significant increase in glucose transport was detected in tissue immediately surrounding the injection site by 2-deoxy[14C]glucose uptake and autoradiography. Such injections did not cause marked cytopathology. Thus, this approach can be used to alter central nervous system physiology in vitro and in vivo.
View details for Web of Science ID A1993KX81600112
View details for PubMedID 8386379
View details for PubMedCentralID PMC46360