Abstract
Preganglionic parasympathetic neurons of the ventromedial part of the superior salivatory nucleus (SSN) mediate vasodilation of orbital and choroidal blood vessels, via their projection to the nitrergic pterygopalatine ganglion (PPG) neurons that innervate these vessels. We recently showed that the baroresponsive part of the nucleus of the solitary tract (NTS) innervates choroidal control parasympathetic preganglionic neurons of SSN in rats. As this projection provides a means by which blood pressure (BP) signals may modulate choroidal blood flow (ChBF), we investigated if activation of baroresponsive NTS evokes ChBF increases in rat eye, using Laser Doppler Flowmetry (LDF) to measure ChBF transclerally. We found that electrical activation of ipsilateral baroresponsive NTS and its efferent fiber pathway to choroidal SSN increased mean ChBF by about 40–80% above baseline, depending on current level. The ChBF responses obtained with stimulation of baroresponsive NTS were driven by increases in both choroidal blood volume (ChBVol; i.e., vasodilation) and choroidal blood velocity (ChBVel; possibly due to orbital vessel dilation). Stimulation of baroresponsive NTS, by contrast, yielded no significant mean increases in systemic arterial blood pressure (ABP). We further found that the increases in ChBF with NTS stimulation were significantly reduced by administration of the neuronal nitric oxide (NO) synthase inhibitor Nω-propyl-l-arginine (NPA), thus implicating nitrergic PPG terminals in the NTS-elicited ChBF increases. Our results show that the NTS neurons projecting to choroidal SSN do mediate increase in ChBF, and thus suggest a role of baroresponsive NTS in the BP-dependent regulation of ChBF.
Highlights
The retina has two separate vascular supplies involved in its support: the retinal vessels within the retina itself, and the choroidal vessels external to Bruch’s membrane and the retinal pigment epithelium (Alm, 1992)
For the time blocks prior to stimulation, we calculated the mean for choroidal blood flow (ChBF), choroidal blood volume (ChBVol), choroidal blood velocity (ChBVel) and arterial blood pressure (ABP), which served as the baseline level for these parameters against which to evaluate stimulation effects
This study shows that ChBF increases significantly upon activation of the baroresponsive part of nucleus of the solitary tract (NTS) or its output fibers to prechoroidal superior salivatory nucleus (SSN), and the increase in ChBF elicited by NTS activation is attenuated by the neuronal NOS inhibitor NPA
Summary
The retina has two separate vascular supplies involved in its support: the retinal vessels within the retina itself, and the choroidal vessels external to Bruch’s membrane and the retinal pigment epithelium (Alm, 1992). The PPG input to choroid and the choroidal feeder vessels employ the vasodilators nitric oxide (NO) and vasoactive intestinal polypeptide (VIP), and as a result the ophthalmic and posterior ciliary arteries in mammals and the choroidal and ophthalmotemporal arteries in birds, as well as choroidal vessels, are densely coated with nerve fibers containing neuronal NO synthase (which synthesizes NO in neurons) and VIP (Stone et al, 1987; Cuthbertson et al, 1997; Reiner et al, 2012). In prior studies on the inputs to the SSN in rats, we found that a major input arose from the nucleus of the solitary tract (NTS) of the medulla (Li et al, 2010), and in more recent studies we have characterized the part of NTS from which this input arises (Li et al, 2015)
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