Cavallaro B, Burnside B
Department of Physiology-Anatomy, University of California, Berkeley 94720.
Invest Ophthalmol Vis Sci. 1988 Jun;29(6):882-91.
In teleosts, retinomotor movements of photoreceptors and retinal pigment epithelium are regulated both by light and by an endogenous circadian rhythm. Light induces cones to contract, rods to elongate and RPE cells to disperse their pigment granules into their long apical projections; darkness induces opposite movements. When fish are maintained in prolonged constant darkness, appropriate movements nonetheless occur at subjective dusk and dawn. To explore the mechanisms of this light and circadian regulation, we have been investigating effects of several extracellular messengers known to be present in retina on retinomotor movements in the green sunfish (Lepomis cyanellus). Here we report that prostaglandin E1 (PGE1) can induce movements characteristic of dark onset (or night) in both cones and RPE in isolated light-adapted retinas in the light; ie, PGE1 induces cone elongation and RPE pigment granule aggregation. The extent of PGE1-induced cone and RPE movements were dose-dependent with maximal movement occurring at 250-500 nM; higher concentrations were not as effective. Incubations with PGE2 and PGD2 also induced dark-adaptive cone and RPE retinomotor movements, but PGF2 alpha did not. Further observations suggest that prostaglandins may play a role in mediating the induction of cone and RPE movements by dark onset: dark-induced movements were inhibited by pretreating light-adapted isolated retinas before dark culture with agents which inhibit endogenous prostaglandin synthesis. Both indomethicin (50 microM) and acetylsalicylic acid (50 microM), two inhibitors of the cyclooxygenase component of specific prostaglandin synthase, inhibited dark-induced cone elongation and pigment aggregation in cultured sunfish retinas. Another cyclooxygenase inhibitor, ibuprofen (50 microM) had no effect. Together the effectiveness of PGE1 inducing dark-adaptive movement and the inhibition of dark adaptive movement by cyclooxygenase inhibitors suggest that prostaglandins may play a role in vivo in mediating the induction of dark-adapted RPE and cone retinomotor movements by dark onset.
在硬骨鱼中,光感受器和视网膜色素上皮的视网膜运动受光线和内源性昼夜节律的调节。光线诱导视锥细胞收缩、视杆细胞伸长,视网膜色素上皮(RPE)细胞将其色素颗粒分散到其长的顶端突起中;黑暗则诱导相反的运动。当鱼类处于长时间持续黑暗中时,在主观黄昏和黎明仍会出现适当的运动。为了探究这种光线和昼夜调节的机制,我们一直在研究几种已知存在于视网膜中的细胞外信使对绿太阳鱼(蓝鳃太阳鱼,Lepomis cyanellus)视网膜运动的影响。在此我们报告,前列腺素E1(PGE1)可在光照下诱导离体的光适应视网膜中的视锥细胞和RPE出现黑暗开始(或夜晚)时的特征性运动;即,PGE1诱导视锥细胞伸长和RPE色素颗粒聚集。PGE1诱导的视锥细胞和RPE运动程度呈剂量依赖性,在250 - 500 nM时出现最大运动;更高浓度则效果不佳。用PGE2和PGD2孵育也可诱导暗适应的视锥细胞和RPE视网膜运动,但PGF2α则不能。进一步观察表明,前列腺素可能在介导黑暗开始对视锥细胞和RPE运动的诱导中起作用:在用抑制内源性前列腺素合成的试剂对光适应的离体视网膜进行黑暗培养前预处理,可抑制黑暗诱导的运动。吲哚美辛(50 μM)和乙酰水杨酸(50 μM)这两种特异性前列腺素合酶环氧化酶成分的抑制剂,均可抑制培养的太阳鱼视网膜中黑暗诱导的视锥细胞伸长和色素聚集。另一种环氧化酶抑制剂布洛芬(50 μM)则无作用。PGE1诱导暗适应运动的有效性以及环氧化酶抑制剂对暗适应运动的抑制作用共同表明,前列腺素可能在体内介导黑暗开始对暗适应的RPE和视锥细胞视网膜运动的诱导中起作用。