DORSOMEDIAL HINDBRAIN PARTICIPATION IN GLUCOPRIVIC FEEDING RESPONSE TO 2DG BUT NOT 2DG-INDUCED HYPERGLYCEMIA OR ACTIVATION OF THE HPA AXIS

Citation
Bk. Edmonds et Gl. Edwards, DORSOMEDIAL HINDBRAIN PARTICIPATION IN GLUCOPRIVIC FEEDING RESPONSE TO 2DG BUT NOT 2DG-INDUCED HYPERGLYCEMIA OR ACTIVATION OF THE HPA AXIS, Brain research, 801(1-2), 1998, pp. 21-28
Citations number
30
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
801
Issue
1-2
Year of publication
1998
Pages
21 - 28
Database
ISI
SICI code
0006-8993(1998)801:1-2<21:DHPIGF>2.0.ZU;2-6
Abstract
2-Deoxy-D-glucose (2DG) is a glucose analogue that inhibits intracellu lar utilization of glucose and produces a characteristic behavioral re sponse known as glucoprivic feeding. The area postrema (AP) is a cauda l hindbrain structure shown previously to be involved in :DG-induced g lucoprivic feeding. In addition, peripheral administration of 2DG is k nown to elicit activation of both the hypothalamic-pituitary-adrenal ( HPA) axis and the sympathoadrenomedullary system. The neural substrate s for these neuroendocrine and neural responses to 2DG are not known a lthough they may also involve the AP. The possible role of the AP in 2 DG-induced feeding, activation of the HPA axis and hyperglycemia was i nvestigated in Sprague-Dawley rats with lesions centered on the area p ostrema (APX) and sham-operated (SHM) rats administered 2DG (200 mg/kg ) or physiological saline (1 ml/kg). Peripheral administration of 2DG evoked a feeding response in SHM rats that was abolished in APX animal s. Interestingly, 2DG administered at this dose produced a significant increase in plasma corticosterone and plasma glucose in both SHM and APX rats for up to 4 h after drug treatment. Collectively, these findi ngs suggest that the AP is involved in the behavioral (feeding) respon se to peripheral administration of 2DG, but does not appear to be a co mmon neural substrate for the neuroendocrine (HPA axis) and sympathoad renal (hyperglycemic) responses to this agent. (C) 1998 Elsevier Scien ce B.V. All rights reserved.