SUBGROUPS OF HINDBRAIN CATECHOLAMINE NEURONS ARE SELECTIVELY ACTIVATED BY 2-DEOXY-D-GLUCOSE INDUCED METABOLIC CHALLENGE

Glucose is a major fuel for body energy metabolism and an essential me tabolic fuel for the brain. Consequently, glucose deficit (glucoprivat ion) elicits a variety of physiological and behavioral responses cruci al for survival. Previous work indicates an important role for brain c atecholamine neurons in mediation of responses to glucoprivation. This experiment was conducted to identify the specific catecholamine neuro ns that are activated by glucoprivation. Activation of hindbrain catec holamine neurons by the antimetabolic glucose analogue, 2-deoxy-D-gluc ose (2DG; 50, 100, 200 or 400 mg/kg, s.c.) was evaluated using double label immunohistochemistry. Fos protein was used as the marker for neu ronal activation and the enzymes tyrosine hydroxylase (TH) and pheneth anolamine-N-methyl transferase (PNMT) were used as the markers for nor epinephrine (NE) and epinephrine (E) neurons. 2-Deoxy-D-glucose (200 a nd 400 mg/kg) produced selective activation of distinct hindbrain cate cholamine cell groups. In the ventrolateral medulla, doubly labeled ne urons were concentrated in the area of A1/C1 and were predominantly ad renergic in phenotype. in the dorsal medulla, doubly labeled neurons w ere limited to C2 and C3 cell groups. In the pens, some A6 neurons wer e Fos-positive. Neurons in rostral C1, ventral C3, A2, A5 and A7 did n ot express Fos-ir in response to 2DG, Our results identify specific su bpopulations of catecholamine neurons that are selectively activated b y 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 pre ferential activation of epinephrine neurons suggests that they may pla y a unique role in the brain's response to glucose deficit. (C) 1998 E lsevier Science B.V. All rights reserved.