P物质可促使豚鼠小肠肌间神经丛释放γ-氨基丁酸。
Substance P provoked gamma-aminobutyric acid release from the myenteric plexus of the guinea-pig small intestine.
作者信息
Tanaka C, Taniyama K
出版信息
J Physiol. 1985 May;362:319-29. doi: 10.1113/jphysiol.1985.sp015680.
The release of [3H]gamma-aminobutyric acid (GABA) from the isolated small intestine of the guinea-pig pre-loaded with [3H]GABA was measured in the presence of substance P and vasoactive intestinal polypeptide (VIP). Substance P (10(-10)-10(-7) M) produced a dose-dependent increase in the fractional rate of [3H]GABA release. VIP, even at 10(-7) M, did not affect the spontaneous [3H]GABA release nor the release of [3H]GABA evoked by electrical transmural stimulation (0.5 ms, 15 V, 10 Hz for 30 s). The release of endogenous GABA from the isolated small intestine was measured in the presence of substance P (10(-9) M). After 60 min superfusion, the spontaneous release of GABA was 4.61 +/- 0.14 pmol min-1 g-1 wet wt. (n = 20). Substance P (10(-9) M) produced an approximate 2-fold spontaneous release of endogeneous GABA (8.74 +/- 0.21 pmol min-1 g-1 wet wt. (n = 10)). Perfusion with Ca-free medium containing 1 mM-EGTA and tetrodotoxin (3 X 10(-7) M) inhibited the release of endogenous GABA evoked by substance P (10(-9) M). (D-Pro2, D-Trp7,9) substance P (10(-6) M) antagonized the release of endogenous GABA evoked by substance P (10(-9) M). These results indicate that substance P induces a neuronal release of GABA through its receptor located in the guinea-pig small intestine. Substance P (10(-11)-10(-7) M) produced a dose-dependent increase in the fractional rate of [3H]acetylcholine (ACh) release from the isolated small intestine pre-loaded with [3H]choline. The release of [3H]ACh evoked by substance P (10(-9) M) was inhibited by perfusion with Ca-free medium containing 1 mM-EGTA, tetrodotoxin (3 X 10(-7) M) and (D-Pro2, D-Trp7,9)substance P (10(-6) M). Bicuculline (10(-6) M) inhibited the release of [3H]ACh evoked by substance P (10(-9) M) by 68.1 +/- 4.6% (n = 5), thereby suggesting that the substance P-evoked ACh release is partly mediated through the endogenous GABA released by substance P. These results provide evidence for the neurotransmitter role of GABA and a possible excitatory role of substance P on the GABAergic neurones in the myenteric plexus of the guinea-pig small intestine.
在存在P物质和血管活性肠肽（VIP）的情况下，测定了预先加载[³H]γ-氨基丁酸（GABA）的豚鼠离体小肠中[³H]GABA的释放。P物质（10⁻¹⁰ - 10⁻⁷ M）使[³H]GABA释放的分数率呈剂量依赖性增加。即使在10⁻⁷ M时，VIP也不影响[³H]GABA的自发释放，也不影响经壁电刺激（0.5毫秒，15伏，10赫兹，持续30秒）诱发的[³H]GABA释放。在存在P物质（10⁻⁹ M）的情况下，测定了离体小肠中内源性GABA的释放。60分钟的超灌注后，GABA的自发释放为4.61±0.14皮摩尔·分钟⁻¹·克⁻¹湿重（n = 20）。P物质（10⁻⁹ M）使内源性GABA的自发释放增加了约2倍（8.74±0.21皮摩尔·分钟⁻¹·克⁻¹湿重（n = 10））。用含有1 mM - EGTA和河豚毒素（3×10⁻⁷ M）的无钙培养基灌注可抑制P物质（10⁻⁹ M）诱发的内源性GABA释放。（D-脯氨酸²，D-色氨酸⁷,⁹）P物质（10⁻⁶ M）拮抗P物质（10⁻⁹ M）诱发的内源性GABA释放。这些结果表明，P物质通过其位于豚鼠小肠中的受体诱导GABA的神经元释放。P物质（10⁻¹¹ - 10⁻⁷ M）使预先加载[³H]胆碱的离体小肠中[³H]乙酰胆碱（ACh）释放的分数率呈剂量依赖性增加。用含有1 mM - EGTA、河豚毒素（3×10⁻⁷ M）和（D-脯氨酸²，D-色氨酸⁷,⁹）P物质（10⁻⁶ M）的无钙培养基灌注可抑制P物质（10⁻⁹ M）诱发的[³H]ACh释放。荷包牡丹碱（10⁻⁶ M）使P物质（10⁻⁹ M）诱发的[³H]ACh释放抑制了68.1±4.6%（n = 5），从而表明P物质诱发的ACh释放部分是通过P物质释放的内源性GABA介导的。这些结果为GABA的神经递质作用以及P物质对豚鼠小肠肌间神经丛中GABA能神经元可能的兴奋作用提供了证据。
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