High-fructose diet initiated during adolescence does not affect basolateral amygdala excitability or affective-like behavior in Sprague Dawley rats.

Patients with type-2 diabetes, obesity, and metabolic syndrome have a significantly increased risk of developing depression. Dysregulated metabolism may contribute to the etiology of depression by affecting neuronal activity in key limbic areas. The basolateral amygdala (BLA) acts as a critical emotional valence detector in the brain's limbic circuit, and shows hyperactivity and abnormal glucose metabolism in depressed patients. Furthermore, administering a periadolescent high-fructose diet (HFrD; a model of metabolic syndrome) to male Wistar rats increases anxiety- and depressive-like behavior. Repeated shock stress in Sprague Dawley rats similarly increases anxiety-like behavior and increases BLA excitability. We therefore investigated whether a metabolic stressor (HFrD) would have similar effects as shock stress on BLA excitability in Sprague Dawley rats. We found that a HFrD did not affect the intrinsic excitability of BLA neurons. Fructose-fed Sprague Dawley rats had elevated body fat mass, but did not show increases in metabolic efficiency and fasting blood glucose relative to control. Finally unlike Wistar rats, fructose-fed Sprague Dawley rats did not show increased anxiety- and depressive-like behavior. These results suggest that genetic differences between rat strains may affect susceptibility to a metabolic insult. Collectively, these data show that a periadolescent HFrD disrupts metabolism, but does not change affective behavior or BLA excitability in Sprague Dawley rats.