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M. Fitzgerald, M.S. LeDoux, S.L. Cuthbertson, A.J. Reiner; Evidence for Facial Nucleus Regulation of Compensatory Choroidal Vasodilation in Response to Systemic Hypotension in Rodents . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1794.
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The parasympathetic component of the facial nucleus, the superior salivatory nucleus (SSN), mediates increases in chorodial blood flow (ChBF) via the pterygopalatine ganglion (PPG). Nitric oxide acting on the choroid plays a major role in this vasodilatory response. Since the SSN has been implicated in cerebral baroregulation, we sought to determine if the SSN neural circuitry was involved in a similar phenomenon for ChBF.
In one group of rats, ChBF regulation was investigated using transcleral laser Doppler flowmetry. ChBF was recorded over a wide range of systemic blood pressures with and without systemic L–NAME (50mg/kg) administration. In a second group of animals, we sought to determine if known CNS regions that regulate blood pressure were in the SSN pathway. The CNS cell groups that projected to the SSN were determined via retrograde transneuronal transport of pseudorabies virus (PRV). PRV was injected into the choroid, with post–injection transport intervals of 52–72 hours. In a third group of animals, a 30 min period of systemic hypotension was used to stimulate the expression of c–fos within baro–responsive CNS neurons. The neurons that responded to hypotension were identified using c–fos immunohistochemistry.
ChBF exhibited strong regulation at blood pressures that were reduced up to 40% below basal blood pressure, with ChBF remaining at basal levels. This baroregulation of ChBF was blocked with systemic administration of L–NAME. PRV retrograde labeling was observed in the following cell groups: the nucleus of tractus solitarius (NTS), the parabrachial nucleus, locus coerulus, the SSN, the periaqueductal grey, and the paraventricular nucleus. Sustained hypotension resulted in c–fos immunoreactivity in the same CNS cell groups observed to be labeled with PRV. Of these cell groups, the NTS has been shown to receive input from the baroreceptive aortic sinuses.
These results suggest that the choroidal vasculature shows compensatory vasodilation in response to systemic hypotension. Our evidence is consistent with the notion that this phenomenon is mediated by nitric oxide released by PPG terminals in the choroid in response to activation of SSN by input from brain regions responding to hypotension. Furthermore, our data provide information on which CNS cell groups may project to the SSN and therefore might mediate this ChBF response.
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