December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Cholinergic Regulation of Retinal Pericyte Physiology
Author Affiliations & Notes
  • DM Wu
    Neuroscience Graduate Program and Department of Ophthalmology & Visual Sciences University of Michigan Ann Arbor MI
  • DG Puro
    Neuroscience Graduate Program and Department of Ophthalmology & Visual Sciences University of Michigan Ann Arbor MI
  • Footnotes
    Commercial Relationships   D.M. Wu, None; D.G. Puro, None. Grant Identification: American Diabetes Association; NIH EY12505, EY07003; Research to Prevent Blindness
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3701. doi:
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      DM Wu, DG Puro; Cholinergic Regulation of Retinal Pericyte Physiology . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3701.

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

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Abstract: : Purpose: Pericytes are contractile cells which ensheathe capillaries and may regulate the flow of blood at the microcirculatory level. One putative mechanism linking neuronal function with blood flow involves neurotransmitters, such as acetylcholine, serving as vasoactive signals. Based on the premise that ion channels play a vital role in mediating the responses of the microvasculature, we monitored the ionic currents of retinal pericytes during exposure to cholinergic compounds. Methods: Retinas were rapidly removed from euthanised rats, incubated in a papain-containing solution, and then gently pressed between two glass coverslips. By this procedure, retinal microvessels adhered to the glass. The perforated-patch configuration of the patch-clamp technique was used to monitor whole-cell currents in pericytes located on the freshly isolated microvessels. Results: We found that exposure of isolated microvessels to carbachol, a nonspecific cholinergic agonist, reversibly activated the transient depolarizing chloride currents of retinal pericytes. In contrast to this effect on the calcium-activated chloride (ClCa) channels, carbachol did not affect a pericyte's basal steady state currents, which are due to the activity of nonspecific cation and voltage-dependent K+ channels. Consistent with involvement of muscarinic receptors, oxotremorime-M activated ClCa currents of pericytes by a mechanism that was sensitive to atropine. A possible role of the M1 subtype of receptor was suggested by our observation that pirenzepine inhibited the effect of oxotremorime-M. In other experiments, we found that cyclopiazonic acid, which depletes calcium stores in many cell types, markedly attenuated the oxotremorime-induced activation of ClCa channels. Conclusion: Our experiments support the hypothesis that activation of muscarinic receptors in retinal microvessels causes release of calcium stores and, thereby, opens ClCa channels, which cause transient depolarizations of the pericyte membrane potential. This may be one mechanism by which acetylcholine serves as a neuron-to-pericyte signal in the retinal microvasculature.

Keywords: 445 ion channels • 614 vascular cells • 305 acetylcholine 

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