强肌健力饮对肾阳虚大鼠CRH、ACTH、Cor水平的影响

目的:观察强肌健力饮对肾阳虚大鼠下丘脑组织中促肾上腺皮质激素释放激素(CRH)及血浆促肾上腺皮质激素(ACTH)、皮质醇(Cor)水平的影响,进一步探讨该方对中医肾阳虚证的防治机理.方法:将大鼠分为正常对照组、肾阳虚模型组、强肌健力饮低、中、高剂量组、右归丸阳性对照组,采用氢化可的松制备肾阳虚大鼠模型.观察动物的一般状态及其胸腺和肾上腺指数,采用放射免疫分析检测CRH、ACTH、Cor的含量.结果:①肾阳虚模型组大鼠体重及胸腺指数、肾上腺指数明显低于正常对照组(P＜0.01),CRH、ACTH、Cor含量均比正常对照组显著降低(P＜0.01).②强肌健力饮各剂量组CRH、ACTH、Cor含量均比肾阳虚模型组显著升高(P＜0.05～0.01).结论:肾阳虚时下丘脑-垂体-肾上腺轴合成、分泌和调控功能低下,而强肌健力饮能够修复该轴功能的损伤,表明该方药具有下丘脑、垂体、肾上腺轴多层次的调节作用.     

下丘脑-垂体-肾上腺轴紊乱对焦虑性抑郁模型大鼠海马结构的影响

目的研究下丘脑-垂体-肾上腺(HPA)轴紊乱对焦虑性抑郁模型大鼠海马结构的影响,探讨焦虑性抑郁的潜在发病机制。方法将大鼠随机分为空白组、溶媒组、焦虑组、抑郁组和焦虑性抑郁组,每组12只。采用慢性束缚应激联合皮质酮注射方法建立焦虑性抑郁大鼠模型,连续21 d;造模后采用高架十字迷宫(EPM)、旷场实验(OFT)、强迫游泳实验(FST)评价大鼠焦虑和抑郁样行为;HE染色检测大鼠HPA轴各组织及海马病理变化;ELISA检测大鼠血浆中促肾上腺皮质激素释放激素(CRH)、促肾上腺皮质激素(ACTH)、皮质酮(CORT)含量;Western blot检测大鼠海马糖皮质激素受体(GR)蛋白表达。结果焦虑性抑郁组大鼠进入开臂的时间、次数及自主活动次数均与焦虑组相当,不动时间显著增加,与对照组及抑郁组比较有显著差异(P0.01或P0.05);HPA轴各组织均出现不同程度损伤,海马神经元肿胀,呈空泡状;同时,血浆中CRH、ACTH和CORT含量显著增加(P0.01或P0.05),海马GR表达显著下降。结论焦虑性抑郁模型组大鼠具有显著的焦虑及抑郁样行为,其发病机制可能与机体HPA轴紊乱及其引发的脑内海马损伤密切相关。     

褪黑素对创伤后应激障碍大鼠下丘脑-垂体-肾上腺轴的影响

目的:探讨褪黑素(MLT)对足部电击所致创伤后应激障碍(PTSD)大鼠下丘脑-垂体-肾上腺(HPA)轴的影响。方法:利用足底电击法制备大鼠PTSD模型,通过腹腔注射方法给予治疗组大鼠MLT。通过拒俘反应测试检测大鼠的行为学变化,利用real time RT-PCR方法检测下丘脑中促肾上腺皮质激素释放激素(CRH)mRNA的表达,利用酶联免疫吸附试验(ELISA)检测血清中促肾上腺皮质激素(ACTH)、肾上腺素(EPI)和糖皮质激素(GC)的含量。结果:PTSD组大鼠拒俘反应明显(P<0.05),下丘脑中CRH mRNA表达升高(P<0.05),血清中ACTH和EPI明显升高(P<0.05),但是GC水平下降(P<0.05)。MLT治疗后可以明显缓解PTSD大鼠拒俘反应(P<0.05),同时降低下丘脑中CRH mRNA表达(P<0.05),降低血清中ACTH和EPI水平并升高GC的水平(P<0.05)。结论:MLT治疗可缓解PTSD大鼠的症状,并恢复HPA轴的神经内分泌平衡。     

下丘脑室旁核CRH神经元激活在慢性充血性心力衰竭中的交感兴奋作用

目的:观察慢性心衰时下丘脑室旁核(PVN)内促肾上腺皮质激素释放激素(CRH)表达变化及其与交感神经活动之间的关系。方法:健康雄性SD大鼠,冠脉结扎制备心衰模型,侧脑室插管渗透压泵持续给药。假手术组和心衰组给予人工脑脊液0.25μL/h,心衰给药组给予CRH抑制剂αh-CRH 15 mg/h。同时,选取健康雄性体内CRH合成不足的Lewis大鼠与同源纯种Fischer 344大鼠分别制备心衰模型和假手术对照进行对比研究。4周后,测定左室舒张末压(LVEDP)、左室内压最大上升和下降速率(±dp/dtmax)、右心室/体重比(RV/BW)、肺/体重比(lung/BW)、肾交感神经放电活动(RSNA)、血浆去甲肾上腺素(NE)浓度和PVN内CRH阳性神经元数目。血浆促肾上腺皮质激素(ACTH)含量。结果:与假手术组相比,SD心衰大鼠PVN内CRH阳性神经元数目明显增加,血浆ACTH浓度升高,RSNA增强,血浆NE浓度增加,LVEDP、lung/BW和RV/BW增加,±dp/dtmax降低;心衰模型后给予αh-CRH可明显逆转上述各种变化(P0.05)。Fisher 344大鼠心衰组和假手术对照相比,PVN内CRH阳性神经元数目明显增加,血浆ACTH浓度升高,RSNA增强,外周血NE浓度升高,LVEDP、RV/BW和lung/BW增加,±dp/dtmax下降(P0.05)。但Lewis大鼠心衰组和假手术对照相比,以上各指标改变均不明显。结论:慢性心衰时,下丘脑室旁核CRH神经元被激活,激活的CRH神经元可增强外周交感神经活动,加重心功能恶化。     

下丘脑-垂体-肾上腺轴在抑郁症发病中的作用

越来越多的研究表明，下丘脑一垂体一肾上腺轴(hypothalamic pituitary adrenal axic，HPA轴)在抑郁的发病机制中发挥着重要的作用。HPA轴的活化机制是：下丘脑通过垂体门脉系统运送下丘脑调节肽(促肾上腺皮质激素释放激素，CRH)到脑垂体，从而调节腺垂体的分泌。腺垂体在调节肽的作用下释放促肾上腺皮质激素(ACTH)，然后作用于肾上腺皮质，释放肾上腺皮质激素到全身。下面我们将从HPA轴的三个水平(CRH、ACTH、肾上腺皮质激素)来论述HPA轴在抑郁发病过程中的作用。     

脑室注射组胺对下丘脑室旁核促皮质素释放激素神经元的作用

目的:观察第三脑室注射组胺对下丘脑室旁核促皮质素释放激素(CRH)神经元活动的影响。方法:Fos癌蛋白免疫组化LSAB法结合双抗原标记法;半定量逆转录聚合酶链反应(RT-PCR)方法。结果:第三脑室注射组胺后,(1)下丘脑室旁核Fos阳性神经元数目明显增加(P＜0.05);(2)室旁核内的Fos阳性神经元中约有31.78%同时呈CRH阳性反应;(3)室旁核CRHmRNA含量明显升高,且有量效关系。结论:中枢组胺可以激活下丘脑室旁核的CRH神经元,并使CRH基因表达增加。     

大鼠腺垂体促肾上腺皮质激素细胞分泌方式的免疫电镜研究

实验用雄性Wistar大鼠,以在无菌条件下腹腔注射松节油的方法制成急性非特异性腹膜炎,取大鼠腺垂体用免疫电镜方法进行染色.发现促肾上腺皮质激素(ACTH)细胞内分泌颗粒向细胞表面突起,并可见细胞间隙内完整的金标记的内分泌颗粒,实验结果表明,ACTH细胞除传统认为的胞吐分泌外还有其它分泌方式.     

