title: Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding.
abstract: OBJECTIVE
  To examine the role of AMP-activated protein kinase (AMPK) in the control of glucoprivic feeding by hindbrain catecholamine neurons.
  
  
  METHODS
  Micropunched hindbrain samples were collected from control and 2-deoxy-d-glucose (2DG)-injected rats for Western blot analysis of phosphorylated (activated) AMPK (pAMPK). Samples also were collected from 2DG-injected rats pretreated with anti-dopamine-β-hydroxylase conjugated to saporin to lesion hindbrain catecholamine neurons. In a second experiment, rats were given a fourth-ventricle injection of compound C (CC) or 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), an inhibitor and activator of AMPK, to identify a role for AMPK in hindbrain neurons required for elicitation of 2DG-induced feeding.
  
  
  RESULTS
  Systemic 2DG stimulated food intake in controls but not in catecholamine-lesioned rats. In controls, but not catecholamine-lesioned rats, 2DG also increased phosphorylated Thr172 at AMPKα subunits (pAMPKα) in hindbrain micropunches containing catecholaminergic cell groups A1 through the middle region of C1 (A1-C1m). Increased pAMPKα was not observed in the adjacent noncatecholaminergic ventromedial medulla or in the A2-C2 catecholamine cell groups in the dorsal hindbrain. Fourth-ventricle injection of CC attenuated 2DG-induced feeding during the first 2 h of the test, and AICAR alone increased food intake only during the first 60 min of the 4-h test.
  
  
  CONCLUSIONS
  Results indicate that AMPK in catecholaminergic A1-C1m neurons is activated by glucoprivation. Therefore, AMPK may contribute to the glucose-sensing mechanism by which these neurons detect and signal a glucose deficit in the service of systemic glucoregulation.
authors.affiliation: Programs in Neuroscience, Washington State University, Pullman, Washington, USA. aijunli@vetmed.wsu.edu
authors.forename: Ai-Jun
authors.initials: AJ
authors.lastname: Li
authors.forename: Qing
authors.initials: Q
authors.lastname: Wang
authors.forename: Sue
authors.initials: S
authors.lastname: Ritter
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000620:Aminoimidazole Carboxamide / Q000031:analogs & derivatives / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D002395:Catecholamines / Q000378:metabolism*; D002408:Catheters, Indwelling; D003847:Deoxyglucose / Q000494:pharmacology; D004299:Dopamine beta-Hydroxylase / Q000378:metabolism; D004435:Eating / Q000187:drug effects / Q000502:physiology*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D008845:Microinjections; D009474:Neurons / Q000378:metabolism*; D010766:Phosphorylation / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012249:Rhombencephalon / Q000187:drug effects / Q000378:metabolism*; D012265:Ribonucleotides / Q000494:pharmacology
chemical_list: D002395:Catecholamines; D007004:Hypoglycemic Agents; D012265:Ribonucleotides; D000620:Aminoimidazole Carboxamide; D003847:Deoxyglucose; D004299:Dopamine beta-Hydroxylase; D055372:AMP-Activated Protein Kinases; C031143:AICA ribonucleotide