論文

査読有り
2011年6月

Dopamine Modulates the Voltage Response of Human Rod Photoreceptors by Inhibiting the h Current

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
  • Fusao Kawai
  • ,
  • Masayuki Horiguchi
  • ,
  • Ei-ichi Miyachi

52
7
開始ページ
4113
終了ページ
4117
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1167/iovs.10-6983
出版者・発行元
ASSOC RESEARCH VISION OPHTHALMOLOGY INC

PURPOSE. The h current (I(h)) is a hyperpolarization-activated current that plays important roles in the physiological functions of different types of cells. In the retina of lower vertebrates, I(h) contributes to the rod responses to light stimuli by bringing the membrane potential back to the dark level in the presence of continuous light. The purpose of this study was to determine how dopamine modulates I(h) in human rods and regulates voltage responses.
METHODS. A patch-clamp recording technique was used on surgically excised human retinas to investigate the effects of dopamine on the I(h) of isolated rods. Dopamine was applied in the superfusate.
RESULTS. Dopamine reversibly decreased the amplitude of the I(h) induced by hyperpolarizing voltage steps from a holding potential of -60 mV. At a voltage step of -100 mV, 20 mu M dopamine decreased the amplitude of I(h). The D2 dopamine agonist quinpirole inhibited I(h), but the D1 agonist SKF-38393 had no effect. Dopamine-induced reduction of I(h) amplitude was blocked by the D2 dopamine antagonist sulpiride. Under current-clamp conditions, an injection of hyperpolarizing current steps to rods produced voltage responses that exhibited a gradual decay. Adding dopamine to the superfusate inhibited the decay in the voltage responses. Quinpirole also inhibited the voltage decay, whereas SKF-38393 was ineffective.
CONCLUSIONS. Dopamine reduced I(h) through a D2 receptor and inhibited the gradual decay in the voltage response through a D2 receptor, indicating that dopamine slows the recovery phase of responses to light stimuli by inhibiting Ih in human rods. (Invest Ophthalmol Vis Sci. 2011;52:4113-4117) DOI: 10.1167/iovs.10-6983

リンク情報
DOI
https://doi.org/10.1167/iovs.10-6983
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21421871
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000293332500025&DestApp=WOS_CPL
ID情報
  • DOI : 10.1167/iovs.10-6983
  • ISSN : 0146-0404
  • PubMed ID : 21421871
  • Web of Science ID : WOS:000293332500025

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