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首页> 外文期刊>Journal of Neurophysiology >Neurotensin excites periaqueductal gray neurons projecting to the rostral ventromedial medulla.
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Neurotensin excites periaqueductal gray neurons projecting to the rostral ventromedial medulla.

机译：神经降压素激发投射到延髓腹膜延髓的导水管周围灰色神经元。

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Microinjection of neurotensin into the midbrain periaqueductal gray (PAG) produces a potent and naloxone-insensitive analgesic effect. To test the hypothesis that neurotensin induces the analgesic effect by activating the PAG-rostral ventromedial medulla (RVM) descending antinociceptive pathway, PAG neurons that project to RVM (PAG-RVM) were identified by microinjecting DiI(C18), a retrograde tracing dye, into the rat RVM. Subsequently, fluorescently labeled PAG-RVM projection neurons were acutely dissociated and selected for whole cell patch-clamp recordings. During current-clamp recordings, neurotensin depolarized retrogradely labeled PAG-RVM neurons and evoked action potentials. Voltage-clamp recordings indicated that neurotensin excited PAG-RVM neurons by opening the voltage-insensitive and nonselective cation channels. Both SR 48692, a selective NTR-1 antagonist, and SR 142948A, a nonselective antagonist of NTR-1 and NTR-2, failed to prevent neurotensin from exciting PAG-RVM neurons. Neurotensin failed to evoke cationic currents after internally perfusing PAG-RVM projection neurons with GDP-beta-S or anti-G(alpha q/11) antiserum. Cellular Ca(2+) fluorescence measurement using fura-2 indicated that neurotensin rapidly induced Ca(2+) release from intracellular stores of PAG-RVM neurons. Neurotensin-evoked cationic currents were blocked by heparin, an IP(3) receptor antagonist, and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a fast chelator of Ca(2+). These results suggest that by activating a novel subtype of neurotensin receptors, neurotensin depolarizes and excites PAG-RVM projection neurons through enhancing Ca(2+)-dependent nonselective cationic conductance. The coupling mechanism via G(alpha q/11) proteins is likely to involve the production of IP(3), and subsequent IP(3)-evoked Ca(2+) release leads to the opening of nonselective cation channels.
机译：将神经降压素微注射入中脑导水管周围灰色区（PAG），可产生有效且对纳洛酮不敏感的镇痛作用。为了验证神经降压素通过激活PAG-玫瑰腹侧延髓（RVM）降抗伤害感受途径诱导镇痛作用的假设，通过微注射DiI（C18）（一种逆行示踪染料）鉴定了投射到RVM（PAG-RVM）的PAG神经元，进入大鼠RVM。随后，将荧光标记的PAG-RVM投射神经元急性解离并选择用于全细胞膜片钳记录。在电流钳记录期间，神经降压素使逆行标记的PAG-RVM神经元去极化并诱发动作电位。电压钳记录表明，神经降压素通过打开对电压不敏感的非选择性阳离子通道来激发PAG-RVM神经元。选择性的NTR-1拮抗剂SR 48692和NTR-1和NTR-2的非选择性拮抗剂SR 142948A均未能阻止神经降压素激发PAG-RVM神经元。在内部将PAG-RVM投射神经元与GDP-β-S或抗G（alpha q / 11）抗血清灌输后，神经降压素未能引起阳离子电流。使用fura-2的细胞Ca（2+）荧光测量表明，神经降压素迅速诱导从PAG-RVM神经元的细胞内存储释放Ca（2+）。神经降压素诱发的阳离子电流被肝素（一种IP（3）受体拮抗剂）和1,2-双（2-氨基苯氧基）乙烷-N，N，N'，N'-四乙酸（BAPTA）（一种快速螯合剂）阻断Ca（2+）。这些结果表明，通过激活一种新型的神经降压素受体亚型，神经降压素可以通过增强Ca（2+）依赖性非选择性阳离子电导去极化和激发PAG-RVM投影神经元。通过G（alpha q / 11）蛋白质的耦合机制可能涉及IP（3）的产生，随后IP（3）诱发的Ca（2+）释放导致非选择性阳离子通道的打开。

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