3-Iodothyronamine Induces Tail Vasodilation Through Central Action in Male Mice.
Endocrinology
; 158(6): 1977-1984, 2017 06 01.
Article
in En
| MEDLINE
| ID: mdl-28368510
ABSTRACT
3-Iodothyronamine (3-T1AM) is an endogenous thyroid hormone (TH)-derived metabolite that induces severe hypothermia in mice after systemic administration; however, the underlying mechanisms have remained enigmatic. We show here that the rapid 3-T1AM-induced loss in body temperature is a consequence of peripheral vasodilation and subsequent heat loss (e.g., over the tail surface). The condition is subsequently intensified by hypomotility and a lack of brown adipose tissue activation. Although the possible 3-T1AM targets trace amine-associated receptor 1 or α2a-adrenergic receptor were detected in tail artery and aorta respectively, myograph studies did not show any direct effect of 3-T1AM on vasodilation, suggesting that its actions are likely indirect. Intracerebroventricular application of 3-T1AM, however, replicated the phenotype of tail vasodilation and body temperature decline and led to neuronal activation in the hypothalamus, suggesting that the metabolite causes tail vasodilation through a hypothalamic signaling pathway. Consequently, the 3-T1AM response constitutes anapyrexia rather than hypothermia and closely resembles the heat-stress response mediated by hypothalamic temperature-sensitive neurons. Our results thus underline the well-known role of the hypothalamus as the body's thermostat and suggest an additional molecular link between TH signaling and the central control of body temperature.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Tail
/
Thyronines
/
Vasodilation
/
Brain
Limits:
Animals
Language:
En
Journal:
Endocrinology
Year:
2017
Document type:
Article
Affiliation country: