Glucose Inhibition of the Glucose-sensitive Neurone in the Rat Lateral Hypothalamus

Abstract

IT is generally accepted that the lateral hypothalamic area (LH) and ventromedial nucleus (VMH) have a reciprocal relationship in the control of feeding behaviour^1–3, and that some neurones in these regions are sensitive to levels of glucose in the blood^4,5 or to electro-osmotically applied glucose⁶. We have demonstrated that although about one-third of the VMH neurones increased their activity when glucose was applied, there are neurones in LH which are specifically inhibited by it. These neurones are activated by direct applications of insulin, 2-deoxy-D-glucose and 3-O-methyl-D-glucose⁷. Booth⁸ demonstrated that the injection of 1 µl of 5% D-glucose in the LH blocked insulin-induced eating. More recently Colin-Jones and Himsworth⁹ reported that an injection of 2-deoxy-D-glucose (2DG) into the LH causes a marked increase in gastric acid secretion and attributed it to the lack of metabolisable glucose in the LH neurones. The fact that the specific glucose-sensitive cells which are inhibited by glucose exist only in LH has been highlighted in a recent report in which gastric secretion induced by the peripheral administration of 2DG in the cat was blocked by specific and discrete lesions in the lateral hypothalamus¹⁰. Here we report that the inhibition of LH neurones induced by direct application of glucose is the result of membrane hyperpolarisation and possibly results from the activation of the sodium pump causing an increased extrusion of internal sodium.