Hypothalamic neurons are regarded as essential for integrating thermal afferent information from skin and core and issuing commands to autonomic and behavioral effectors that maintain core temperature (Tc) during cold exposure and for control of energy expenditure. Caudal brainstem neurons are necessary elements of the hypothalamic effector pathway and also are directly driven by skin and brain cooling. To assess whether caudal brainstem processing of thermal afferent signals is sufficient to drive endemic effectors for thermogenesis - heart rate (HR), Tc and activity responses of chronic decerebrate (CD) and control rats adapted to 23 °C were compared during cold exposure (4, 8, 12 °C) for 6 h. Other CDs and controls were exposed to 4 or 23 °C for 2 h and tissues were processed for norepinephrine turnover (NETO), a neurochemical measure of sympathetic drive. Controls maintained Tc for all temperatures. CDs maintained Tc for 8 and 12 °C exposures, but Tc declined 2 °C during 4 °C exposure. Cold exposure elevated HR in CDs and controls alike. Tachycardia magnitude correlated with decreases in environmental temperature for controls, but not CDs. Cold increased NETO in brown adipose tissue, heart, and some white adipose tissue pads in CDs and controls compared with their respective room temperature controls. These data demonstrate that in neural isolation from the hypothalamus, cold exposure drives caudal brainstem neuronal activity and engages local effectors that trigger sympathetic energetic and cardiac responses that are comparable in many, but not in all, respects to those seen in neurologically-intact rats