Many neurotransmitters, hormones and metabolites have been shown to be involved in pathophysiology of anorexia nervosa (AN). By central and/or peripheral administration in experimental animals, the majority of these bioactive substances are also known to affect feeding. A few of them such as noradrenaline (NA), dopamine (DA), corticotropin releasing factor (CRF) and glucocorticoids (GC) are considered as causal factors of AN. Central administration of NA or DA induces feeding, while in AN, NA and DA mechanisms are impaired. Plasma concentration of CRF and GC that suppress feeding, however, is elevated in AN. Other substances, which may be secondary factors of the disease, behave differently : CSF or plasma level of feeding suppressors (e.g. serotonin, somatostatin, glucagon, estrogen etc.) is reduced ; and that of a feeding stimulant (growth hormone) increases in AN.To elucidate neuronal pathophysiological mechanisms leading to the development of the disease, understanding of central catecholaminergic mechanisms in the primate feeding control is important. Therefore, neuron activity of the hypothalamus, amygdala and orbitofrontal cortex during operant feeding task was analyzed and catecholaminergic involvement in modulation of feeding related neuron activity was investigated in awake monkeys. In the hypothalamus and the orbitofrontal cortex, β-adrenergic receptors were involved in regulation of bar press related firing rate decrease, while DA modulated bar press related firing facilitation. The hypothalamic DA system also modulated cue signals to excitation. In the amygdala, β-adrenergic and DA system regulated reward related firing rate decrease and increase, respectively. These data suggest that the dopaminegic transmission is involved in initiation of motivated food acquisition behavior, while α-adrenergic receptors modulate reward mechanisms. The β-adrenergic system participates in the regulation of food acquisition in a different manner from that of the DA system.In AN, dysfunction of the DA and β-adrenergic systems may cause disturbance of adaptive control of food acquisition, and dysfunction of the α-adrenergic mechanisms may result in abnormal reward-sensation or lack of suitable recognition of the reward.
