Disinhibition of neurons of the nucleus of solitary tract that project to the superior salivatory nucleus causes choroidal vasodilation: Implications for mechanisms underlying choroidal baroregulation

NEUROSCIENCE LETTERS

卷:633

Article

Li, Chunyan¹  Fitzgerald, Malinda E. C.^1,2,3  Del Mar, Nobel¹  Reiner, Anton^1,2 

[1] Univ Tennessee, Dept Anat & Neurobiol, Memphis, TN 38163 USA

[2] Univ Tennessee, Dept Ophthalmol, Memphis, TN 38163 USA

[3] Christian Bros Univ, Dept Biol, Memphis, TN USA

关键词: Choroidal blood flow;    Superior salivatory nucleus;    Nucleus of solitary tract;    Autonomic;    Parasympathetic;    Disinhibition;    GABA;   

DOI  :  10.1016/j.neulet.2016.09.029

来源: Elsevier

【 摘 要 】

Preganglionic neurons in the superior salivatory nucleus (SSN) that mediate parasympathetic vasodilation of choroidal blood vessels receive a major excitatory input from the baroresponsive part of the nucleus of the solitary tract (NTS). This input appears likely to mediate choroidal vasodilation during systemic hypotension, which prevents decreases in choroidal blood flow (ChBF) due to reduced perfusion pressure. It is uncertain, however, how low blood pressure signals to NTS from the aortic depressor nerve (ADN), which fires at a low rate during systemic hypotension, could yield increased firing in the NTS output to SSN. The simplest hypothesis is that SSN-projecting NTS neurons are under the inhibitory control of ADN-receptive GABAergic NTS neurons. As part of evaluating this hypothesis, we assessed if SSN-projecting NTS neurons, in fact, receive prominent inhibitory input and if blocking GABAergic modulation of them increases ChBF. We found that SSN-projecting NTS neuronal perikarya identified by retrograde labeling are densely coated with GABAergic terminals, but lightly coated with excitatory terminals. We also found that, infusion of the GABA-A receptor antagonist GABAzine into NTS increased ChBF. Our results are consistent with the possibility that low blood pressure signals from the ADN produce vasodilation in choroid by causing diminished activity in ADN-receptive NTS neurons that tonically suppress SSN-projecting NTS neurons. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

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