Abstract
Autonomic nerves, consisting of both sympathetic and parasympathetic nerves, regulatevarious bodily functions such as blood pressure, body temperature, glucose metabolism,energy metabolism, and digestion. Our studies in rats and mice have demonstrated thatfood, flavor, and music affect physiological phenomena via changes in autonomicneurotransmissions. Intestinal injection of Lactobacillus johnsonii La1(NCC533) suppressed sympathetic nerves that innervate the adrenal gland and kidney ofurethane-anesthetized rats, lowering blood glucose and blood pressure levels, and excitedthe gastric parasympathetic nerve, elevating appetite and body weight. In contrast,intestinal injection of Lactobacillus paracasei ST11 (NCC2461) excitedsympathetic nerves that innervate white and brown fat and the adrenal gland, increasinglipolysis and body temperature, and suppressed the gastric parasympathetic nerve, reducingappetite and body weight. Interestingly, we found that the hypothalamic suprachiasmaticnucleus (SCN), a master circadian clock, and histamine receptors in histaminergic neuronsplay important roles in peripheral autonomic control. To investigate the possible role ofSCN and histamine receptors in lactobacilli-mediated pathology, we created an SCN-lesionmodel and experimented with histaminergic blocker injections. SCN lesion or injection ofthioperamide, a histamine H3-receptor antagonist, eliminated the suppression of renalsympathetic nerve activity by NCC533, preventing blood pressure decline, and inhibited theenhancement of the gastric parasympathetic nerve induced by NCC533. In addition,diphenhydramine, a histamine H1-receptor antagonist, abolished the increases in renalsympathetic nerve activity and blood pressure caused by NCC2461. Infradiaphragmaticvagotomy eliminated the suppression of renal sympathetic nerve activity by NCC533, but didnot affect the excitation of the renal sympathetic nerve by NCC2461. Collectively, thesefindings strongly suggest that SCN and histamine neurons are involved in thelactobacilli-mediated pathology of autonomic nerves and relatedphysiological changes through abdominal afferent vagal pathway input to the centralnervous system.
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