RELEASE OF SUBSTANCE-P FROM THE CAT SPINAL-CORD
RELEASE OF SUBSTANCE-P FROM THE CAT SPINAL-CORD
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DOI：
10.1113/jphysiol.1987.sp016731
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发表时间：
1987-10-01
影响因子：
5.5
通讯作者：
YAKSH, TL
中科院分区：
文献类型：
--
作者：
GO, VLW;YAKSH, TL
1.本实验研究了释放P物质样免疫反应性（SP-1. i.）的生理学和药理学，脊髓中的氟烷麻醉，人工通气猫。2. SP-l. i的静息释放为36 +/-4 fmol/30 min（平均值+/-S.E.; n = 106）。以诱发以A β传导速度（大于40 m/s）传导的纤维活动的强度双侧刺激坐骨神经，未导致血压、瞳孔直径或SP-I. i释放发生变化。以小于2 m/s的速度激活纤维传导的刺激强度导致血压升高、瞳孔缩小和SP-I. i释放升高。(278+/-16%对照）。3.神经刺激频率和释放之间的关系在高达约20 Hz时是单调的。较高的刺激频率不会增加SP-I. i的量。发布在200 Hz时，有一个减少。4.辣椒素（0.1 mM）增加SP-I. i.并导致对随后的神经刺激的急性脱敏。这种急性效应不伴有SP-l. i脊髓节段的降低。刺激后2小时测量。5.颈髓冷阻滞导致SP-I. i的量增加。通过神经刺激释放出来6.实验前7天鞘内注射5，6-二羟色胺（300微克）预处理导致SP-I. i.但对SP-I. i的释放没有影响。由神经刺激引起的。鞘内辣椒素（300微克）的类似预处理导致SP-l. i消耗在脊髓背角，但不是在腹角，并减少了SP-l. i的释放。由神经刺激引起的。7.侧腹的强烈热刺激导致SP-I. i释放的小幅（20 - 35%）但可靠的增加。高于控制。8.阿片μ受体（吗啡，10 - 100 μ M;舒芬太尼，1 μ M）和δ受体（D-Ala 2-D-Leu 5-脑啡肽，1 - 10 μ M; D-Pen 2-D-Pen 5-脑啡肽，10 μ M）的假定激动剂，但不是κ受体（U 50488 H，100 - 1000 μ M）的假定激动剂，产生了剂量依赖性纳洛酮可逆的SP-1. i诱发释放减少，但不是静息释放减少。（-）-纳洛酮（而非（+）-纳洛酮）导致诱发的而非静息的SP-1. i显著增加。release.（400字处截断摘要）
1. The present experiments examine the physiology and pharmacology of the release of substance P‐like immunoreactivity (SP‐l.i.), from the spinal cord in the halothane‐anaesthetized, artificially ventilated cat. 2. Resting release of SP‐l.i. was 36 +/‐ 4 fmol/30 min (mean +/‐ S.E.; n = 106). Bilateral stimulation of the sciatic nerves at intensities which evoked activity in fibres conducting at A beta conduction velocities (greater than 40 m/s), resulted in no change in blood pressure, pupil diameter or release of SP‐l.i. Stimulation intensities which activate fibres conducting at velocities less than 2 m/s resulted in increased blood pressure, miosis and elevated release of SP‐l.i. (278 +/‐ 16% of control). 3. The relationship between nerve‐stimulation frequency and release was monotonic up to approximately 20 Hz. Higher stimulation frequencies did not increase the amounts of SP‐l.i. released. At 200 Hz there was a reduction. 4. Capsaicin (0.1 mM) increased the release of SP‐l.i. from the spinal cord and resulted in an acute desensitization to subsequent nerve stimulation. This acute effect was not accompanied by a reduction in spinal levels of SP‐l.i. measured 2 h after stimulation. 5. Cold block of the cervical spinal cord resulted in an increase in the amounts of SP‐l.i. released by nerve stimulation. 6. Pre‐treatment with intrathecal 5,6‐dihydroxytryptamine (300 micrograms) 7 days prior to the experiment caused a reduction in the dorsal and ventral horn stores of SP‐l.i., but had no effect on the release of SP‐l.i. evoked by nerve stimulation. Similar pre‐treatment with intrathecal capsaicin (300 micrograms) resulted in depletion of SP‐l.i. in the dorsal but not in the ventral horn of the spinal cord and diminished the release of SP‐l.i. evoked by nerve stimulation. 7. Intense thermal stimulation of the flank resulted in small (20‐35%), but reliable increases in the release of SP‐l.i. above control. 8. Putative agonists for the opioid mu‐receptor (morphine, 10‐100 microM; sufentanil, 1 microM), and for the delta‐receptor (D‐Ala2‐D‐Leu5‐enkephalin, 1‐10 microM; D‐Pen2‐D‐Pen5‐enkephalin, 10 microM), but not the kappa‐receptor (U50488H, 100‐1000 microM), produced a dose‐dependent, naloxone‐reversible reduction of the evoked, but not of the resting release of SP‐l.i. (‐)‐Naloxone, but not (+)‐naloxone, resulted in a significant increase in evoked but not resting SP‐l.i. release.(ABSTRACT TRUNCATED AT 400 WORDS)