思春期の暴飲暴食は、マウスの皮質微小回路に長期的な変化をもたらす Adolescent binge drinking leads to long-lasting changes in cortical microcircuits in mice
Avery R. Sicher, William D. Starnes, Keith R. Griffith, Nigel C. Dao, Grace C. Smith, Dakota F. Brockway, Nicole A. Crowley
Neuropharmacology Available online :1 May 2023
•Adolescent binge alcohol increases excitability of prelimbic somatostatin neurons.
•Hyperexcitability persists 30 days after alcohol with no change in SST cell density.
•Initial pyramidal neuron excitability decreases, then rebounds in females after alcohol.
•Binge drinking does not change SST-mediated GABA transmission in prelimbic circuits.
Adolescent drug consumption has increased risks to the individual compared to consumption in adulthood, due to the likelihood of long-term and permanent behavioral and neurological adaptations. However, little is known about how adolescent alcohol consumption influences the maturation and trajectory of cortical circuit development. Here, we explore the consequences of adolescent binge drinking on somatostatin (SST) neuronal function in superficial layers of the prelimbic (PL) cortex in male and female SST-Ai9 mice. We find that adolescent drinking-in-the-dark (DID) produces sex-dependent increases in intrinsic excitability of SST neurons, with no change in overall SST cell number, persisting well into adulthood. While we did not find evidence of altered GABA release from SST neurons onto other neurons within the circuit, we found a complementary reduction in layer II/III pyramidal neuron excitability immediately after binge drinking; however, this hypoexcitability rebounded towards increased pyramidal neuron activity in adulthood in females, suggesting long-term homeostatic adaptations in this circuit. Together, this suggests that binge drinking during key developmental timepoints leads to permanent changes in PL microcircuitry function, which may have broad behavioral implications.