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A. Reiner, M. E. C. Fitzgerald, C. Li, N. Del Mar; Effects on Rat Retina of Disrupted Parasympathetic Choroidal Blood Flow Regulation by Superior Salivatory Nucleus Lesions. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6323.
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The parasympathetic output of the superior salivatory nucleus (SSN) to the pterygopalatine ganglion (PPG) regulates choroidal blood flow (ChBF) via a vasodilatory projection of PPG to choroid. We have found that SSN is integrated into central cardiovascular circuitry, with SSN receiving inputs from such major cell groups involved in blood pressure (BP) - related vascular control as the paraventricular nucleus of the hypothalamus, the lateral parabrachial nucleus and the nucleus of the solitary tract. These various inputs may enable SSN output to choroidally projecting neurons of the PPG to mediate compensatory choroidal vasodilation to allow ChBF stability during low systemic BP. In the present study we sought to determine if impairment of this adaptive reflex was damaging to the retina.
Right SSN was stereotaxically lesioned in rats, and histological analysis of the retina carried out 8 weeks later. For comparison, we also examined the effects of bilateral removal of the superior cervical ganglion (SCG). In some rats, full field scotopic flash ERGs (10 cd.s/m2 white light) were measured for both eyes at 2, 4 and/or 8 weeks after the SSN lesion.
Two months after destruction of choroidal SSN, GFAP was upregulated in retinal Müller cells throughout the ipsilateral retina, and somewhat in contralateral retina. By contrast, in control cases with no lesions, and in lesion cases without choroidal SSN damage, GFAP immunolabeling of Müller cells was limited to their vitreal endfeet. For SCGectomy cases, Müller cell GFAP was elevated 2 weeks postsurgery. In three rats with complete unilateral destruction of choroidal SSN, the a-wave and b-wave in the right eye exceeded that in the left eye by about 30%. In one of these rats, we also measured ERGs at 2 and 4 weeks. At these earlier time points, we observed a 30% reduction in the ipsilateral a-wave and b-wave. In control eyes and in eyes from rats with lesions that missed SSN, there was no difference between the two eyes at any time point postlesion.
Our overall findings indicate that impairment of the adaptive neural control of ChBF by the facial parasympathetic and the sympathetic input to the choroid adversely affects retinal health. Thus, both the overperfusion of the retina prevented by SCG input and the underperfusion prevented by SSN-PPG input are harmful to the retina.
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