The NAc lesions disrupted the hippocampus-mPFC theta coherence during intravenous cocaine administration in rats.

Synchronization and desynchronization of neuronal oscillatory activities between different brain areas play an important role in effective information communication. The hippocampus-mPFC circuit is well recognized as an important neural circuit pathway involved in drug addiction. We aimed to examine cocaine-related changes in oscillation synchronization in the hippocampus-mPFC circuit and to explore the role of the NAc in oscillation synchronization between the hippocampus and the mPFC during intravenous cocaine administration. In our experiment, adult male Sprague-Dawley rats were divided into the Saline group, Cocaine group and Lesion group by the random number table method. Using an electrophysiological method, we continuously recorded the local field potentials (LFPs) of the hippocampus and the mPFC after pulse intravenous cocaine or saline. Our results showed that theta coherence occurred in the hippocampus-mPFC circuit during intravenous cocaine administration (Coherenceθ, Pre-drug = 0.2212 ± 0.0126, Coherenceθ, Post-drug = 0.3118 ± 0.0149, t = 4.894, P < 0.001), and the NAc Lesions could disrupt hippocampus-mPFC theta coherence (Coherenceθ, Pre-drug = 0.3164 ± 0.0188, Coherenceθ, Post-drug = 0.2628 ± 0.0248, t = 2.408, P < 0.05). These findings indicated that the NAc could influence oscillation synchronization between the hippocampus and mPFC during intravenous cocaine administration, which might help to elucidate the neurophysiological mechanisms of the neural circuits that underlie the function of the NAc during the strengthening of drug addiction.