Doly M, Oustrin J
Laboratoire de Biophysique, Facultés de Médecine et de Pharmacie, Clermont-Ferrand.
Ann Pharm Fr. 1996;54(2):64-7.
The Platelet Activating Factor (PAF) have been shown to alter the transretinal potential recorded from light stimulated isolated retina. In the present study, we investigated the effect of cholera and pertussis toxins on PAF-induced electroretinogram (ERG) impairment. Administrated alone, 2.10(-7) M PAF induced a very marked and rapid drop in the b-wave amplitude of the ERG. When 75 micrograms/l of cholera toxin was coadministrated with PAF (2.10(-7) M) into the perfusion solution, the fall of the b-wave was not observed, suggesting that PAF effect on retinal function was mediated through GTP-binding protein (G-protein). Similarly, low-dose of pertussis toxin (5 micrograms/l) 1) were sufficient to antagonize PAF (2.10(-7) M) consequence on the ERG. Our results suggest that the irreversible and deleterious effect of PAF on ERG is mediated by a G-protein mechanism, located in the neural retina.
血小板活化因子（PAF）已被证明会改变从光刺激的离体视网膜记录到的经视网膜电位。在本研究中，我们研究了霍乱毒素和百日咳毒素对PAF诱导的视网膜电图（ERG）损伤的影响。单独给予2.10（-7）M PAF会导致ERG的b波振幅非常明显且迅速下降。当将75微克/升的霍乱毒素与PAF（2.10（-7）M）共同加入灌注溶液中时，未观察到b波下降，这表明PAF对视网膜功能的影响是通过鸟苷三磷酸结合蛋白（G蛋白）介导的。同样，低剂量的百日咳毒素（5微克/升）足以拮抗PAF（2.10（-7）M）对ERG的影响。我们的结果表明，PAF对ERG的不可逆和有害作用是由位于神经视网膜中的G蛋白机制介导的。
