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Diabetes 50:2431-2437, 2001
© 2001 by the American Diabetes Association, Inc.

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Xiao Hui Liu1, Richard Morris2, David Spiller3, Michael White3, and Gareth Williams1

1 Diabetes and Endocrinology Research Group, Department of Medicine University of Liverpool, Liverpool, U.K.
2 Department of Preclinical Veterinary Science University of Liverpool, Liverpool, U.K.
3 School of Biological Science, University of Liverpool, Liverpool, U.K.

Falls in blood glucose induce hunger and initiate feeding. The lateral hypothalamic area (LHA) contains glucose-sensitive neurons (GSNs) and orexin neurons, both of which are stimulated by falling blood glucose and are implicated in hypoglycemia-induced feeding. We combined intracellular electrophysiological recording with fluorescein labeling of GSNs to determine their neuroanatomic and functional relationships with orexin neurons. Orexin A (1 µmol/l) caused a 500% increase (P < 0.01) in spontaneous firing rate and rapid and lasting depolarization that was tetrodotoxin-resistant and thus a direct postsynaptic effect. Orexin A altered the intrinsic neuronal properties of GSNs, consistent with increased excitability. Confocal microscopy showed that GSNs were intimately related to orexin neurons: orexin-immunoreactive axons were frequently entwined around GSN dendrites, establishing close and putatively synaptic contacts. Orexin-cell axons also passed in close proximity to glucose-responsive neurons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and only a 200% increase in spontaneous firing rate (P < 0.05 vs. GSN). We conclude that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in part, the acute appetite-stimulating effect of orexin A. Orexin neurons may regulate GSNs so as to control the onset and termination of hypoglycemia-induced feeding.


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