Neurotransmitters and neuroimaging findings in eating disorders
GONIDAKIS FR.

The main difficulty in studying neurotransmitters' abnormalities in eating disorders and especially in anorexia nervosa is the distinction between what consists the biological basis of the disorder and the biological consequences of starvation.

The most well studied neurotransmitter in eating disorders and especially in anorexia nervosa is serotonin. The main three reasons for the above are: the regulatory role of serotonin in appetite, mood, impulse control and compulsive behavior, the efficacy of SSRI's in the treatment of depression and anxiety disorders and finally the dysfunction of serotonin system in starvation. The short allele of the serotonin transporter has been linked in genetic studies with the development of eating disorders, mainly anorexia nervosa. Neurobiological and neuroimaging studies have shown that in anorexia nervosa serotonin level as well as the activity of 5HT_2A receiver in the brain is reduced. After recovery serotonin levels are higher than normal while 5HT_2A receiver activity remains reduced. In bulimia nervosa the level of serotonin is reduced, the 5HT_2A receiver activity is normal while the presynaptic 5HT_1A receiver activity is increased. After recovery from bulimia nervosa serotonin level is normalized while 5HT_2A activity is lower and 5HT_1A activity is higher than normal. Serotonin dysfunction has also been linked with certain symptoms of anorexia and bulimia nervosa. Drive for thinness has been negatively correlated with 5HT_2A activity in the left parietal cortex while body image distortion has been linked with 5HT_2A hypo activity in left parietal cortex.

Noradrenalin activity is reduced both in anorexia and bulimia nervosa. This finding has been attributed to the starvation in anorexia and the eating patterns in bulimia nervosa. There are far less published studies on noradrenalin than on serotonin. Considering the genetic factors it has been reported that the presence of both the L allele of the MAOA gene and the NETpPR-L4 polymorphism of the promoter region for the noradrenalin transporter gene doubles the risk for anorexia nervosa. Noradrenalin activity is lowered both in anorexia and bulimia nervosa and is returned to normal levels in recovered patients. It is interesting that while noradrenalin levels in CSF are within normal range in anorectic patients they are lower than normal 6 months after recovery.

Dopamine is the third neurotransmitter that has been studied mainly because of dopamine role in regulating food intake, mood, anxiety, sexual and social behavior, aggressiveness, motor activity and rewarding activities. So far there has been no indication that there is a relation between the dopamine receptors genes and eating disorders. A connection between the val158Met polymorphism of the COMT gene and anorexia nervosa has been reported but newer studies did not duplicate this result. In anorexia nervosa the dopaminergic activity is lowered both in the restricted and the binging/purging type. There are indications that some kind of dopamine hypo activity remains even after recovery. A lower concentration of homovanilic acid in CSF and an increase in the sensitivity of the D₂/D₃ receptors in the striatum has been found in recovered restrictive type anorectic patients, indicating thus a dopamine involvement in the pathopysiology of anorexia nervosa. Dopamine activity is also lowered in bulimia nervosa especially in patients with repeatedly bulimic episodes. Dopamine activity returns to normal after recovery.

Key words: Eating disorders, neurotrasmitters, neuroimaging.