These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Selective uptake of (3H)beta-alanine by glia: association with glial uptake system for GABA.
    Author: Schon F, Kelly JS.
    Journal: Brain Res; 1975 Mar 21; 86(2):243-57. PubMed ID: 234775.
    Abstract:
    On the basis of inhibitor studies it has been suggested that the high-affinity GABA uptake system in glial cells differs in its chemical specificity from that present in nerve terminals. In this paper it has been demonstrated that the GABA analogue, beta-alanine, is almost as good a substrate as GABA itself in the glial cell uptake system whilst not being transported at all into nerve terminals. Not only has [3H]beta-alanine been shown autoradiographically to be exclusively accumulated in glial sites in toeh sensory ganglia and slices of cerebral cortex, but in addition a virtually identical high-affinity uptake process for [3H] beta-alanine was demonstrated at both these sites. Furthermore, non-radioactive GABA was shown to be an equipotent inhibitor of [3H]beta-alanine uptake in sensory ganglia as well as in both small slices and synaptosomes prepared from cerebral cortical tissue, Finally, the competitive inhibition kinetics of GABA on [3H]beta-alanine uptake in cortical slices furnishes proof that intact glial sites of GABA uptake were present in such slices in addition to the more prominent and well documented uptake system in nerve terminals. The possible imporatnce of such glial fragments in brain slice and crude synaptosomal preparations is discussed.
    [Abstract] [Full Text] [Related] [New Search]