Department of Anatomy and Neurobiology, USA.
Department of Anatomy and Neurobiology, USA; Department of Ophthalmology, University of Tennessee, 855 Monroe Ave, Memphis, TN, 38163, USA; Department of Biology, Christian Brothers University, Memphis, TN, 38104, USA.
Exp Eye Res. 2021 May;206:108541. doi: 10.1016/j.exer.2021.108541. Epub 2021 Mar 16.
The vasodilatory pterygopalatine ganglion (PPG) innervation of the choroid is under the control of preganglionic input from the superior salivatory nucleus (SSN), the parasympathetic portion of the facial motor nucleus. We sought to confirm that choroidal SSN drives a choroid-wide vasodilation and determine if such control is important for retinal health. To the former end, we found, using transscleral laser Doppler flowmetry, that electrical activation of choroidal SSN significantly increased choroidal blood flow (ChBF), at a variety of choroidal sites that included more posterior as well as more anterior ones. We further found that the increases in ChBF were significantly reduced by inhibition of neuronal nitric oxide synthase (nNOS), thus implicating nitrergic PPG terminals in the SSN-elicited ChBF increases. To evaluate the role of parasympathetic control of ChBF in maintaining retinal health, some rats received unilateral lesions of SSN, and were evaluated functionally and histologically. In eyes ipsilateral to choroidal SSN destruction, we found that the flash-evoked scotopic electroretinogram a-wave and b-wave peak amplitudes were both significantly reduced by 10 weeks post lesion. Choroidal baroregulation was evaluated in some of these rats, and found to be impaired in the low systemic arterial blood pressure (ABP) range where vasodilation normally serves to maintain stable ChBF. In retina ipsilateral to SSN destruction, the abundance of Müller cell processes immunolabeled for glial fibrillary acidic protein (GFAP) and GFAP message were significantly upregulated. Our studies indicate that the SSN-PPG circuit mediates parasympathetic vasodilation of choroid, which appears to contribute to ChBF baroregulation during low ABP. Our results further indicate that impairment in this adaptive mechanism results in retinal dysfunction and pathology within months of the ChBF disturbance, indicating its importance for retinal health.
翼腭神经节(PPG)对脉络膜的血管扩张作用受到来自面神经核副交感部分的节前输入的控制,即上涎核(SSN)。我们试图证实 SSN 对脉络膜的驱动作用是脉络膜广泛血管扩张,并确定这种控制对视网膜健康是否重要。为此,我们发现,使用巩膜激光多普勒血流仪,电刺激 SSN 可显著增加脉络膜血流(ChBF),刺激部位包括更靠后的脉络膜部位以及更靠前的部位。我们进一步发现,神经元型一氧化氮合酶(nNOS)的抑制显著减少了 ChBF 的增加,这表明 SSN 诱导的 ChBF 增加涉及到 nitrergic PPG 末梢。为了评估副交感神经对 ChBF 的控制在维持视网膜健康中的作用,一些大鼠接受了单侧 SSN 损伤,并进行了功能和组织学评估。在 SSN 破坏的脉络膜同侧眼,我们发现闪光诱发的暗视视网膜电图 a 波和 b 波峰值振幅在损伤后 10 周均显著降低。在这些大鼠中评估了脉络膜的血压调节,发现其在低全身动脉血压(ABP)范围内受损,在正常情况下,血管扩张可维持稳定的 ChBF。在 SSN 破坏的同侧视网膜中,免疫标记胶质纤维酸性蛋白(GFAP)和 GFAP 信使的 Müller 细胞突起的丰度显著上调。我们的研究表明,SSN-PPG 回路介导脉络膜的副交感神经血管扩张,这似乎有助于在低 ABP 期间进行 ChBF 血压调节。我们的结果进一步表明,这种适应性机制的损害会导致视网膜功能障碍和病理学改变,这表明其对视网膜健康的重要性。