4.5 Article

Localization of a GABA Transporter to Glial Cells in the Developing and Adult Olfactory Pathway of the Moth Manduca sexta

期刊

JOURNAL OF COMPARATIVE NEUROLOGY
卷 518, 期 6, 页码 815-838

出版社

WILEY
DOI: 10.1002/cne.22244

关键词

glia; GAT; invertebrate; insect; antennal

资金

  1. National Institutes of Health [R01DC008597]

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Glial cells have several critical roles in the developing and adult olfactory (antennal) lobe of the moth Manduca, sexta. Early in development, glial cells occupy discrete regions of the developing olfactory pathway and processes of gamma-aminobutyric acid (GABA)ergic neurons extend into some of these regions. Because GABA is known to have developmental effects in a variety of systems, we explored the possibility that the glial cells express a GABA transporter that could regulate GABA levels to which olfactory neurons and glial cells are exposed. By using an antibody raised against a characterized high-affinity M. sexta GABA transporter with high sequence homology to known mammalian GABA transporters (Mbungu et al. [1995] Arch. Biochem. Biophys. 318:489-497; Umesh and Gill [2002] J. Comp. Neurol. 448:388-398), we found that the GABA transporter is localized to subsets of centrally derived glial cells during metamorphic adult development. The transporter persists into adulthood in a subset of the neuropil-associated glial cells, but its distribution pattern as determined by light-and electron-microscopic-level immunocytochemistry indicates that it could not serve to regulate GABA concentration in the synaptic cleft. Instead, its role is more likely to regulate extracellular GABA levels within the glomerular neuropil. Expression in the sorting zone glial cells disappears after the period of olfactory receptor axon ingrowth, but may be important during ingrowth if GABA regulates axon growth. Glial cells take up GABA, and that uptake can be blocked by L-2,4-diaminobutyric acid (DABA). This is the first molecular evidence that the central glial cell population in this pathway is heterogeneous. J. Comp. Neurol. 518:815-838, 2010. (C) 2009 Wiley-Liss, Inc.

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