Transient effects of junk food on NAc core MSN excitability and glutamatergic transmission in obesity-prone female rats.

Abstract

The nucleus accumbens (NAc) plays critical roles in eating and food seeking in rodents and humans. Diets high in fats and sugars ("junk food") produce persistent increases in NAc function in male obesity-prone rats. This study examines effects of junk food and junkfood deprivation on NAc core medium spiny neuron (MSN) excitability and glutamate transmission in females. Obesity-prone female rats were given access to ad libitum junkfood for 10 days, and recordings were made from MSNs in the NAc core immediately or after a short (27-72 hours) or long (14-16 days) junk food deprivation period in which rats were returned to ad libitum standard chow. Controls remained on chow throughout. Whole-cell slice electrophysiology was used to examine MSN intrinsic membrane and firing properties and glutamatergic transmission. The study found that intrinsic excitability was reduced, whereas glutamatergic transmission was enhanced, after the short, but not long, junk food deprivation period. A brief junk food deprivation period was necessary for increases in NAc calcium-permeable-AMPA receptor transmission and spontaneous excitatory postsynaptic current (sEPSC) frequency, but not for increases in sEPSC amplitude. This study reveals that females are protected from long-lasting effects of sugary fatty foods on MSN neuronal function and provides evidence for sex-specific effects on plasticity in brain centers that influence food-seeking and feeding behavior.