Dynamic interaction between hippocampus, orbitofrontal cortex, and subthalamic nucleus during goal conflict in the stop signal task in rats

Action stopping depends on at least two (fast, slow) frontal circuits depending on the urgency of execution of the 'go' response. Human EEG suggests a third (even slower, limbic) circuit that activates frontal areas at frequencies typical of 'hippocampal theta'. Here we test in male rats whether stop-go conflict engages the hippocampus and so may send theta-modulated information via the frontal cortex to the subthalamic nucleus. We recorded from multi-electrode arrays in the hippocampus, orbitofrontal cortex, and subthalamus in 5 male Long Evans rats performing a stop signal task and, as in previous human experiments, assessed stop-signal specific power for effects of goal conflict. Conflict increased 11-12 Hz theta power modestly in all three structures but with the largest increase in power being at 5 Hz in the frontal cortex but not the hippocampus. There was increased conflict-related coherence in all circuits in the range 5-8 Hz and particularly at 5-6 Hz. Increased coherence coupled with an increase in conflict-induced low frequency power in the frontal cortex may reflect communi-cation with the hippocampus. The data are consistent with a third limbic circuit that can generate stopping when go responses are particularly slow (as, e.g., in a go/no go task). [199 words; 200 max]

Automated summary

The cessation of action relies on at least two frontal circuits and a third limbic circuit that operates in the frequency typical of hippocampal theta. The study investigates in male rats whether stop-go conflict involves the hippocampus and whether theta-modulated information is transmitted to the subthalamic nucleus through the frontal cortex. The results suggest the presence of a third limbic circuit that contributes to stopping action when go responses are slow.