Thyroid hormone is well known for its profound direct effects on cardiovascular 
function and metabolism. Recent evidence, however, suggests that the hormone 
also regulates these systems indirectly through the central nervous system. 
While some of the molecular mechanisms underlying the hormone's central control 
of metabolism have been identified, its actions in the central cardiovascular 
control have remained enigmatic. Here, we describe a previously unknown 
population of parvalbuminergic neurons in the anterior hypothalamus that 
requires thyroid hormone receptor signaling for proper development. Specific 
stereotaxic ablation of these cells in the mouse resulted in hypertension and 
temperature-dependent tachycardia, indicating a role in the central autonomic 
control of blood pressure and heart rate. Moreover, the neurons exhibited 
intrinsic temperature sensitivity in patch-clamping experiments, providing a new 
connection between cardiovascular function and core temperature. Thus, the data 
identify what we believe to be a novel hypothalamic cell population potentially 
important for understanding hypertension and indicate developmental 
hypothyroidism as an epigenetic risk factor for cardiovascular disorders. 
Furthermore, the findings may be beneficial for treatment of the recently 
identified patients that have a mutation in thyroid hormone receptor α1.