Excess intake of fat and sugar potentiates epinephrine-induced hyperglycemia in male rats.

Aims: Over the past five decades, per capita caloric intake has increased significantly, and diet- and stress-related diseases are more prevalent. The stress hormone epinephrine stimulates hepatic glucose release during a stress response. The present experiment tested the hypothesis that excess caloric intake alters this ability of epinephrine to increase blood glucose.

Remembering to eat: hippocampal regulation of meal onset.

A wide variety of species, including vertebrate and invertebrates, consume food in bouts (i.e., meals).

High energy diets prevent the enhancing effects of emotional arousal on memory.

Over the past five decades, per capita caloric intake has increased by approximately 28% in the United States. Excessive intake of calories from fats and sugars (high energy diets; HEDs) negatively impacts hippocampal-dependent memory. These deleterious effects of HEDs on hippocampal function involve HED-induced decreases in neuronal growth factors, neurogenesis, and synaptic plasticity.

Atomoxetine reverses attentional deficits produced by noradrenergic deafferentation of medial prefrontal cortex.

Background: The majority of studies assessing executive function in attention deficit disorder (ADD) have shown deficits in attentional set shifting using either the Wisconsin card sorting task or the intra-dimensional/extra-dimensional set-shifting task (ID/ED). Damage to the prefrontal cortex in humans, primates, and rodents impairs extra-dimensional (ED) shifts. Noradrenergic depletion of the medial prefrontal cortex in rats is sufficient to impair attentional set shifting.