6 research outputs found
IH significantly decreases glutamate transporters, MAP2 and GFAP immunoreactivity.
<p>EAAT1, EAAT2, GFAP and MAP2 immunoreactivity in slices exposed to 7 days RA, SH or IH. EAAT1 and EAAT2 expression was unchanged by SH while significantly reduced in IH. MAP2 and GFAP expression decreased in both SH and IH.</p
Long term sustained or Intermittent hypoxia decreases cell viability.
<p>Propidium iodide (red) and Fluorescein diacetate (green) staining of slices exposed to 7 days RA, SH or IH (A) without and (B) with 100 µM ceftriaxone (n = 4-6).</p
Ceftriaxone effect on cell tolerance to glutamate is significantly greater in IH-exposed slices.
<p>Propidium iodide staining quantification of ceftriaxone (+) treated slices exposed to RA, SH and IH at baseline (BL), after 200 µM glutamate, and 10 mM glutamate, followed by a second 200 µM glutamate challenge. n = 12–18 for RA<sup>-</sup>, SH<sup>-</sup>, IH<sup>-</sup> and n = 9-12 for RA+, SH<sup>+</sup>, IH<sup>+</sup>; IH<sup>-</sup> > IH<sup>+</sup>: *At BL (p = .005), <sup>&</sup>At 10 mM (p<.001) & ∧At 200 µM#2 (p = .005).</p
Ceftriaxone prevents hypoxia-induced cell death and improves tolerance to excitotoxicity.
<p>Propidium iodide staining (A) and quantification of PI positive cells presented as mean <u>+</u> SD (B) of slices exposed to 100 µM ceftriaxone during 7 days RA, SH or IH at baseline (BL), after 200 µM glutamate, and 10 mM glutamate, followed by a second 200 µM glutamate challenge. baseline (BL) n = 9–12, <sup>#</sup> At 10 mM & 200 µM#2: RA<sup>+</sup>; IH<sup>+</sup>; SH<sup>+</sup>> their respective BL (p<.01).</p
Intermittent hypoxia decreases cell viability and impairs glutamate response.
<p>Propidium iodide staining (A) and quantification of PI positive cells presented as mean <u>+</u> SD (B) of slices exposed to 7 days RA, SH or IH at baseline (BL), after 200 µM glutamate, and 10 mM glutamate, followed by a second 200 µM glutamate challenge. n = 12–18. *: At all concentrations RA<sup>-</sup> < SH<sup>-</sup> & IH<sup>-</sup> (p<.001). <sup>+</sup> At 10mM: SH<sup>-</sup> < IH<sup>-</sup> (p<.05). <sup>#</sup> At 10 mM & 200 µM#2: BL < SH<sup>-</sup> & IH<sup>-</sup> (p<.05 and p<.001 respectively).</p
Graphic representation of glutamate transporters, MAP2 and GFAP immunoreactivity with or without ceftriaxone.
<p>Quantification of EAAT1, EAAT2, GFAP and MAP2 immunofluorescence per unit area of slices exposed to 7 days RA, SH or IH in presence (+ve) or in absence (-ve) of 100 µM ceftriaxone. Data are presented as mean immunofluorescence <u>+</u> SD. n =  4-13 for RA<sup>+</sup>, IH<sup>+</sup>, SH<sup>+</sup>; n = 5–11 for RA<sup>-</sup>, IH<sup>-</sup>, SH *: IH<sup>-</sup> or SH<sup>-</sup> - (p≤0.01). <sup>+</sup>: IH<sup>+</sup> < SH<sup>+</sup> (p≤0.01).</p