Lack of α2C-Adrenoceptor Results in Contrasting Phenotypes of Long Bones and Vertebra and Prevents the Thyrotoxicosis-Induced Osteopenia.

A series of studies have demonstrated that activation of the sympathetic nervous system (SNS) causes osteopenia via β2-adrenoceptor (β2-AR) signaling. However, in a recent study, we found an unexpected and generalized phenotype of high bone mass in female mice with chronic sympathetic hyperactivity, due to double gene inactivation of adrenoceptors that negatively regulate norepinephrine release, α2A-and α2C-AR (α2A/2C-AR-/-). These findings suggest that β2-AR is not the single adrenoceptor involved in bone turnover regulation and show that α2-AR signaling may also mediate the SNS actions in the skeleton.

Temporal and topographic ultrastructural alterations of rat heart myofibrils caused by thyroid hormone.

In order to further our understanding regarding the temporal and topographic ultrastructural aspects of the myocardium under thyrotoxicosis, thyroxine (T4; 25 and 100 microg/100 g bw) was administered to young rats 24 hours after birth until 15 days. The animals were then sacrificed, the hearts excised and weighed, and the ventricle tissue samples were then processed for confocal and transmission electron microscopy. At 48/72 hours and 1 week after initiation of T4 treatment with 100 microg/100 g bw, numerous lamellar bodies (probably formed by phospholipids) progressively accumulated in the heart.