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- W2416131567 endingPage "1424" @default.
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- W2416131567 abstract "Kim, Chang-Ju, Jeong-Seop Rhee, and Norio Akaike. Modulation of high-voltage activated Ca 2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol. 77: 1418–1424, 1997. The effect of μ-type opioid receptor agonist, D-Ala 2 ,N-MePhe 4 ,Gly 5 -ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca 2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 118 PAG neurons tested, the HVA Ca 2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca 2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca 2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca 2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of ω-conotoxin-GVIA occluded the inhibitory effect of DAMGO ∼70%. So, HVA Ca 2+ channels inhibited by DAMGO were mainly the N-type Ca 2+ channels. The inhibitory effect of DAMGO on HVA Ca 2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8–10 h, suggesting that DAMGO modulation on N-type Ca 2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that μ-type opioid receptor modulates N-type HVA Ca 2+ channels via PTX-sensitive G proteins in PAG neurons of rats." @default.
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- W2416131567 date "1997-03-01" @default.
- W2416131567 modified "2023-10-17" @default.
- W2416131567 title "Modulation of High-Voltage Activated Ca<sup>2+</sup> Channels in the Rat Periaqueductal Gray Neurons by μ-Type Opioid Agonist" @default.
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- W2416131567 doi "https://doi.org/10.1152/jn.1997.77.3.1418" @default.
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