Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure

K. Knecht, A. Michalak, C. Rose, Jeffrey D Rothstein, R. F. Butterworth

Research output: Contribution to journalArticle

Abstract

It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-I was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT- 1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.

Original languageEnglish (US)
Pages (from-to)201-203
Number of pages3
JournalNeuroscience Letters
Volume229
Issue number3
DOIs
StatePublished - Jul 4 1997

Fingerprint

Amino Acid Transport System X-AG
Acute Liver Failure
Frontal Lobe
Glutamic Acid
Hepatic Encephalopathy
Surgical Portacaval Shunt
Hepatic Artery
Brain Edema
Liver Failure
Brain
Coma
Reverse Transcriptase Polymerase Chain Reaction
Astrocytes
Ligation
Western Blotting
Neurons
Antibodies
Proteins

Keywords

  • Astrocytes
  • Gene expression
  • GLT-1
  • Hepatic encephalopathy
  • Neuron-astrocyte trafficking
  • RT-PCR
  • Western blotting

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure. / Knecht, K.; Michalak, A.; Rose, C.; Rothstein, Jeffrey D; Butterworth, R. F.

In: Neuroscience Letters, Vol. 229, No. 3, 04.07.1997, p. 201-203.

Research output: Contribution to journalArticle

Knecht, K. ; Michalak, A. ; Rose, C. ; Rothstein, Jeffrey D ; Butterworth, R. F. / Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure. In: Neuroscience Letters. 1997 ; Vol. 229, No. 3. pp. 201-203.
@article{b65397d293c0474f99f52dbf9f037d68,
title = "Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure",
abstract = "It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-I was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT- 1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.",
keywords = "Astrocytes, Gene expression, GLT-1, Hepatic encephalopathy, Neuron-astrocyte trafficking, RT-PCR, Western blotting",
author = "K. Knecht and A. Michalak and C. Rose and Rothstein, {Jeffrey D} and Butterworth, {R. F.}",
year = "1997",
month = "7",
day = "4",
doi = "10.1016/S0304-3940(97)00444-8",
language = "English (US)",
volume = "229",
pages = "201--203",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

TY - JOUR

T1 - Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure

AU - Knecht, K.

AU - Michalak, A.

AU - Rose, C.

AU - Rothstein, Jeffrey D

AU - Butterworth, R. F.

PY - 1997/7/4

Y1 - 1997/7/4

N2 - It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-I was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT- 1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.

AB - It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-I was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT- 1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.

KW - Astrocytes

KW - Gene expression

KW - GLT-1

KW - Hepatic encephalopathy

KW - Neuron-astrocyte trafficking

KW - RT-PCR

KW - Western blotting

UR - http://www.scopus.com/inward/record.url?scp=0030789808&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030789808&partnerID=8YFLogxK

U2 - 10.1016/S0304-3940(97)00444-8

DO - 10.1016/S0304-3940(97)00444-8

M3 - Article

C2 - 9237493

AN - SCOPUS:0030789808

VL - 229

SP - 201

EP - 203

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -