NEUROPEPTIDE-E-I ANTAGONIZES THE ACTION OF MELANIN-CONCENTRATING HORMONE ON STRESS-INDUCED RELEASE OF ADRENOCORTICOTROPIN IN THE RAT
NEUROPEPTIDE-E-I ANTAGONIZES THE ACTION OF MELANIN-CONCENTRATING HORMONE ON STRESS-INDUCED RELEASE OF ADRENOCORTICOTROPIN IN THE RAT
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DOI：
10.1111/j.1365-2826.1995.tb00761.x
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发表时间：
1995-04-01
影响因子：
3.2
通讯作者：
NAHON, JL
中科院分区：
文献类型：
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作者：
BLUETPAJOT, MT;PRESSE, F;NAHON, JL
在哺乳动物中，黑色素浓缩激素（melanin-concentrating hormone， MCH）的生理作用尚不清楚，但该肽可能参与了下丘脑垂体肾上腺（hypothalamopititary adrenaline， HPA）轴在适应应激过程中的中枢控制。对大鼠MCH (rMCH) cDNA的克隆和测序发现，MCH前体中存在编码的其他肽，其中：神经肽(N)谷氨酸(E)异亮氨酸(I)酰胺（NEI）在大鼠下丘脑与MCH共同加工和分泌。在目前的工作中，我们审查了：(1) rMCH mRNA表达的模式在光明与黑暗条件下大鼠下丘脑和(2)的影响intracerebroventricular (ICV)注射rMCH和NEI控制基底或醚stress-modified释放促肾上腺皮质激素(ACTH)、催乳素(PRL)和生长激素(GH)分泌体内点灯和点火条件,我们的数据表明,rMCH mRNA水平在点灯期间不改变,但是增加后的黑暗,无论是单独使用还是联合使用，rMCH和NEI在任何测试时间都不会改变GH和PRL的基础分泌，也不会改变应激引起的这两种激素分泌的变化。在与ACTH昼夜节律高峰相对应的光照期结束时，施用rMCH而不是NEI导致ACTH水平下降，而MCH在周期的光照期（即基础ACTH水平已经很低的时候）无效。使用适度的醚诱导应激，ACTH水平仅在周期的黑暗阶段受到刺激，rMCH（63或210 nmol）阻止ACTH释放的增加，而NEI单独不改变应激反应，在应激前给药两种肽可消除rMCH诱导的ACTH血浆水平抑制。这些数据表明，rMCH可能作为一种中枢促肾上腺皮质激素抑制因子参与血浆ACTH水平的昼夜节律性，而NEI可以拮抗其作用。
The physiological role of melanin-concentrating hormone (MCH) in mammals is still very elusive, but this peptide might participate in the central control of the hypothalamopituitary adrenal (HPA) axis during adaptation to stress, Cloning and sequencing of the rat MCH (rMCH) cDNA revealed the existence of additional peptides encoded into the MCH precursor, Among these peptides, neuropeptide (N) glutamic acid (E) isoleucine (I) amide (NEI) is co-processed and secreted with MCH in rat hypothalamus. In the present work we examined: (1) The pattern of rMCH mRNA expression during the light and dark conditions in the rat hypothalamus and (2) The effect of intracerebroventricular (ICV) injections of rMCH and NEI in the control of basal or ether stress-modified release of corticotropin (ACTH), prolactin (PRL) and growth hormone (GH) secretion in vivo in light-on and light-off conditions, Our data indicate that rMCH mRNA levels do not change during the light-on period, but increase after the onset of darkness, Either alone or co-administered, rMCH and NEI do not modify basal secretion of GH and PRL at any time tested nor do they alter ether stress-induced changes in these two hormonal secretions. At the end of the light on period corresponding to the peak of the circadian rhythm in ACTH, administration of rMCH but not NEI leads to a decrease in ACTH levels while MCH is not effective during the light off period of the cycle (i.e. when basal ACTH levels are already low). Using a moderate ether induced stress, ACTH levels are only stimulated during the dark phase of the cycle, rMCH (63 or 210 nmoles) prevents the rise in ACTH release while NEI alone does not modify the stress response, Go-administration of both peptides before stress results in an abolition of the rMCH induced inhibition of ACTH plasma levels, Taken together, these data indicate that rMCH may act as a central corticotropin inhibitory factor involved in the circadian rhythmicity of plasma ACTH levels and that NEI antagonizes its action.