THE SUPRACHIASMATIC NUCLEUS IS PART OF A NEURAL FEEDBACK CIRCUIT ADAPTING BLOOD PRESSURE RESPONSE

被引:43
作者
Buijs, F. N. [1 ]
Cazarez, F. [1 ]
Basualdo, M. C. [1 ]
Scheer, F. A. J. L. [3 ,4 ]
Perusquia, M. [1 ]
Centurion, D. [2 ]
Buijs, R. M. [1 ]
机构
[1] Univ Nacl Autonoma Mexico, Inst Invest Biomed, Mexico City, DF, Mexico
[2] CINVESTAV, Dept Farmacobiol, Mexico City 14000, DF, Mexico
[3] Brigham & Womens Hosp, Div Sleep Med, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Boston, MA USA
关键词
hypertension; circadian rhythm; nucleus tractus solitarius; cardiovascular; hypothalamus; SOLITARY TRACT NUCLEUS; CIRCADIAN-RHYTHMS; HEART-RATE; REGULATES EXPRESSION; PRIMARY HYPERTENSION; COMMISSURAL NTS; LESIONS; RAT; PROJECTIONS; LIGHT;
D O I
10.1016/j.neuroscience.2014.02.018
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The suprachiasmatic nucleus (SCN) is typically considered our autonomous clock synchronizing behavior with physiological parameters such as blood pressure (BP), just transmitting time independent of physiology. Yet several studies show that the SCN is involved in the etiology of hypertension. Here, we demonstrate that the SCN is incorporated in a neuronal feedback circuit arising from the nucleus tractus solitarius (NTS), modulating cardiovascular reactivity. Tracer injections into the SCN of male Wistar rats revealed retrogradely filled neurons in the caudal NTS, where BP information is integrated. These NTS projections to the SCN were shown to be glutamatergic and to terminate in the ventrolateral part of the SCN where light information also enters. BP elevations not only induced increased neuronal activity as measured by c-Fos in the NTS but also in the SCN. Lesioning the caudal NTS prevented this activation. The increase of SCN neuronal activity by hypertensive stimuli suggested involvement of the SCN in counteracting BP elevations. Examining this possibility we observed that elevation of BP, induced by alpha 1-agonist infusion, was more than twice the magnitude in SCN-lesioned animals as compared to in controls, indicating indeed an active involvement of the SCN in short-term BP regulation. We propose that the SCN receives BP information directly from the NTS enabling it to react to hemodynamic perturbations, suggesting the SCN to be part of a homeostatic circuit adapting BP response. We discuss how these findings could explain why lifestyle conditions violating signals of the biological clock may, in the long-term, result in cardiovascular disease. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:197 / 207
页数:11
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