UCL  IRIS
Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
Modulation of non-vesicular glutamate release by pH.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Billups B, Attwell D
  • Publication date:
    11/01/1996
  • Pagination:
    171, 174
  • Journal:
    Nature
  • Volume:
    379
  • Issue:
    6561
  • Status:
    Published
  • Country:
    England
  • Print ISSN:
    0028-0836
  • Language:
    eng
  • Keywords:
    ATP-Binding Cassette Transporters, Amino Acid Transport System X-AG, Animals, Biological Transport, Glutamic Acid, Hydrogen-Ion Concentration, In Vitro Techniques, Neuroglia, Neurons, Patch-Clamp Techniques, Potassium, Purkinje Cells, Receptors, N-Methyl-D-Aspartate, Retina, Urodela
Abstract
Glutamate uptake into glial cells helps to keep the brain extracellular glutamate concentration, [glu]o, below levels that kill neurons. Uptake is powered by the transmembrane gradients of Na+, K+ and pH. When the extracellular [K+] rises in brain ischaemia, uptake reverses, releasing glutamate into the extracellular space. Here we show, by monitoring glutamate transport electrically and detecting released glutamate with ion channels in neurons placed outside glial cells, that a raised [H+] inhibits both forward and reversed glutamate uptake. No electroneutral reversed uptake was detected, contradicting the idea that forward and reversed uptake differ fundamentally. Suppression of reversed uptake by the low pH occurring in ischaemia will slow the Ca(2+)-independent release of glutamate with can raise [glu]o to a neurotoxic level, and will thus protect the brain during a transient loss of blood supply.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Author
Neuro, Physiology & Pharmacology
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by