注射IL-1β后大鼠下丘脑室旁核内CRR/AVP基因转录的动态变化

目的 探讨IL-1β对下丘脑室旁核(PVN)内促肾上腺皮质素释放激素(CRH)和血管加压素(AVP)基因转录的影响.方法 麻醉下于Wistar大鼠右心房内留置导管,48 h后将清醒大鼠分为5组,分别于右心房内注射IL-1β(1.4 μg/kg)或生理盐水(300 μ1)后于15、120 min后断头,以及无任何处置的空白对照组.取各组大鼠躯干血,采用放射免疫分析法测定促.肾上腺皮质激素(ACTH)和AVP的浓度.利用[35S]UTP、[35S]CTP双标记RNA探针采用原位杂交组织化学方法检测各组大鼠PVN内CRH hnRNA、CRH mRNA和AVPhnRNA、AVPmRNA的表达.结果 与空白对照组相比,血浆ACTH和AVP浓度均在注射IL-1β 15 min后显著增加(P<0.01),在120 min后恢复正常.CRH hnRNA表达水平在注射IL-1β 15 min后显著增加(P<0.01),120 min后恢复正常;CRH mRNA表达水平在注射IL-1β 120min后显著增加(P<0.01).小细胞内AVP hnRNA表达水平在注射IL-1β 15 min后显著增加(P<0.01),且持续增加至120 min后,而大细胞内AVP hnRNA表达水平在注射IL-1β 120 min后显著增加(P<0.01);小细胞内AVP mRNA表达水平在注射IL-1β120 min后显著增加(P<0.01),而大细胞内AVP mRNA表达水平在注射IL-1β 15和120 min后均无明显改变.结论 共存于小细胞内的CRH、AVP基因转录的调控机制不同,而共存于大、小细胞内的AVP基因转录的调控机制也完全不同,表明不同细胞内同一基因转录的动态变化不同.     

褪黑素对SD大鼠下丘脑-垂体-肾上腺皮质的影响

目的 研究褪黑素对正常和糖尿病大鼠下丘脑-垂体-肾上腺皮质功能和超微结构的影响.方法 应用放射免疫法分别观察了低、中、高剂量(0.5mg/kg、10mg/kg、50mg/kg)褪黑素及对照药物硫辛酸(100mg/kg)连续腹腔注射3周,对SD大鼠血浆促肾上腺皮质激素释放激素(CRH)、促肾上腺皮质激素(ACTH)、皮质酮(COR)水平的影响.并运用电镜观察用药前后大鼠垂体、肾上腺皮质超微结构的变化.结果 1.正常和糖尿病大鼠低、中、高剂量褪黑素处理组CRH水平与相应对照组相比显著降低;正常大鼠低、中、高剂量褪黑素及硫辛酸处理组和糖尿病大鼠低剂量(0.5mg/kg)褪黑素、硫辛酸处理组ACTH水平比相应对照组明显降低(P＜0.05);正常大鼠低、中、高剂量褪黑素处理组和糖尿病大鼠中高剂量褪黑素处理组皮质酮水平比相应对照组显著降低(P＜0.05).2.褪黑素对正常大鼠下丘脑-垂体-肾上腺皮质超微结构无明显影响.糖尿病大鼠垂体细胞和肾上腺皮质细胞出现功能受抑制状态,褪黑素(50mg/(kg·d))处理21d后垂体促肾上腺皮质细胞和肾上腺皮质细胞代谢较处理前明显活跃.结论 褪黑素能在不同层次直接或间接地发挥对正常和糖尿病大鼠下丘脑-垂体-肾上腺(HPA)轴的抑制作用.     

褪黑素水平对抑郁症患者下丘脑-垂体-肾上腺轴功能的影响

目的探讨抑郁症患者褪黑素(MT)水平对下丘脑-垂体-肾上腺轴(HPA)功能的影响。方法对86例抑郁症患者,检测血清MT、促肾上腺皮质激素释放激素(CRH)、促肾上腺皮质激素(ACTH)、皮质醇(COR),并分析其相互关系。结果1以MT中位数(51.3ng/L)为切点,将所有抑郁症患者分为MT高值组(51.3ng/L,n=43)与MT低值组(51.3ng/L,n=43),前者血清CRH、ACTH、COR均显著低于后者(t=3.330,3.315,2.314;P0.01,0.01,0.05);2血清MT水平与CRH、ACTH水平负相关(r=-0.414,-0.329;P0.01,0.05)。结论褪黑素对抑郁症患者的HPA轴功能可能有一定的抑制作用。     

The role of hypothalamo-hypophyseal-adrenocortical system hormones in controlling pain sensitivity

The present review addresses analysis of data demonstrating the role of the hypothalamo-hypophyseal-adrenocortical axis (HHACA) in controlling pain sensitivity. Experiments on rats have demonstrated the analgesic effects of exogenous hormones of all components of the HHACA — corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and glucocorticoids — in the same models, and have also shown that the opioid and non-opioid mechanisms contribute to the development of the analgesia induced by these hormones. Endogenous glucocorticoids are involved in the development of analgesia mediated by non-opioid mechanisms. Along with the non-opioid mechanisms associated with endogenous glucocorticoids, the analgesic effect of ACTH can be mediated by the opioid mechanism. Unlike the situation with ACTH, the analgesic effect of CRH is mediated exclusively by non-opioid mechanisms, one of which is associated with HHACA hormones, while the other, appearing only on systemic administration, is not associated with these hormones. The actions of glucocorticoids on pain are mediated by neurons in the central gray matter of the midbrain. __________ Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 93, No. 11, pp. 1252–1262, November, 2007.     

急性高台应激对大鼠神经内分泌激素、相关受体及脑神经递质的影响

目的 高台应激是一种不可逃避应激,是研究应激对机体神经生理病理变化的重要模型.本研究对急性高台应激后神经内分泌激素、受体表达、脑神经递质变化以及地西泮的干预作用进行探讨.方法 大鼠随机分为空白对照组、应激+地西泮(DAP)组与应激+溶剂组.后两组于应激前30 min分别腹腔注射地西泮2 mg/kg与等量生理盐水.采用酶联免疫法测量应激后各组的血浆促肾上腺皮质激素(ACTH)、血清皮质酮(CORT)水平;采用实时定量PCR测量下丘脑促肾上腺皮质激素分泌激素(CRH)mRNA、海马糖皮质激素受体(GR)mRNA、盐皮质激素受体(MR) mRNA、5-羟色胺1a受体(5-HT1aR)mRNA水平;采用高效液相色谱电化学法测量大脑皮层匀浆液中去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)及其代谢产物5-羟吲哚乙酸(5-HIAA)水平.结果 与空白组相比,应激+溶剂组大鼠血浆ACTH、血清CORT以及海马5-HT1aR mRNA水平升高(P均＜0.05),此变化可由DAP逆转(P均＜0.05).此外,DAP还可降低应激后的下丘脑CRH mRNA,海马GR mRNA以及MR mRNA水平(P均＜0.05).然而大脑皮层匀浆液中NE、DA、5-HT、5-HIAA在应激后无变化.结论 急性高台应激可引起大鼠相关神经内分泌激素与受体表达变化,且该效应可被DAP逆转.     

不同应激方式中小鼠下丘脑与垂体中促肾上腺皮质激素释放激素、促肾上腺皮质激素表达与血清糖皮质激素水平的变化规律及加味逍遥丸的调节作用

目的了解心理和生理（小站台水环境复合）应激及纯心理（情绪）应激后不同时间小鼠下丘脑与垂体促肾上腺皮质激素释放激素（CRH）、促。肾上腺皮质激素（ACTH）的表达和血清糖皮质激素（GC）变化规律及加味逍遥丸的调节作用。方法利用小站台水环境装置应激动物和多功能条件反应箱电刺激小鼠激怒,而致试验鼠情绪紧张的纯心理应激方法制造动物模型;中药加味逍遥丸按2mg／g体重灌胃给药;免疫组化法检测CRH、ACTH蛋白;放射免疫法检测血清糖皮质激素含量。结果小站台水环境应激状态下,下丘脑CRH和垂体ACTH的表达面积都于3h明显增多;血清糖皮质激素于12h升高,并随应激时间延长继续升高。加味逍遥丸在小站台水环境应激72h时能减少下丘脑CRH、垂体ACTH的表达面积和降低反应强度,并下调血清糖皮质激素水平。在情绪应激状态下,下丘脑CRH和垂体ACTH表达面积和强度都于1d增多和增强,延长应激时间,下丘脑CRH、垂体ACTH表达和GC含量均维持在1d水平;加味逍遥丸在情绪应激5d时能降低下丘脑CRH表达强度,减少垂体ACTH的表达面积和降低强度,并下调血清糖皮质激素水平。结论小站台水环境应激状态下下丘脑CRH和垂体ACTH表达面积增多和反应强度明显增强;加味逍遥丸对应激造成的下丘脑CRH和垂体ACTH高表达有调节作用。情绪应激状态下下丘脑CRH和垂体ACTH表达面积增多和反应强度明显增强,加味逍遥丸对应激造成的下丘脑CRH和垂体ACTH高表达有调节作用。     

