Potassium channels underlie postsynaptic but not presynaptic GABAB receptor-mediated inhibition on ventrolateral periaqueductal gray neurons
Zhi-Liang Liua, Hongyu Mab✉, Ruxiang Xua, Yiwu Daia, Hongtian Zhanga, Xue-qin Yaoa, Kun Yangc d✉
- aBayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing 100700, China
- bClinical Laboratory Center, Air Force General Hospital, Beijing 100142, China
- cDepartment of Anatomy and K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi’an 710032, China
- dDepartment of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
- ✉Corresponding author
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Abstract
γ-Aminobutyric acid (GABA) is the principle inhibitory neurotransmitter in adult mammalian brain. GABA receptors B subtype (GABA(B)Rs) are abundantly expressed at presynaptic and postsynaptic neuronal structures in the rat ventrolateral periaqueductal gray (PAG), an area related to pain regulation. Activation of GABA(B)Rs by baclofen, a selective agonist, induces presynaptic inhibition by decreasing presynaptic glutamate release. At the same time, baclofen induces a postsynaptic inhibitory membrane current or potential. We here report that in the ventrolateral PAG, the postsynaptic inhibition is mediated by activation of G protein-coupled inwardly rectifying K(+) (GIRK) channels. Blockade of K(+) channels largely prevents postsynaptic action of baclofen. In contrast, presynaptic inhibition of baclofen is insensitive to K(+) channel blockade. The data indicate that potassium channels play different roles in GABA(B)R-mediated presynaptic and postsynaptic inhibition on PAG neurons.