大鼠深部松果体的神经支配和去双侧颈上节后深部松果体的变化

应用电镜观察18只正常大白鼠和8只切除双侧颈上节8周后大白鼠的深部松果体。在非手术大鼠的深部松果体中可见交感神经无髓纤维终末,它含有小颗粒泡,多位于血管周隙,也见于松果体细胞间。具有大颗粒泡的无髓神经纤维终末见于深部松果体,且与含清亮泡的神经末梢有突触性联系。深部松果体中存在大量来自缰核和后连合的有髓和无髓神经纤维。切除双侧颈上节后,大鼠深部松果体发生变化,松果体细胞核明显增大,胞浆中有不同形态空泡形成。细胞膜出现大量皱褶,细胞体积变小。交感神经终末呈清亮型溃变象。     

松果体内的神经纤维终末同松果体细胞的联系—电镜定量研究

目的研究松果体内神经纤维终末同松果体细胞间的联系方式.方法取12只成年雄性SD大鼠浅松果体,作常规电镜包埋,电镜下等距随机选点观察拍照并作形态定量测试.结果(1)松果体细胞体积约占松果体体积的75.9%±3.8(X±S-x),松果体细胞间隙和血管周围间隙体积占整个松果体体积的22.0%±3.5;在血管周围间隙中松果体细胞游离面表面积占松果体细胞整个界面面积的46%;(2)松果体细胞的球状突起轮廓数共计数155个,其中101个游离在血管周围间隙内;(3)共计数各种类型的神经纤维终末轮廓数248个,其中221个游离在血管周围间隙内,23个与松果体细胞胞体相贴,1个与细胞突起相贴,3个与松果体细胞形成突触.结论提示进入松果体的交感神经纤维终末对松果体细胞活动的调控主要是通过神经体液途径.     

松果体的神经支配

电镜观察松果体实质,证明充满联合神经分支的薄层有神经纤维,这些纤维与明、暗细胞及神经胶质细胞的胞体和突起紧密相贴。接触点,胞膜增厚,髓鞘内主致密线消失,周期间线空隙加宽,出现施兰氏切迹样结构。无髓交感神经纤维终末膨大,含致密中心小泡,多分布于松果体细胞旁及血管周。本文阐明松果体系由联合神经及交感神经双重支配。     

荧光金顺行追踪结合免疫荧光组化法在大鼠松果体神经供给研究中的应用

哺乳类动物的松果体 ( Pineal body)是一个重要的神经内分泌器官 ,具有多种生理功能 ,这些功能与其神经供给有着密切的关系。以往的许多研究曾通过摘除双侧颈上交感神经节 ,逆行追踪等手段来证明松果体主要接受颈上交感神经节的节后神经纤维支配 ,但尚未见将示踪剂直接注入双侧颈上交感神经节以了解颈上交感神经节内直接投射到松果体的神经纤维数量、分布及性质的详细报道。为此 ,我们将荧光金 ( fluoro- gold,FG)顺行追踪结合免疫荧光组化法应用于松果体神经供给的研究之中。1　材料和方法1 .1　动物选择 :成年健康雄性 SD大鼠 (华西医大…     

大鼠松果体内生长抑素免疫反应阳性细胞和纤维

哺乳动物松果体除了分泌胺类激素(如褪黑素)外,在松果体内也发现了多种肽类物质,如生长抑素等[1-4].但是,关于生长抑素是存在于有突起的松果体细胞内,还是位于支配松果体的神经纤维内,以及数量的多少,不同研究者间的报道差异较大[5-6].因此,本研究对大鼠松果体进行生长抑素的免疫组织化学显色观察,以探讨松果体合成与分泌生长抑素的情况.     

成年牦牛松果体的光镜和电镜观察

目的 探讨成年牦牛松果体形态结构特征,为哺乳动物松果体形态结构研究积累资料.方法 光镜HE染色、浸银染色和透射电子显微镜技术.结果 光镜下,牦牛松果体由松果体细胞、少量的神经胶质细胞、毛细血管和神经等组成.电镜下,松果体细胞电子致密度低,细胞质内含丰富的线粒体、粗面内质网、滑面内质网、微管、微丝和核糖体;高尔基复合体数量极少,典型异质细胞器突触带呈球形,多位于质膜附近.神经胶质细胞的细胞质内含丰富的线粒体,其胞体突起呈球形膨大伸入到松果体细胞之间.松果体细胞以及神经胶质细胞间均存在突触和连接复合体.牦牛松果体内毛细血管为连续型,其远腹侧血管周围可见色素细胞.结论 成年牦牛松果体细胞内存在神经上皮样和腺上皮样2种细胞连接方式.毛细血管为连续型.松果体细胞内细胞器发达,但很少观察到高尔基复合体.     

大鼠松果体内含5-羟色胺,血管活性肠多肽及P物质纤维的免疫组化观察

用免疫组化ABC法,研究了正常和摘除双侧颈上神经节后的大鼠松果体浅部内含5-羟色胺、血管活性肠多肽及P物质纤维.结果显示:(1)对照组松果体浅部内含5-羟色胺纤维非常丰富.且松果体细胞也呈阳性反应.实验组含5-羟色胺纤维显著减少,细胞的免疫反应强度也降低,与对照组相比,差异有显著性(P<0.01 ).(2)含血管活性肠多肽纤维主要分布在血管周围间隙,数量较少.实验组和对照组间纤维数量无明显差异.(3)含P物质纤维数量很少,呈典型的串珠状,主要分布在腺细胞之间.摘除双侧颈上神经节后对P物质纤维数量没有影响.     

大鼠松果体衰老的形态学研究

目的 探讨松果体形态结构的衰老性变化,为进一步研究松果体与衰老的关系提供形态学基础。方法 随机选取3月龄和34月龄SD大鼠10只分别作为青年组和老年组,用光镜和电镜结合形态计量学分法分析松果体细胞和神经胶质细胞密度及其指数;松果体细胞线粒体的Vv、Sv、Nv,高尔基器的Vv、Sv、粗面内质网的Sv、溶酶体的Vv;松果体神经终末的Vv及其线粒体的Vv、Sv、Nv、小颗粒囊泡的NA。结果 与青年组相比,老年组松果体细胞核形状不规则,核膜皱褶增多和加深。细胞浆内粗面内质网减少,排列紊乱,分散,脱颗粒明显;线粒体结构不清、肿胀、嵴断裂、消失、空泡化等。老年组松果体细胞密度比青年组减少,而神经胶质细胞密度增加,差异有高度显著性(P<0.01)。老年组神经胶质细胞指数比青年组高(P<0.01)。老年线粒体Vv与青年组无差别,但老年组线粒体Sv、Nv均比青年组减少(P<0.01)。老年组高尔基器的Vv、Sv均比青年组减少(P<0.01);老年组粗面内质网Sv比青年组减少,而老年组溶酶体Vv比青年组增加(P<0.01);老年组神经终末Vv比青年组减少(P<0.01);老年组神经终末中小颗粒囊泡NA比青年组减少(P<0.01);老年组线粒体Sv、Nv比青年组减少(P<0.05),两组神经终末中线粒体Vv无差别(P>0.05)。结论 老年大鼠松果体已发生衰老性变化,这可能与机?     

SVHRP对Aβ_(1-40)处理后大鼠海马突触形态学改变的抑制作用

目的:探索蝎毒耐热蛋白(SVHRP)对淀粉样β蛋白(Aβ)神经毒性的抑制作用。方法:在大鼠海马内每侧注射Aβ1-40(10μg/2μl)后1d,给予腹腔SVHRP(0.5～2μg/100g),1次/d,连续10次。建模16d后分别进行海马部位的突触体素免疫组织化学分析和突触超微结构计量观察。结果:与对照组比较,Aβ组大鼠突触体素免疫反应强度和电镜下突触密度明显下降(P0.01),小突触丢失为主,突触终末可见突触小泡大量集聚,突触活性区平均长度增加。SVHRP干预组大鼠实触体素免疫反应强度和电镜下突触密度明显高于Aβ组大鼠(P0.01),突触终末内未见突触小泡过量集聚,但小突触比例显著增加(P0.01)。结论:以上结果强有力的提示,Aβ是突触退变的始动因素,SVHRP可抑制Aβ引起的突触退变,有可能成为治疗Alzheimer病(AD)的一种药物。     

大鼠松果体的中枢神经支配──病毒跨神经元顺行追踪研究

大量研究证明，松果体（Pi）的功能同它的神经支配密切相关，因此，研究Pi的神经支配就十分必要。但长期以来对此存在着异议，一些学者认为Pi的神经支配仅来源于双侧颈上交感神经节（SCG），另一些又提出Pi的神经支配不仅来源于SCG，而且也接受来自脑或其它地方的纤维投射。本研究用假狂犬病毒（PRV）作顺行跨神经元追踪，进一步探讨Pi的神经支配。17只雄性SD大鼠在单侧眼球内注入3一PRV（Bartha株、5X10’PFU／ml）前施行双侧SCG摘除术，术后分别存活56、72和96hr。PRV标记的神经元用免疫组化ABC法显示。结果；（1）56hr组仅在视交叉上核（SCN）内在极少数神经元被PRV标记；（2）72hr组除SCN外，在丘脑下部前区、下丘脑室旁核（PVN）、缰核（Hb）和外侧膝状体（LGH）出现了PRV标记的神经元。与此同时，在松果体的被膜内和松果体细胞之间也呈现出PRV标记的神经纤维；（3）随着动物存活时！和延长，96hr组在上述提及区域内被PRV标记的神经元和神经纤维数量增多。以上结果表明松果体接受了来自视网膜节细胞（RGC）的光信息。结合其他学者的报道，我们推测从视网膜及下丘脑投射到松果体的神经通路可能有以下几条：①RGC～LGH～Pi。＠PGC～Hb～Pi，＠SCN～PVN—Pi，＠SCN～LGH～Pi和⑤SCN～Hb－Pi。不论从哪     

Non-sympathetic synaptic innervation of the pinealocyte of the Mongolian gerbil (Meriones unguiculatus): an electron microscopic study

Summary Direct synaptic innervation of pinealocytes was observed in the superficial pineal gland of the Mongolian gerbil (Meriones unguiculatus) by electron microscopy. This innervation consisted of nerve fibres terminating in boutons with clear transmitter vesicles with a diameter of 40–60 nm. The boutons made synaptic junctions with the cell membrane of the pinealocyte displaying thickenings of both the pre- and postsynaptic membranes. Such boutons persisted in the gland 1 week after removal of both superior cervical ganglia. In contrast, all the sympathetic boutons containing transmitter vesicles with a small dense core disappeared after ganglionectomy. This direct synaptic innervation reveals a neuronal character of the pinealocyte and might underlie reports of action potentials in electrophysiological recordings from the gland.     

Synaptic junctions between sympathetic axon terminals and pinealocytes in the monkey Macaca fascicularis

Summary The distribution of axon terminals in the pineal gland of monkeys was studied by electron microscopy. Numerous terminals bearing small pleomorphic agranular and dense-cored vesicles were localized in the perivascular space and among the pinealocytes in the parenchyma in normal monkeys. Following bilateral superior cervical ganglionectomy, they underwent degenerative changes, including the accumulation of glycogen masses, appearance of dense residual bodies and the displacement of synaptic vesicles. Some of these degenerating terminals showed synaptic contacts with the cell bodies of pinealocytes. At the synaptic junction the postsynaptic membrane was thickened asymmetrically. Examples of synaptic contacts were most frequently observed in 5 and 7 days postoperative animals. In the longer surviving (30 days) monkey, most of the axon terminals showed round agranular vesicles, and they were mainly presynaptic to the intrapineal ganglion cells with some of the pinealocytes. They remained structurally unchanged following the resection of both the superior cervical ganglia. A few axon terminals containing small dense-cored vesicles appeared to have survived the initial insult, but some of their vesicles appeared swollen 30 days after the operation. It is concluded from this study that some of the pinealocytes are under the influence by the postganglionic neurons in the superior cervical ganglia through direct synaptic contacts. The intrapineal ganglion cells are postsynaptic to fibres originating exclusively from the central nervous system. Some of these fibres, however, may be presynaptic directly to pinealocytes.     

Adrenalectomy but not gonadectomy affects rat pineal beta-adrenergic receptor density

Bilateral adrenalectomy, like chronic pineal denervation by means of superior cervical ganglionectomy, induced an increase in the morning levels of [125I]iodopindolol (IPIN) binding to rat pineal membranes; this change may be related to the reduced input of catecholamines to the pinealocytes as suggested by the decrease in nocturnal pineal melatonin synthesis previously reported in adrenalectomized rats. Castrated rats did not show changes in IPIN binding to pineal membranes when measured either at middark or in chronically superior cervical ganglionectomized rats, suggesting that the regulation of pineal beta-adrenergic receptors is independent from gonadal control.     

Neural control of glycogen content and its diurnal rhythm in mouse pineal cell.

In adult male dd mice, possible mechanisms regulating the glycogen content in the pineal cell were investigated by a semiquantitative histochemical method, with particular reference to the role of the sympathetic innervation. Reserpine, superior cervical ganglionectomy (SCGX), or decentralization of the ganglia (DC), as well as continuous light, prevented the nocturnal decrease in the glycogen content, causing a marked increase, and caused a gradual decrease in the size of the pineal cell. In the SCGX or DC group, the glycogen content reached a peak at 2 days and then decreased gradually. The nocturnal decrease was also prevented by propranolol. Noradrenaline caused a marked decrease in the glycogen content. These findings support the hypothesis that the glycogen metabolism and its diurnal rhythm in the pineal cell are regulated by the sympathetic nerve terminals innervating the pineal gland, presumably by the release of noradrenaline. In addition, the nature of the internal mechanism in the organism generating the pineal glycogen rhythm was examined. Light was considered to induce a phase shift in such a mechanism, but reserpine was not.     

Expression of protein gene product 9.5, tyrosine hydroxylase and serotonin in the pineal gland of rats with streptozotocin-induced diabetes

Hyperglycemia is a well-known factor in reducing nocturnal pineal melatonin production. However, the mechanism underlying diabetes-induced insufficiency of pineal melatonin has remained uncertain. This study was undertaken to examine the structure, innervation and functional activity of the pineal gland in streptozotocin (STZ)-induced diabetes in rats by immunohistochemistry, