A reduction of heat loss to the environment through increased cutaneous vasoconstrictor (CVC) sympathetic outflow contributes to elevated body temperature during fever. We determined the role of neurons in the dorsomedial hypothalamus (DMH) in the increases in CVC tone evoked by prostaglandin E₂ (PGE₂) into the preoptic area (POA) in chloralose/urethane-anesthetized rats. The action potential frequency of CVC sympathetic ganglion cell axons recorded from the surface of the tail artery was increased by 1.8Hz following nanoinjections of bicuculline (50 pmol) into the DMH. PGE₂ nanoinjection into the POA elicited a similar excitation of tail CVC neurons (+2.1Hz). Subsequent to PGE₂ into the POA, muscimol (400 pmol/side) into the DMH did not alter the activity of tail CVC neurons. Inhibition of neurons in the raphe pallidus (rRPa) eliminated spontaneous discharges of tail CVC neurons, but only reduced the PGE₂-evoked activity. Residual activity was abolished by muscimol into the rostral ventrolateral medulla. Transections through the neuraxis caudal to the POA increased the activity of tail CVC neurons which was sustained through transections caudal to DMH. We conclude that while activation of neurons in the DMH can activate tail CVC neurons, it is not necessary for their PGE₂-evoked activity. These results support a CVC component of the increased core temperature elicited by PGE₂ in POA that arises from relief of a tonic inhibition, from neurons in POA, of CVC sympathetic premotor neurons in rRPa and is dependent on the excitation of CVC premotor neurons from a site caudal to DMH.