April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Hydrostatic Pressure Causes Ryanodine Receptor-Mediated Calcium Release in Cultured Rat Optic Nerve Astrocytes
Author Affiliations & Notes
  • A. Mandal
    University of Arizona, Tucson, Arizona
  • M. Shahidullah
    University of Arizona, Tucson, Arizona
  • N. A. Delamere
    Physiology and Ophthalmology,
    University of Arizona, Tucson, Arizona
  • Footnotes
    Commercial Relationships  A. Mandal, None; M. Shahidullah, None; N.A. Delamere, None.
  • Footnotes
    Support  NIH Grant EY014069
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1472. doi:
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      A. Mandal, M. Shahidullah, N. A. Delamere; Hydrostatic Pressure Causes Ryanodine Receptor-Mediated Calcium Release in Cultured Rat Optic Nerve Astrocytes. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1472.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Elevated intraocular pressure (IOP) is linked to glaucomatous optic nerve damage. Other investigators have shown protein expression changes in cultured optic nerve head (ONH) astrocytes exposed for 24h or more to elevated hydrostatic pressure (HP). Here we examined the immediate response of astrocytes to a 15 mmHg hydrostatic pressure challenge.

Methods: : Rat optic nerve astrocytes were grown on glass cover slips and loaded with Fura-2. The cover slip was mounted in a closed imaging chamber and cytoplasmic calcium concentration was measured ratiometrically while HP of 15 mmHg was applied.

Results: : HP caused a slow rise in cytoplasmic calcium concentration that started soon after the pressure increase. The response was similar in calcium-containing bathing solution or nominally calcium-free solution. The nonselective calcium channel antagonist nickel chloride (4 mM) failed to block the HP-induced cytoplasmic calcium rise. The purinergic receptor antagonist, suramin (50 µM) also failed to block the HP-induced cytoplasmic calcium rise. In contrast ruthenium red (10 µM) and dantrolene (25 µM), ryanodine receptor (RyR) antagonists, inhibited the pressure-induced calcium rise. Consistent with RyR-mediated calcium release, when ryanodine-sensitive calcium stores were first depleted by exposure to caffeine (3 mM), the magnitude of the HP-induced cytoplasmic calcium rise was significantly reduced. HP was observed to cause ERK1/2 phosphorylation. The magnitude of the ERK1/2 response was reduced by ruthenium red.

Conclusions: : Increasing HP by 15 mmHg causes a detectable rise in cytoplasmic calcium caused by release from a ryanodine-sensitive cytoplasmic store. The rise in cytoplasmic calcium appears to be associated with ERK1/2 activation. Further studies are needed to determine if these events lead to the long term changes of protein expression known to occur in pressure-stressed astrocytes.

Keywords: astrocytes: optic nerve head • signal transduction • calcium 

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