Serotonergic fibers induce a long-lasting inhibition of monosynaptic reflex in the neonatal rat spinal cord
Serotonergic fibers induce a long-lasting inhibition of monosynaptic reflex in the neonatal rat spinal cord
复制标题
血清素能纤维诱导新生大鼠脊髓单突触反射的长期抑制
DOI：
10.1016/0306-4522(92)90162-u
复制
发表时间：
1992
期刊：
影响因子：
3.3
通讯作者：
K. Yoshioka
中科院分区：
文献类型：
--
作者：
H. Yomono;H. Suzuki;K. Yoshioka
在新生大鼠的脊髓上，研究了长时间下行抑制单突触反射的递质机制。从腰前根(L3-L5)细胞外记录刺激背根引起的单突触反射。电刺激半横断脊髓的上胸段，对单突触反射的抑制作用持续约40 S。利血平(1μM)或5，7-二羟色胺(10μM)灌流2~6 h可明显减轻这种下行抑制作用，利血平(1μM)灌流4 h可显著降低新生大鼠脊髓5-羟色胺、多巴胺和去甲肾上腺素的含量，而5，7-二羟色胺(10μM)灌流4 h则降低5-羟色胺和多巴胺的含量。5-羟色胺摄取阻断剂西酞普兰(10 NM)可明显增强这种下行抑制作用，而5-羟色胺拮抗剂酮丝氨酸(10-100 nM)可阻断该抑制作用。脊髓内应用5-羟色胺可抑制单突触反射，后者的一部分可被酮丝氨酸阻断。酮色林也适度地阻断了去甲肾上腺素和多巴胺引起的单突触反射的抑制。酚妥拉明(10μM)可阻断去甲肾上腺素和多巴胺的抑制作用，但不影响5-羟色胺的抑制作用和下行抑制作用，提示5-羟色胺参与下行抑制作用，但不参与多巴胺和去甲肾上腺素的作用。除酮色林外，与5-羟色胺2受体有亲和力的利坦色林、氟哌啶醇和哌安酮，以及5-羟色胺1和5-羟色胺2受体(均为1μM)的拮抗剂螺环酮和甲硫平也可阻断这种下行抑制作用。另一方面，5-羟色胺1C和5-羟色胺2拮抗剂Mesulergine(1μM)和5-羟色胺3拮抗剂ICS205-930和Qupazine(均为1μM)既不抑制下行抑制，也不抑制5-羟色胺引起的单突触反射抑制。使用这些拮抗剂的结果有利于5-羟色胺2受体的参与，而使用Mesulergine的结果与这一观点不一致。5-羟色胺1激动剂，如8-羟基-2-(二正丙氨基)四氢呋喃、丁螺环酮和5-羧氨基色胺，以及5-羟色胺3激动剂2-甲基-5-羟色胺，对单突触反射有持久的抑制作用，这种抑制可被酮丝氨酸阻断，而5-羟色胺2激动剂S-(+)-α-甲基-5-羟色胺则引起双相抑制，仅后一种成分被酮丝氨酸阻断。5-carboxyamidotryptamine，8-OH-hydroxy-2-(di-n-propyl-amino)tetralin和丁螺环酮的强烈兴奋作用表明，负责抑制单突触反射的受体类似于5-羟色胺1型。因此，参与抑制的5-羟色胺受体不能简单地归类为5-羟色胺1、5-羟色胺2或5-羟色胺3亚型。连续两次50ms刺激后，第二单突触反射小于第一单突触反射。对上胸段的条件性刺激或应用5-羧氨基色胺或丁螺环酮，以及低钙介质，增加了第二单突触反射与第一单突触反射的幅度之比，因此第二反应通常在…中变得更大
The transmitter mechanism of a long-lasting descending inhibition of the monosynaptic reflex was investigated in the isolated spinal cord of the neonatal rat. The monosynaptic reflex elicited by dorsal root stimulation was recorded extracellularly from a lumbar ventral root (L3–L5). Electrical stimulation of the upper thoracic part of the hemisected cord caused an inhibition lasting about 40 s of the monosynaptic reflex. This descending inhibition was markedly attenuated by perfusing the spinal cord with reserpine (1 μM) or 5,7-dihydroxytryptamine (10 μM) for 2–6 h. The perfusion with reserpine (1 μM) for 4 h significantly decreased the contents of 5-hydroxytryptamine, dopamine, and norepinephrine of the neonatal rat spinal cord, whereas the perfusion with 5,7-dihydroxy-tryptamine (10 μM) for 4 h decreased the contents of 5-hydroxytryptamine and dopamine. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine uptake blocker, citalopram (10 nM), and was blocked by a 5-hydroxytryptamine antagonist, ketanserin (10–100 nM). Application of 5-hydroxytryptamine to the spinal cord induced an inhibition of the monosynaptic reflex, a later part of which was blocked by ketanserin. Ketanserin also moderately blocked inhibitions of the monosynaptic reflex caused by norepinephrine and dopamine. Phentolamine (10 μM) abolished the depressant actions of norepinephrine and dopamine, but did not affect that of 5-hydroxytryptamine or the descending inhibition.These results strongly suggest the involvement of 5-hydroxytryptamine, but not dopamine nor norepinephrine, in the descending inhibition. Besides ketanserin, the descending inhibition was blocked by ritanserin, haloperidol, and pipamperone, which have affinities to 5-hydroxytryptamine2receptors, and also by spiperone and methiothepin, which are antagonists at both 5-hydroxytryptamine1and 5-hydroxy-tryptamine2receptors (all 1 μM). On the other hand, a 5-hydroxytryptamine1Cand 5-hydroxytryptamine2antagonist, mesulergine (1 μM), and 5-hydroxytryptamine3antagonists, ICS 205–930 and quipazine (both 1 μM), did not depress either the descending inhibition or the 5-hydroxytryptamine-evoked inhibition of the monosynaptic reflex. The results with these antagonists favor the involvement of 5-hydroxytryptamine2receptors although the results with mesulergine disagree with this notion. 5-Hydroxytryptamine1agonists, such as8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, and 5-carboxyamidotryptamine, and a 5-hydroxytryptamine3agonist, 2-methyl-5-hydroxytryptamine, induced a long-lasting inhibition of the monosynaptic reflex, which was blocked by ketanserin whereas a 5-hydroxytryptamine2agonist, S-(+)-α-methyl-5-hydroxytryptamine, evoked a biphasic inhibition, in which only the later component was blocked by ketanserin. The potent agonistic action of 5-carboxyamidotryptamine,8-OH-hydroxy-2-(di-n-propyl-amino)tetralin and buspirone suggests that the receptor responsible for the inhibition of the monosynaptic reflex has a resemblance to 5-hydroxytryptamine1type. Thus the 5-hydroxytryptamine receptors involved in the inhibition cannot be classified simply as 5-hydroxytryptamine1, 5-hydroxytryptamine2, or 5-hydroxytryptamine3subtypes. When two successive stimuli with an interval of 50 ms were given to the dorsal root, the second monosynaptic reflex was smaller than the first. The conditioning stimulation of the upper thoracic segments or applications of 5-carboxyamidotryptamine or buspirone, as well as a Iow-Ca2+medium, increased the ratio of the amplitude of the second monosynaptic reflex to the first so that the second response often became larger …
血清素受体的亚型。
DOI：
10.1146/annurev.pa.30.040190.001515
发表时间：
1990
影响因子：
12.5
作者：
Frazer,A;Maayani,S;Wolfe,BB
通讯作者：
Wolfe,BB