Activation of α1-adrenoceptors enhances excitatory synaptic transmission via a pre- and postsynaptic protein kinase C-dependent mechanism in the medial prefrontal cortex of rats

Authors

  • Fei Luo,

    Corresponding author
    1. Institute of Neurobiology & State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Fudan University, Shanghai, China
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  • Hua Tang,

    1. Center for Neuropsychiatric Diseases, Institute of Life Science, Nanchang University, Nanchang, China
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  • Bao-ming Li,

    1. Institute of Neurobiology & State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Fudan University, Shanghai, China
    2. Center for Neuropsychiatric Diseases, Institute of Life Science, Nanchang University, Nanchang, China
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  • Si-hai Li

    1. Center for Neuropsychiatric Diseases, Institute of Life Science, Nanchang University, Nanchang, China
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Abstract

The physiological effects of α1-adrenoceptors (α1-ARs) have been examined in many brain regions. However, little is known about the mechanism of modulation on synaptic transmission by α1-ARs in the medial prefrontal cortex (mPFC). The present study investigated how α1-AR activation regulates glutamatergic synaptic transmission in layer V/VI pyramidal cells of the rat mPFC. We found that the α1-AR agonist phenylephrine (Phe) induced a significant enhancement of the amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs). The facilitation effect of Phe on the frequency of mEPSCs involved a presynaptic protein kinase C-dependent pathway. Phe produced a significant enhancement on the amplitude of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R)- and N-methyl-d-aspartic acid receptor (NMDA-R)-mediated evoked excitatory postsynaptic currents (eEPSCs). Phe enhanced inward currents evoked by puff application of glutamate or NMDA. The Phe-induced facilitation of AMPA-R- and NMDA-R-mediated eEPSCs required, in part, postsynaptic Gq, phospholipase C and PKC. These findings suggest that α1-AR activation facilitates excitatory synaptic transmission in mPFC pyramidal cells via both pre- and post-synaptic PKC-dependent mechanisms.

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