前庭功能锻炼对运动病大鼠血浆应激相关激素水平的影响

 目的：探讨前庭功能锻炼对运动病大鼠接受旋转刺激后血浆应激相关内分泌指标的变化,进一步阐明激素与运动病的内在联系。方法：旋转刺激72只雌性SD大鼠,根据大鼠条件性味觉厌恶程度判断其运动病敏感性。用放射免疫分析法测定血浆皮质酮、促肾上腺皮质激素（ACTH）、促肾上腺皮质素释放激素（CRH）和精氨酸加压素（AVP）水平,观察旋转刺激对血浆激素水平的影响。接着,进行前庭功能锻炼1个月,等大鼠对运动病产生耐受后,再观察旋转刺激对血浆激素水平的影响。结果：（1）大鼠经过1个月的前庭功能锻炼后,糖精水厌饮行为完全被抑制,说明达到了习服的效果;（2）旋转刺激可引起大鼠血浆皮质酮、ACTH和AVP水平升高（P<0.05或P<0.01）,但经前庭功能锻炼后,旋转刺激对皮质酮的升高作用明显减弱;（3）不敏感组大鼠血浆皮质酮、ACTH、CRH和AVP的水平均高于敏感组,尤其是旋转刺激后的皮质酮、ACTH水平与CRH的基础水平（P<0.05或P<0.01）。并且,经过前庭功能锻炼,皮质酮、ACTH与CRH的基础水平在2组均高于前庭功能锻炼前（P<0.05或P<0.01）,AVP基础水平也有一定程度的升高。结论：（1）给大鼠进行前庭功能锻炼可以达到习服的目的,抑制运动病的发生;（2）大鼠运动病敏感性的个体差异可能与血浆应激相关激素基础水平的高低相关。     

Histological and morphofunctional parameters of the hypothalamic–pituitary–adrenal system are sensitive to daidzein treatment in the adult rat

The isoflavone, daidzein is a biologically active, plant-derived compound that interacts with estrogen receptors. Data from previous studies have suggested that daidzein exerts beneficial effects in many diseases; however, as an endocrine disrupter, it may also alter the functioning of the endocrine system. Data regarding the effect of daidzein on the morphofunctional and histological parameters of the hypothalamic–pituitary–adrenal (HPA) system is still lacking. Therefore, using the newCAST stereological software, we investigated the effects of chronic (21 days) daidzein treatment on corticotropin-releasing hormone (CRH) neurons within the hypothalamus and corticotropes (ACTH cells) in the pituitary, while image analysis was employed to-examine the intensity of fluorescence of CRH in the median eminence (ME) and adrenocorticotropin hormone in the pituitary in adult orchidectomized (Ovx) rats. Circulating ACTH and corticosterone levels were also analyzed. This study showed that daidzein treatment decreased the volume density of CRH neurons within the paraventricular nucleus as well as CRH immunofluorescence in the ME. The total number of ACTH cells was decreased, while ACTH cell volume and the intensity of ACTH fluorescence were increased following daidzein treatment. Both ACTH and corticosterone blood levels were increased after daidzein administration. The results of performed experiments clearly demonstrate that volume density of CRH neurons; total number and volume of ACTH cells, as well as stress hormones levels are vulnerable to the effects of daidzein.     

Factors and common conditions associated with adolescent dietary supplement use: an analysis of the National Health and Nutrition Examination Survey (NHANES)

Background

Studies show that electroacupuncture (EA) has beneficial effects in patients with inflammatory diseases. This study investigated the mechanisms of EA anti-inflammation, using a rat model of complete Freund's adjuvant (CFA)-induced hind paw inflammation and hyperalgesia.

