Stress-induced changes in nucleus accumbens glutamate synaptic plasticity

Area of Science:

• Neuroscience
• Neurobiology
• Behavioral Neuroscience

Background:

• Stress hormones impact neural function across brain regions like the hippocampus and amygdala.
• The nucleus accumbens (NAc), crucial for motivation and reward, receives input from stress-affected areas.
• Investigating stress-induced plasticity in the NAc is vital for understanding its role in behavior.

Purpose of the Study:

• To determine if acute stress induces synaptic plasticity in the nucleus accumbens (NAc).
• To assess changes in glutamate receptor function within the NAc following stress exposure.
• To elucidate the role of corticosteroid signaling in stress-induced NAc plasticity.

Main Methods:

• Adult mice were exposed to a two-day cold water forced swim stress paradigm.
• Electrophysiological recordings were performed on NAc medium spiny neurons (MSNs) 18-24 hours post-stress.
• AMPA receptor (AMPAR)/N-methyl-d-aspartate receptor (NMDAR) ratios and miniature postsynaptic currents were measured.

Main Results:

• Stress significantly increased AMPAR/NMDAR ratios in the NAc shell MSNs, indicating enhanced synaptic strength.
• These stress-induced changes were blocked by glucocorticoid receptor (GR) antagonist RU486.
• Exogenous corticosterone (CORT) administration mimicked the effect of stress on AMPAR/NMDAR ratios in the NAc shell.
• Increased AMPAR-mediated currents, but not NMDAR currents, were observed in stressed NAc shell MSNs.

Conclusions:

• Acute stress induces corticosteroid-dependent synaptic plasticity in the NAc shell.
• Enhanced AMPAR function in the NAc shell may underlie stress-related alterations in reward processing.
• This plasticity could contribute to behaviors like stress-induced drug seeking and relapse.