title: The role of catecholamine innervation in the medial prefrontal cortex on the regulation of body weight and food intake.
abstract: Effects of 6-hydroxydopamine (6-OHDA) lesions in the medial prefrontal cortex with or without protection of norepinephrine (NE) fibers were examined on basic regulatory processes of feeding. Daily body weight, food and water intake were measured. Locomotor activity, ingestion after food or water deprivation, and preference for 5% and 10% glucose solution were examined. Dopamine (DA) and NE content, as well as, tyrosine hydroxylase immunoreactivity were assessed to confirm the neurotoxic effect of treatments. 6-OHDA lesions of the medial prefrontal cortex with or without NE fiber protection resulted in body weight loss. Diminished habituation in open field tests, i.e. a persistently high motor activity, was also observed. Application of 6-OHDA with NE fiber protection led to increased food consumption following food-deprivation and to enhanced glucose preference. Enhanced intake of 10% over 5% glucose solution was also detected. 6-OHDA lesion resulted in a decrease to 20% of NE tissue concentration and only to 75% of DA concentration. In case of lesion with NE protection the NE content decreased to 69% and DA level to 51% with significant loss of tyrosine hydroxylase positive fibers in the deeper layers of the medial prefrontal cortex. DA depletion in the medial prefrontal cortex resulted in increased behavioral responsiveness to hunger and glucose, as well as, to open field environment. Pronounced lesion of NE terminals caused increased reaction to the environment in open field but not to hunger or glucose solution.
authors.affiliation: Institute of Physiology, University of Pécs Medical School, Pécs, Hungary. Electronic address: rita.galosi@aok.pte.hu.
authors.forename: Rita
authors.initials: R
authors.lastname: Gálosi
authors.affiliation: Department of Neural and Behavioral Sciences, Penn State University, College of Medicine, The Milton S. Hershey Medical Center, Hershey, PA, USA.
authors.forename: Andras
authors.initials: A
authors.lastname: Hajnal
authors.affiliation: Institute of Physiology, University of Pécs Medical School, Pécs, Hungary; Molecular Neurophysiology Research Group, University of Pécs, Szentágothai Research Center, Pécs, Hungary.
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Petykó
authors.affiliation: Institute of Physiology, University of Pécs Medical School, Pécs, Hungary.
authors.forename: Géza
authors.initials: G
authors.lastname: Hartmann
authors.affiliation: Institute of Physiology, University of Pécs Medical School, Pécs, Hungary; Molecular Neurophysiology Research Group, University of Pécs, Szentágothai Research Center, Pécs, Hungary.
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Karádi
authors.affiliation: Institute of Physiology, University of Pécs Medical School, Pécs, Hungary; Molecular Neurophysiology Research Group, University of Pécs, Szentágothai Research Center, Pécs, Hungary.
authors.forename: László
authors.initials: L
authors.lastname: Lénárd
mesh_terms: D018663:Adrenergic Agents / Q000633:toxicity; D000818:Animals; D001835:Body Weight / Q000502:physiology*; D004298:Dopamine / Q000378:metabolism*; D060766:Drinking Water / Q000008:administration & dosage; D004435:Eating / Q000502:physiology*; D005106:Exploratory Behavior / Q000502:physiology; D005518:Food Preferences / Q000502:physiology; D005947:Glucose / Q000008:administration & dosage; D006185:Habituation, Psychophysiologic / Q000502:physiology; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism*; D016627:Oxidopamine / Q000633:toxicity; D017397:Prefrontal Cortex / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D017208:Rats, Wistar; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D018663:Adrenergic Agents; D060766:Drinking Water; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D005947:Glucose; D004298:Dopamine; D009638:Norepinephrine
keywords: Body weight; Catecholamine; Glucose preference; Medial prefrontal cortex