PT  - JOURNAL ARTICLE
AU  - Kang, Ling
AU  - Routh, Vanessa H.
AU  - Kuzhikandathil, Eldo V.
AU  - Gaspers, Larry D.
AU  - Levin, Barry E.
TI  - Physiological and Molecular Characteristics of Rat Hypothalamic Ventromedial Nucleus Glucosensing Neurons
AID  - 10.2337/diabetes.53.3.549
DP  - 2004 Mar 01
TA  - Diabetes
PG  - 549--559
VI  - 53
IP  - 3
4099  - http://diabetes.diabetesjournals.org/content/53/3/549.short
4100  - http://diabetes.diabetesjournals.org/content/53/3/549.full
SO  - Diabetes2004 Mar 01; 53
AB  - To evaluate potential mechanisms for neuronal glucosensing, fura-2 Ca2+ imaging and single-cell RT-PCR were carried out in dissociated ventromedial hypothalamic nucleus (VMN) neurons. Glucose-excited (GE) neurons increased and glucose-inhibited (GI) neurons decreased intracellular Ca2+ ([Ca2+]i) oscillations as glucose increased from 0.5 to 2.5 mmol/l. The Kir6.2 subunit mRNA of the ATP-sensitive K+ channel was expressed in 42% of GE and GI neurons, but only 15% of nonglucosensing (NG) neurons. Glucokinase (GK), the putative glucosensing gatekeeper, was expressed in 64% of GE, 43% of GI, but only 8% of NG neurons and the GK inhibitor alloxan altered [Ca2+]i oscillations in ∼75% of GK-expressing GE and GI neurons. Insulin receptor and GLUT4 mRNAs were coexpressed in 75% of GE, 60% of GI, and 40% of NG neurons, although there were no statistically significant intergroup differences. Hexokinase-I, GLUT3, and lactate dehydrogenase-A and -B were ubiquitous, whereas GLUT2, monocarboxylate transporters-1 and -2, and leptin receptor and GAD mRNAs were expressed less frequently and without apparent relationship to glucosensing capacity. Thus, although GK may mediate glucosensing in up to 60% of VMN neurons, other regulatory mechanisms are likely to control glucosensing in the remaining ones.