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首页> 外文期刊>Brain research >Serotonergic mechanism of the lateral parabrachial nucleus and relaxin-induced sodium intake.
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Serotonergic mechanism of the lateral parabrachial nucleus and relaxin-induced sodium intake.

机译：臂外侧臂旁核的血清素能机制和松弛素诱导的钠摄入。

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It has been shown that central or peripheral injections of the peptide relaxin induces water intake, not sodium intake in rats. Important inhibitory mechanisms involving serotonin and other neurotransmitters in the control of water and NaCl intake have been demonstrated in the lateral parabrachial nucleus (LPBN). In the present study, we investigated the effects of bilateral injections of methysergide (serotonergic receptor antagonist) into the LPBN on intracerebroventricular (i.c.v.) relaxin-induced water and NaCl intake in rats. Additionally, the effect of the blockade of central angiotensin AT(1) receptors with i.c.v. losartan on relaxin-induced water and NaCl intake in rats treated with methysergide into the LPBN was also investigated. Male Holtzman rats with cannulas implanted into the lateral ventricle (LV) and bilaterally in the LPBN were used. Intracerebroventricular injections of relaxin (500 ng/1 microl) induced water intake (5.1+/-0.7 ml/120 min), but not significant 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Bilateral injections of methysergide (4 microg/0.2 microl) into the LPBN strongly stimulated relaxin-induced 1.8% NaCl intake (34.5+/-10.9 ml/120 min) and slightly increased water intake (10.5+/-4.9 ml/120 min). The pretreatment with i.c.v. losartan (100 microg/1 microl) abolished the effects of i.c.v. relaxin combined with LPBN methysergide on 1.8% NaCl intake (0.5+/-0.4 ml/120 min). Losartan (100 microg/1 microl) also abolished relaxin-induced water intake in rats injected with methysergide into the LPBN (1.6+/-0.8 ml/120 min) or not (0.5+/-0.3 ml/120 min). Losartan (50 microg/1 microl) partially reduced the effects of relaxin. The results show that central relaxin interacting with central angiotensinergic mechanisms induces NaCl intake after the blockade of LPBN serotonergic mechanisms.
机译：已经显示，中央或周边注射肽松弛素诱导大鼠进水，而不是钠摄入。在臂外侧臂旁核（LPBN）中已证明了涉及5-羟色胺和其他神经递质控制水和NaCl摄入的重要抑制机制。在本研究中，我们调查了LPBN双边注射美塞麦肽（5-羟色胺能受体拮抗剂）对大鼠脑室内（i.c.v.）松弛素诱导的水和NaCl摄入的影响。此外，i.c.v。阻断中央血管紧张素AT（1）受体的作用。还研究了氯沙坦对松弛素诱导的水和NaCl摄入量的影响，该大鼠用美塞麦肽治疗了LPBN。使用雄性Holtzman大鼠，将插管植入侧脑室（LV）并在LPBN两侧植入。脑室内注射松弛素（500 ng / 1微升）诱导水摄入（5.1 +/- 0.7 ml / 120分钟），但没有明显的1.8％NaCl摄入（0.5 +/- 0.4 ml / 120分钟）。向LPBN双边注射甲基化麦角麦角（4微克/0.2微升）可以强烈刺激松弛素诱导的1.8％NaCl摄入（34.5 +/- 10.9 ml / 120分钟）和略微增加的水摄入（10.5 +/- 4.9 ml / 120分钟） 。 i.c.v.的预处理氯沙坦（100 microg / 1 microl）取消了i.c.v.松弛素与LPBN甲基麦角甘油酯联合摄取1.8％NaCl（0.5 +/- 0.4 ml / 120分钟）。氯沙坦（100微克/ 1微升）也取消了在向LPBN中注射美塞麦肽（1.6 +/- 0.8毫升/ 120分钟）或未注射（0.5 +/- 0.3毫升/ 120分钟）大鼠中松弛素诱导的水摄入。氯沙坦（50微克/ 1微升）部分降低了松弛素的作用。结果表明，中枢松弛素与中枢血管紧张素能机制相互作用可诱导LPBN血清素能机制被阻断后NaCl的摄入。

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