Neurobiology driving hyperactivity in activity-based anorexia.
Hyperactivity in anorexia nervosa is difficult to control and negatively impacts outcome. Hyperactivity is a key driving force to starvation in an animal model named activity-based anorexia (ABA). Recent research has started unraveling what mechanisms underlie this hyperactivity. Besides a general increase in locomotor activity that may be an expression of foraging behavior and involves frontal brain regions, the increased locomotor activity expressed before food is presented (food anticipatory behavior or FAA) involves hypothalamic neural circuits. Ghrelin plays a role in FAA, whereas decreased leptin signaling is involved in both aspects of increased locomotor activity. We hypothesize that increased ghrelin and decreased leptin signaling drive the activity of dopamine neurons in the ventral tegmental area. In anorexia nervosa patients, this altered activity of the dopamine system may be involved not only in hyperactivity but also in aberrant cognitive processing related to food.
Department of Neuroscience and Pharmacology, Rudolf Magnus Institute of Neuroscience, University Medical Centre, Utrecht, The Netherlands. r.a.h.adan@umcutrecht.nl
R A H
RA
Adan
J J G
JJ
Hillebrand
U N
UN
Danner
S
S
Cardona Cano
M J H
MJ
Kas
L A W
LA
Verhagen
D000701:Analgesics, Opioid; D000818:Animals; D000855:Anorexia / Q000150:complications* / Q000523:psychology; D004195:Disease Models, Animal; D004298:Dopamine; D054439:Ghrelin / Q000378:metabolism; D006801:Humans; D006948:Hyperkinesis / Q000150:complications*; D020738:Leptin / Q000378:metabolism; D053486:Melanocortins; D009446:Neurobiology; D009478:Neuropeptide Y
D000701:Analgesics, Opioid; D054439:Ghrelin; D020738:Leptin; D053486:Melanocortins; D009478:Neuropeptide Y; D004298:Dopamine