In the previous funding periods, a circuit controlling choroidal blood flow in pigeons via the Edinger-Westphal nucleus (EWN) and ciliary ganglion (CG) was described. Light-mediated regulation of choroidal blood flow, a role for nitric oxide (NO) released by CG fibers, and the importance of parasympathetic neural control of choroidal blood flow were shown. These mechanisms will be further examined in pigeons, while additional studies will be performed in rabbits to test whether these observations are extendible into a mammalian eye. A major hypothesis to be tested is that NO is responsible for choroidal vasodilatation during high frequency activation (through the postganglionic parasympathetic terminals of the choroid) and that basal activation is under control of cholinergic endothelial-dependent NO. In rabbits and pigeons, immunolabeling will be used to identify the inputs to the facial nucleus preganglionic parasympathetic neurons controlling choroidal blood flow via the pterygopalatine ganglion (PPG) and laser doppler will be used in conjunction with inhibitors of nitric oxide synthase (NOS) to evaluate the roles of different isoforms of NOS in choroidal vasodilatation mediated by the PPG. The role of the EWN-CG circuit in control of choroidal blood flow will be investigated in rabbits. The role of vasointestinal peptide (VIP) in PPG-mediated choroidal blood flow dilatation via NO will be explored. Finally, the role of muscarinic receptors and endothelial NO in choroidal vasodilatation via CG will be examined. It will be determined if disruption of neural control of choroidal blood flow by EWN lesions results in retinopathy when combined with transient ischemia of the eye. These studies will provide additional knowledge of the neural control of choroidal blood flow. Abnormalities of this controlling system may be associated with retinal damage in diseases such as diabetes, hypertension, myopia, and senile macular disease.
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