title: Blockade of presynaptic 4-aminopyridine-sensitive potassium channels increases initial neurotransmitter release probability, reinstates synaptic transmission altered by GABAB receptor activation in rat midbrain periaqueductal gray.
abstract: The activation of γ-aminobutyric acid receptor subtype B (GABAB) receptors in the midbrain ventrolateral periaqueductal gray (vlPAG) induces both postsynaptic and presynaptic inhibition. Whereas the postsynaptic inhibition is mediated by G protein-coupled inwardly rectifying K channels, the presynaptic inhibition of neurotransmitter release is primarily mediated by voltage-gated calcium channels. Using whole-cell recordings from acute rat PAG slices, we report here that the bath application of 4-aminopyridine, a voltage-gated K channel blocker, increases the initial GABA and glutamate release probability (P) and reinstates P depressed by presynaptic GABAB receptor activation at inhibitory and excitatory synapses, respectively. However, Ba, which blocks G protein-coupled inwardly rectifying K channels, does not produce similar effects. Our data suggest that the blockade of presynaptic 4-aminopyridine-sensitive K channels in vlPAG facilitates neurotransmitter release and reinstates synaptic transmission that has been altered by presynaptic GABAB receptor activation. Because vlPAG is involved in the descending pain control system, the present results may have potential therapeutic applications.
authors.affiliation: aDepartment of Psychology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin bBayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing cDepartment of Basic Medical Sciences, School of Medicine dAffiliated Hospital Electrophysiology Laboratory, Jiangsu University, Zhenjiang, Jiangsu, China.
authors.forename: Guangying
authors.initials: G
authors.lastname: Li
authors.forename: Zhi-Liang
authors.initials: ZL
authors.lastname: Liu
authors.forename: Wei-Ning
authors.initials: WN
authors.lastname: Zhang
authors.forename: Kun
authors.initials: K
authors.lastname: Yang
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology*; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002413:Cations, Divalent / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D018408:Patch-Clamp Techniques; D010487:Periaqueductal Gray / Q000187:drug effects* / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D015221:Potassium Channels / Q000378:metabolism; D017729:Presynaptic Terminals / Q000187:drug effects* / Q000502:physiology; D011336:Probability; D017207:Rats, Sprague-Dawley; D018080:Receptors, GABA-B / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology; D046509:Tissue Culture Techniques; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D002413:Cations, Divalent; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D018080:Receptors, GABA-B; D001464:Barium; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D015761:4-Aminopyridine