December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Superior Salivatory Nucleus (SSN) Regulates Choroidal Blood Flow in Rats
Author Affiliations & Notes
  • ME C Fitzgerald
    Anatomy & Neurobiology/Biology University of TN/Christian Brothers University Memphis TN
  • SV Jones
    Anatomy & Neurobiology University of TN Memphis TN
  • SL Cuthbertson
    Anatomy & Neurobiology University of TN Memphis TN
  • A Reiner
    Anatomy & Neurobiology University of TN Memphis TN
  • Footnotes
    Commercial Relationships   M.E.C. Fitzgerald, None; S.V. Jones, None; S.L. Cuthbertson, None; A. Reiner, None. Grant Identification: NIH-EY-05298
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2624. doi:
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      ME C Fitzgerald, SV Jones, SL Cuthbertson, A Reiner; Superior Salivatory Nucleus (SSN) Regulates Choroidal Blood Flow in Rats . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2624.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Parasympathetic control of choroidal blood flow (ChBF) in mammals is mediated via the pterygopalatine ganglion (PPG), which uses NO and VIP to increase ChBF. Our studies in rats using viral transneuronal retrograde labeling have shown that a set of neurons within the Superior Salivatory Nucleus (SSN) projects to the PPG and may thereby regulate ChBF (Cuthbertson et al., ARVO, 2001). The present study sought to confirm that these SSN neurons do mediate choroidal vasodilation. Methods: NADPHd histochemistry was used to characterize the nitrergic innervation of choroidal vessels. ChBF was measured using transcleral laser Doppler flowmetry at a site behind the ora serrata and a more posterior site, both on the superior aspect of the eye. The SSN was stimulated by a stereotaxically placed electrode, and NOS inhibition with i.v. L-NAME was used to assess the role of NO in SSN-mediated effects. Results: Vessels at both choroidal sites were extensively innervated by nitrergic fibers. Stimulation of the SSN resulted in 200% increases in ChBF over baseline levels at both sites. L-NAME administration significantly both decreased basal ChBF and attenuated the ChBF increases yielded by SSN stimulation. Systemic blood pressure (BP) was monitored throughout each experiment, and it was noted that ChBF remained relatively stable over a ±30 BP range, especially at the more anterior choroidal recording site. Conclusion: These results suggest that SSN activation yields increased ChBF and this effect may involve NO release from orbital perivascular or intrachoroidal PPG fibers. The compensation exhibited by the choroid during variations in systemic BP suggests that a mechanism exists to stabilize ChBF during BP fluctuations. Given the input of hypothalamic and solitary nucleus BP sensitive sites to the prechoroidal neurons of the SSN (Cuthbertson et al., ARVO, 2000), at least part of the choroidal compensation to BP may be SSN-PPG mediated.

Keywords: 345 choroid • 491 nitric oxide • 331 blood supply 

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