Abstract
Purpose :
The parasympathetic component of the facial nucleus, the superior salivatory nucleus (SSN) mediates choroidal blood flow (ChBF) increases via the pterygopalatine ganglion (PPG) in rats. We have reported that baroreceptive portions of the nucleus of tractus solitarius (NTS) mediate nitric-oxide vasodilation of the choroid in rats. We have identified pontine raphe serotonergic (5HT) cell group (PPR, B3) that also projects to SSN. PPR includes several regions of the hind brain: raphe magnus, raphe pallidus, parapyramidal region, lateral paragigantocellular and gigantocellular reticular alpha. These neurons play a role in the sympathetic control of blood pressure by innervating the pre-ganglionic neurons in the spinal cord. Therefore, we sought to determine their influence on choroidal blood flow, since during times of low blood pressure, the ChBF remains at a constant baseline flow rate, which provides a consistant diffusion gradiant for the outer retina.
Methods :
Physiological studies of the ChBF vasodilatory response to PPR electrical stimulation were conducted using laser Doppler flowmetry with and without IV administration of a 5HT antagonist, ritanserin. In addition, the nitrergic system was investigated using LNAME or NPA as pharmacological blockers. Single and double label immunocytochemical data using combinations of antibodies to: 5HT, nitric oxide synthase, or 5HT2A (5HT receptor) were used to characterize the SSN and PPR relationship.
Results :
Up to 70% of the PPR-mediated vasodilation was initially blocked with 0.1mg ritanserin administered IV. In some animals the PPR response began to recover after 30 minutes. While the PPR-mediated vasodilation was only initially blocked 30% with LNAME or NPA. Systemic blood pressure was not affected with PPR stimulation. Confirmation of electrode location was made in PPR and serotoninergic terminals were identified on SSN neurons.
Conclusions :
Choroidal blood flow increases from PPR electrical stimulation indicates these neurons are result in vasodilation of choroidal vessels. Both serotonin and nitric oxide are involved in this pathway, based on administration of antagonists and choroidal vasculature response to PPR stimulation. These data taken together suggest that the serotonergic PPR neurons are part of the central parasympathetic circuit regulating choroidal vasodilation via SSN.
This is a 2020 ARVO Annual Meeting abstract.