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The prefrontal cortex (PFC) of our brain can properly perform its “braking” function to suppress impulses when excitatory and inhibitory signals are in balance. To investigate how chronic drug exposure disrupts this balance, the research team conducted cocaine administration experiments on mice. During this process, they tracked when inhibitory neurons in the PFC were activated and how they sent signals to downstream brain regions.

The experimental results showed that parvalbumin (PV) cells, which account for about 60–70% of the inhibitory neurons in the PFC, were highly active when the mice attempted to seek cocaine. However, when “extinction training”—training to stop seeking the drug—was conducted, the activity of these cells significantly decreased. This demonstrates that the activity patterns of PV cells are not permanently fixed by addiction but can be readjusted through the extinction process.

The research team confirmed that artificially suppressing PV cell activity significantly reduced cocaine-seeking behavior in mice. Conversely, activating these cells caused the drug-seeking behavior to persist even after the extinction process. This effect was specifically observed in drug-addiction behavior and did not appear with general rewards like sugar water. Furthermore, this phenomenon was not observed in somatostatin (SOM) cells—another type of inhibitory neuron—indicating that PV cells selectively regulate drug addiction behavior.

The team also identified the specific brain circuit through which these PV cells operate. Signals originating from the prefrontal cortex are transmitted to the reward circuit of the Ventral Tegmental Area (VTA), a key brain region related to reward. This pathway emerged as the central channel for regulating addiction behavior, determining whether or not to seek the drug again. In this process, PV neurons act as a “regulatory switch,” controlling the flow of signals to influence dopamine signaling and deciding whether to maintain or suppress addictive behavior. ScienceMission sciencenewshighlights.

Drug addiction carries an extremely high risk of relapse, as cravings can be reignited by minor stimuli even long after one has stopped using. Previously, this phenomenon was attributed to a decline in the function of the prefrontal cortex (PFC), which regulates impulses. However, a joint international research team has recently revealed that the cause of addiction relapse is not a simple decline in brain function, but rather an imbalance in specific neural circuits.

The researchers have identified the core principle by which specific inhibitory neurons in the prefrontal cortex regulate cocaine-seeking behavior.