Glucose is a major fuel for body energy metabolism and an essential metabolic fuel for the brain. Consequently, glucose deficit (glucoprivation) elicits a variety of physiological and behavioral responses crucial for survival. Previous work indicates an important role for brain catecholamine neurons in mediation of responses to glucoprivation. This experiment was conducted to identify the specific catecholamine neurons that are activated by glucoprivation. Activation of hindbrain catecholamine neurons by the antimetabolic glucose analogue, 2-deoxy-d-glucose (2DG; 50, 100, 200 or 400 mg/kg, s.c.) was evaluated using double label immunohistochemistry. Fos protein was used as the marker for neuronal activation and the enzymes tyrosine hydroxylase (TH) and phenethanolamine-N-methyl transferase (PNMT) were used as the markers for norepinephrine (NE) and epinephrine (E) neurons. 2-Deoxy-d-glucose (200 and 400 mg/kg) produced selective activation of distinct hindbrain catecholamine cell groups. In the ventrolateral medulla, doubly labeled neurons were concentrated in the area of A1/C1 and were predominantly adrenergic in phenotype. In the dorsal medulla, doubly labeled neurons were limited to C2 and C3 cell groups. In the pons, some A6 neurons were Fos-positive. Neurons in rostral C1, ventral C3, A2, A5 and A7 did not express Fos-ir in response to 2DG. Our results identify specific subpopulations of catecholamine neurons that are selectively activated by 2DG. Previously demonstrated connections of these subpopulations are consistent with their participation in the feeding and hyperglycemic response to glucoprivation. Finally, the predominant and seemingly preferential activation of epinephrine neurons suggests that they may play a unique role in the brain's response to glucose deficit.