Effects of intra-cerebroventricular 2-DG infusion and subsequent hypothalamic lesion on adrenal nerve activity in the rat.

It is known that hyperglycemic response to 2-deoxy-D-glucose (2-DG), a competitive inhibitor of glycolysis [1,22], is neurogenic through the sympathetic activation of adrenal catecholamine secretion [2,6,8]. An increase in the efferent discharge of adrenal nerve filaments after systemic administration of 2-DG was reported by Niijima [12]. Several studies have indicated that neural elements which may be important in this response exist in the central nervous system [2,5,7,19]. To evaluate the involvement of the hypothalamus in the sympathoadrenal response, we have studied the effects of intra-cerebroventricular (i.c.v.) administration of 2-DG and subsequent hypothalamic electrical lesion on the efferent discharge rate of the adrenal nerve. Thirteen male Wistar rats, weighing 250-300 g, were used. Under ketamine (100 mg/kg) anesthesia, a 29-gauge stainless steel tube was implanted into the third ventricle. To prevent leakage of cerebrospinal fluid, a stainless steel wire (100 ~tm in diameter) was inserted into the cannula. For electrical lesion experiments, concentric bipolar electrodes (outer diameter, 26 gauge stainless steel tube insulated except for 0.25 mm at the tip; inner diameter, 0.1 mm stainless steel wire insulated except for 0.25 mm at the tip; 0.5 mm tip separation) were implanted bilaterally into either the lateral hypothalamic area (LHA, A, 2.3 posterior to the bregma; L, 1.5; H, 3.2), or the ventromedial nucleus (VMH, A, 2.3 posterior to the bregma; L, 0.5; H, -3 .5) , each in 3 rats.