December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Modulation by Arachidonic Acid of Neuronal Electrical Coupling between Retinal Neurons
Author Affiliations & Notes
  • D-Q Zhang
    Dept of Physiology University of Kentucky Lexington KY
  • DG McMahon
    Lexington KY
  • Footnotes
    Commercial Relationships   D. Zhang, None; D.G. McMahon , None. Grant Identification: Supported by NEI grant EY09256
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4754. doi:
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      D-Q Zhang, DG McMahon; Modulation by Arachidonic Acid of Neuronal Electrical Coupling between Retinal Neurons . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4754.

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

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Abstract: : Purpose:Arachidonic acid, a cis-polyunsaturated fatty acid released from cell membrane-bound phospholipids, plays an important role in modulation of ion channel activity in CNS as well as in retina. Here we examined arachidonic acid (AA) gating of electrical coupling between retinal neurons. Methods:Experiments were performed on cultured bass dendrite-dendrite contacting horizontal cell pairs using the dual whole-cell patch clamp configuration. Results:External application of 3 µM AA produced a significant reduction of horizontal cell macroscopic gap junction conductance with two time-dependent peak amplitudes. After cell pairs were exposed to AA for 30 seconds, the amplitude of junctional currents decreased to 86 ± 7 % of its control value (n=5, mean ± SD) and this action persisted for 1.3 ± 0.3 min. Then a pronounced almost complete suppression of junction currents was obtained with a rising time of 0.95 ± 0.3 min. Upon washout with normal extracellular solution, the AA's uncoupling slowly recovered to 41 ±12% of its control value within 15 minutes. However, 0.5% bovine serum albumin, an AA scavenger, promoted complete recovery from the AA uncoupling effect in 0.8 ± 0.3 min (n=4). In addition, 5,8,11,14-eicosatetranoic acid (ETYA, 3 µM), an AA nonmetabolizable analog, only decreased the amplitude of junctional currents to 84 ± 5% without a further inhibition during prolonged ETYA application (n=6). Conclusion:The rapid and slight effect by AA is mediated by a direct action on gap junctional channels, whereas the slow and strong effect may be mediated by AA metabolic substrates. AA as a light-released substrate may play an important role in retinal neuronal networks.

Keywords: 426 horizontal cells • 416 gap junctions/coupling • 394 electrophysiology: non-clinical 

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