CP-AMPARs in the nucleus accumbens (NAc) mediate cue-triggered motivation for food and cocaine. In addition, increases in NAc CP-AMPAR expression and function can be induced by cocaine or sugary, fatty junk-foods. However, the precise nature of these alterations and the degree to which they rely on the same underlying mechanisms is not well understood. This has important implications for understanding adaptive vs. maladaptive plasticity that drives food- and drug-seeking behaviors. Furthermore, effects of junk-foods on glutamatergic plasticity in females are unknown. Here, we use a combination of protein biochemistry and whole-cell patch clamping to determine effects of diet manipulation on glutamatergic plasticity within the NAc of males and females. We found that junk-food consumption increases silent synapses and subsequently increases CP-AMPAR levels in males in the NAc of male rats. In addition, a brief period of junk-food deprivation is needed for the synaptic insertion of CP-AMPARs and the maturation of silent synapses in males. In contrast, junk-food did not induce AMPAR plasticity in females but may instead alter NMDAR-mediated transmission. Thus, these studies reveal sex differences in the effects of junk-food on NAc synaptic plasticity. In addition, they provide novel insights into how essential food rewards alter NAc function.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Feb 2021|
Bibliographical noteFunding Information:
This work was supported by NIDDK R01DK106188 and NIDDK 1R01DK115526-01 to CRF; TEB was supported by NIDA R01DA040965; YA-C was supported by R01DK106188-02-S1 and 1F99NS108549-01; TLF was supported by NIDA T32DA007268 and R01DK106188; and ETJ was supported by NIDA R01DA040965. The authors declare no competing interests.
© 2020, The Author(s).