Aleman T S, LaVail M M, Montemayor R, Ying G, Maguire M M, Laties A M, Jacobson S G, Cideciyan A V
Department of Ophthalmology, Scheie Eye Institute, University of Pennsylvania, 51 North 39th Street, Philadelphia, PA 19104, USA.
Vision Res. 2001 Sep;41(21):2779-97. doi: 10.1016/s0042-6989(01)00157-2.
Physiological consequences of early stages of photoreceptor degeneration were examined in heterozygous P23H rhodopsin transgenic (Tg) and in aging normal Sprague-Dawley rats. Rod photoreceptor and rod bipolar (RB) cell function were estimated with maximum value and sensitivity parameters of P3 and P2 components of the electroretinogram. In both Tg and aging normal rats, the age-related rate of decline of P3 amplitude was steeper than that of the P2 amplitude. Tg rats showed greater than normal sensitivity of the rods. A new model of distal RB pathway connectivity suggested photoreceptor loss could not be the sole cause of physiological abnormalities; there was an additional increase of post-receptoral sensitivity. We propose that changes at rod-RB synapses compensate for the partial loss of rod photoreceptors in senescence and in early stages of retinal degeneration.
在杂合P23H视紫红质转基因(Tg)大鼠和衰老的正常斯普拉格-道利大鼠中,研究了光感受器变性早期阶段的生理后果。通过视网膜电图P3和P2成分的最大值和敏感性参数来评估视杆光感受器和视杆双极(RB)细胞的功能。在Tg大鼠和衰老正常大鼠中,P3振幅随年龄下降的速率均比P2振幅更为陡峭。Tg大鼠的视杆表现出比正常大鼠更高的敏感性。一种新的远端RB通路连接模型表明,光感受器丧失并非生理异常的唯一原因;感受器后敏感性还有额外增加。我们提出,视杆-RB突触的变化可补偿衰老和视网膜变性早期阶段视杆光感受器的部分丧失。