Abstract Seifert, Gerald, Min Zhou, and Christian Steinhäuser. Analysis of AMPA receptor properties during postnatal development of mouse hippocampal astrocytes. J. Neurophysiol . 78: 2916–2923, 1997. Glial cells in the mammalian brain express various types of voltage- and ligand-gated ion channels, including glutamate receptors (GluRs) of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-subtype. In the present study we followed developmental changes in the functional properties of AMPA receptor (AMPA-R) channels expressed by astrocytes of the mouse hippocampus between postnatal days (P) 5–35 to learn more about the physiological significance of these glial receptors. A fast concentration clamp technique was applied to cells acutely isolated from the CA1 stratum radiatum subregion to quantitatively analyze rapidly activating and desensitizing receptor responses. The equilibrium responses of glutamate and kainate differed between P5 and P12. Although the maximum current induced by kainate was almost the same at all developmental stages, a steep rise in the maximum glutamate response was observed within the same time range. Between P5 and P12 there was an increase in the potentiation of AMPA-R currents with cyclothiazide (CTZ); at the same time, the dissociation kinetics of CTZ became significantly slower. These changes in the pharmacological properties suggested a variation in splice variant expression. With proceeding maturation, we observed an increase in the degree of desensitization of the glutamate- and AMPA-induced receptor currents. In addition to the shift in flip/flop splicing, these findings could hint at a developmental regulation of RNA editing in the arginine/glycine site. Altogether, the present results demonstrate changes in astrocytic AMPA-R functioning early in postnatal development, although after P12 the receptor properties remained almost constant. Although the overall Ca 2+ permeability did not vary during development, the prolonged receptor opening in the early postnatal period causes an enhanced Na + /Ca 2+ influx into the immature astrocytes. This could influence glial proliferation and differentiation during CNS ontogenesis. Footnotes Address for reprint requests: C. Steinhäuser, Institute of Physiology, Dept. of Neurophysiology, University of Jena, Teichgraben 8, 07740 Jena, Germany. Copyright © 1997 the American Physiological Society
Journal of Neurophysiology – The American Physiological Society
Published: Dec 1, 1997
It’s your single place to instantly
discover and read the research
that matters to you.
Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.
All for just $49/month
Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly
Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.
Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.
Read from thousands of the leading scholarly journals from SpringerNature, Wiley-Blackwell, Oxford University Press and more.
All the latest content is available, no embargo periods.
“Hi guys, I cannot tell you how much I love this resource. Incredible. I really believe you've hit the nail on the head with this site in regards to solving the research-purchase issue.”Daniel C.
“Whoa! It’s like Spotify but for academic articles.”@Phil_Robichaud
“I must say, @deepdyve is a fabulous solution to the independent researcher's problem of #access to #information.”@deepthiw
“My last article couldn't be possible without the platform @deepdyve that makes journal papers cheaper.”@JoseServera