Design

Four experiments were conducted on male Sprague-Dawley rats (n = 6–7/per group). Inflammation was induced by injecting CFA into the plantar surface of one hind paw. Experiment 1 examined whether EA increases plasma adrenocorticotropic hormone (ACTH) levels. Experiments 2 and 3 studied the effects of the ACTH and corticotropin-releasing hormone (CRH) receptor antagonists, ACTH_(11–24) and astressin, on the EA anti-edema. Experiment 4 determined whether EA activates CRH neurons in the paraventricular nucleus of the hypothalammus. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice for 20 min each, once immediately post and again 2 hr post-CFA. Plasma ACTH levels, paw thickness, and paw withdrawal latency to a noxious thermal stimulus were measured 2 h and 5 h after the CFA.

Results

EA significantly increased ACTH levels 5 h (2 folds) after CFA compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in ACTH. ACTH_(11–24) and astressin blocked EA anti-edema but not EA anti-hyperalgesia. EA induced phosphorylation of NR1, an essential subunit of the N-methyl-D-aspartic acid (NMDA) receptor, in CRH-containing neurons of the paraventricular nucleus.

Conclusion

The data demonstrate that EA activates CRH neurons to significantly increase plasma ACTH levels and suppress edema through CRH and ACTH receptors in a rat model of inflammation.     

Corticotropin releasing hormone and gonadotropin secretion in physically active males after acute exercise

Summary Plasma concentrations of corticotropin releasing hormone (CRH) and the serum concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, adrenocorticotropic hormone (ACTH) and cortisol were measured in seven physically active males after acute exercise on a treadmill using the Bruce protocol. Measurements were made in the basal pre-exercise state, immediately after exercise, and at 30-min intervals for 3 h after exercise. Serum LH concentrations declined following exercise reaching nadir values between 60 and 180 min after exercise (90 min post exercise in the group). The nadir values in individual volunteers were significantly lower than both the baseline and post-exercise levels. This fall in serum LH concentration appeared to follow a slight but significant elevation of the plasma concentration of CRH which reached peak levels when measured immediately post exercise. Plasma ACTH concentrations paralleled the rise in CRH, but fell to undetectable levels of below 13.8 nmol · l^–1 (< 5 ng · l^–1) 60 min after exercise. Plasma cortisol concentrations peaked approximately 30 min after the rise in ACTH, after which they gradually declined to baseline levels. Plasma testosterone concentrations paralleled the concentrations of LH. The data suggest that CRH, on the basis of its previously described gonadotropin-depressant property, may be the hormone involved in the exercise-mediated decline in serum LH. Alternatively, some as yet unidentified factor(s), may be involved in producing the altered concentrations of both LH and CRH.     

Immunoreactivity of hypothalamo-neurohypophysial neurons which secrete corticotropin-releasing hormone (CRH) and vasopressin (Vp): immunocytochemical evidence for a correlation with their functional state in colchicine-treated rats

Summary The specific immunoreactivity of neurons containing corticotropin-releasing hormone (CRH) or vasopressin (Vp) was studied both centrally, in the parvocellular division of the paraventricular nucleus, and distally, in the external median eminence. Control rats were compared with adrenalectomized rats and with animals supplemented with corticosterone or dexamethasone, either without additional treatment, or 24, and 48 h after an intraventricular injection of colchicine. In all groups of animals, colchicine induced a progressive and parallel decrease in both CRH and Vp immunoreactivity within the axons of the external median eminence. A semi-quantitative estimation of this axonal immunostaining showed that the decrease was clearly correlated with the axons' releasing activity according to the different functional states of the adrenocorticotropic system. Increased rates of hormonal release induced by adrenalectomy could be seen in the accelerated depletion of axonal immunoreactivity whereas corticosteroid supplementation had the opposite effect. Correspondingly, the progressive intensification of the CRH and Vp immunoreactivity within the perikarya following colchicine treatment was further markedly enhanced in adrenalectomized rats and diminished after corticosteroid supplementation. Taken together, these data suggest that in these neurons, perikaryal hormone synthesis may be closely related to the releasing activity of the axon terminals. They further point to appropriate colchicine treatment as useful tool for evaluating the functional state of CRH and Vp neurons of the parvocellular paraventricular nucleus under various experimental conditions.