兴奋性氨基酸介导的膜电流可被吗啡阻断

MORPHINE BLOCKED THE EXITATORY AMINO ACID MEDIATED MEMBRANE CURRENT IN AMBIGUAL MOTONEURONS OF TEE RAT

在Ｓｐｒａｙｕｅ－Ｄａｗｉｅｙ大鼠的含有孤束核中央亚核及疑核神经元密集区的脑薄片上，吗啡（３—５ｐｍｏｌ）对疑核细胞内记录到的自发兴奋性突触后电位有抑制作用；向灌流液内注入吗啡可使电刺激孤束核在疑核记录到的兴奋性突触后电位的幅度降低７１．１±６．２％（Ｐ＜Ｏ．００１），纳洛酮（５０ｎｍｏｌ／Ｌ）可翻转这种抑制效应；含有１０μｍｏｌ／Ｌ吗啡的灌流液对ＮＭＤＡ（０．５—１ｐｍｏｌ）、乙酰胆碱（３ｐｍｏｌ）及ＱＵｉｓｑｕａｌａｔｅ（０．１—０．５ｐｍｏｌ）引起的细胞膜去极化有不同程度的抑制作用，分别为３８．１±５．７％（Ｐ＜０．００１），３２．８±５．５％（Ｐ＜０．０１）和２９．６±７．１％（Ｐ＜０．０５）。这些结果可能是由于吗啡兴奋μ和δ受体后，增加了Ｋ＋电流而降低Ｎａ＋，Ｃａ２＋离子通透性的缘故。

Excitutory postsynaptic potentials (EPSPs) and responses of neurons in the compact formation of the neucleus ambiguus (AMBc) to pressure-ejected or bath-applied test subetunces were recorded intracellularly from sagittul slices of Sprague-Dawley rat medulla containing subllucleus centralis of solitary complex (NTSc), AMBc and solitarioambigual pathway. In 5 cells, recorded spontaneous EPSPs could be blocked by morphine (3-5 pmol) to AMBc. Electrical stimulation of NTSc evoked EPSPs in AMBc neurons, the amplitude of which were decreased to 71. 1 ± 6. 2 % (P<O. 001 ) with the addition to morphine. The morphine effect could be abolished by bath-applied naloxone (50 nmol/L). The amplitude of membrane depolarization induced by pressure-ejected N-methyl-D-aspartate (NMDA, 0. 5-1.0 pmol ), acetylcholine (3 pmol ) and quisqualate (0. 1-0. 5 pmol) to NTSc could also be decreased by bath-applied morphine (10 μmol/L) respectively to 38. 1 ± 5. 7 % (P<0. 001 ), 32. 8± 5. 5% (P<0. 01) and 29. 6± 7. 1 % (P<0. 05). The above results suggest that morphine is capable of block by NMDA, ACh and non-NMDA receptors, increaseing the M-current and decreasing the permeability of Na+ and Ca2+.