Abstract
In depression model rats, the phase coupling of theta and gamma oscillations between vCA1 and mPFC was found to be disrupted, which was correlated with impaired synaptic plasticity. It is well known that both dopamine and serotonin were involved in depression. Our results showed that the blockage of D1 receptor could lead to depression-like decrement on theta phase coupling, which could not be enhanced by LTP induction. In addition, the activation of 5-HT1A receptor facilitated vCA1–mPFC coupling on gamma oscillations, and attenuated CA1 theta-fast gamma cross-frequency coupling. These data suggested that the theta phase coupling between vCA1 and mPFC could be modulated by dopamine system that reflected the impaired synaptic plasticity as an underlying mechanism of the cognitive dysfunction in depression.
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