liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Vesicular uptake and exocytosis of L-aspartate is independent of sialin.
Department of Anatomy and Center for Molecular Biology and Neuroscience, University of Oslo, Oslo, Norway.
Department of Anatomy and Center for Molecular Biology and Neuroscience, University of Oslo, Oslo, Norway.
Center for Molecular Biology and Neuroscience, University of Oslo, Oslo, Norway; Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID iD: 0000-0003-3584-7829
Department of Neurology and Neurological Sciences and Graduate Program in Neuroscience, Stanford University School of Medicine, Stanford, California, USA.
Show others and affiliations
2013 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 27, no 3, 1264-1274 p.Article in journal (Refereed) Published
Abstract [en]

The mechanism of release and the role of l-aspartate as a central neurotransmitter are controversial. A vesicular release mechanism for l-aspartate has been difficult to prove, as no vesicular l-aspartate transporter was identified until it was found that sialin could transport l-aspartate and l-glutamate when reconstituted into liposomes. We sought to clarify the release mechanism of l-aspartate and the role of sialin in this process by combining l-aspartate uptake studies in isolated synaptic vesicles with immunocyotchemical investigations of hippocampal slices. We found that radiolabeled l-aspartate was taken up into synaptic vesicles. The vesicular l-aspartate uptake, relative to the l-glutamate uptake, was twice as high in the hippocampus as in the whole brain, the striatum, and the entorhinal and frontal cortices and was not inhibited by l-glutamate. We further show that sialin is not essential for exocytosis of l-aspartate, as there was no difference in ATP-dependent l-aspartate uptake in synaptic vesicles from sialin-knockout and wild-type mice. In addition, expression of sialin in PC12 cells did not result in significant vesicle uptake of l-aspartate, and depolarization-induced depletion of l-aspartate from hippocampal nerve terminals was similar in hippocampal slices from sialin-knockout and wild-type mice. Further, there was no evidence for nonvesicular release of l-aspartate via volume-regulated anion channels or plasma membrane excitatory amino acid transporters. This suggests that l-aspartate is exocytotically released from nerve terminals after vesicular accumulation by a transporter other than sialin.

Place, publisher, year, edition, pages
Federation of American Societies for Experimental Biology , 2013. Vol. 27, no 3, 1264-1274 p.
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-133048DOI: 10.1096/fj.12-206300ISI: 000315585200038PubMedID: 23221336Scopus ID: 2-s2.0-84874607595OAI: oai:DiVA.org:liu-133048DiVA: diva2:1054580
Available from: 2016-12-08 Created: 2016-12-08 Last updated: 2016-12-13Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMedScopus

Search in DiVA

By author/editor
Larsson, Max
In the same journal
The FASEB Journal
Neurosciences

Search outside of DiVA

GoogleGoogle Scholar

Altmetric score

Total: 8 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf