Dopamine in anorexia nervosa

Abstract

Anorexia nervosa (AN) is a chronic relapsing psychiatric disorder with a largely unknown pathophysiology. Dopamine has been implicated in the pathophysiology of the disorder by preclinical and clinical evidence. Preclinical studies have examined two main characteristics of AN: reduction in food intake (diet restriction) and hyperactivity. Diet restriction has been associated with reduced dopamine levels in the hypothalamus, hippocampus, and the dorsal striatum. Animal hyperactivity following diet restriction has been linked to increased dopamine in the hypothalamus. Increased dopamine in the nucleus accumbens was associated with food administration, but not food expectation. Tyrosine and dopaminergic antagonists normalized anorexia-like behaviors in animal models of AN, but did not restore body weight. Clinical studies on the etiology of AN have produced contradictory findings. Cerebrospinal fluid concentrations of dopamine and its metabolites have been reported to be decreased or normal under conditions of low weight, whereas they tended to normalize when the weight was restored. Plasma and urinary levels of dopamine and its metabolites have been found to be normal, increased, and decreased. Neuroendocrine studies suggest that dopaminergic neurotransmission is increased in AN. However, recent neuroimaging studies lend support to the increase in binding of dopaminergic receptors in the striatum, which favors the opposite theory that intrasynaptic dopamine is indeed decreased. Genetic studies implicate dopamine D2 receptors, the dopamine transporter, and the enzyme COMT. There are promising results with respect to the use of atypical antipsychotics against symptoms of AN beyond weight gain, but further trials are required.

Fatty acids rehabilitated long-term neurodegenerative: like symptoms in olfactory bulbectomized rats

“…EFA group. See text for TNFa data Fatty acids rehabilitated long-term neurodegenerative and food intake (Kontis and Theochari 2012), and thermoregulatory physiological and behavioral effects (Yehuda and Sheleff 1985). Previous studies showed that OBX modified its level and many dopaminergic brain functions (e.g., Yehuda 1976).…”

Striatal dopamine type 2 receptor availability in anorexia nervosa

“…No data are available regarding striatal DA levels, and animal studies suggest that weight loss is associated with decreases in such levels (Pothos et al, 1995). In addition, other human data (e.g., CSF DA and metabolites; plasma DA metabolite studies; genetic studies) suggest the possibility of dopaminergic abnormalities [reviewed in (Kontis and Theochari, 2012)].…”

Eating Disorders in Late-life

“…However, recent neuroimaging studies demonstrated an increased binding of dopaminergic receptors in the striatum, thus supporting the opposite theory, stating the decrease of intrasynaptic dopamine. This finding could explain the efficacy of atypical antipsychotics, going beyond weight gain, on the symptoms of AN [16].…”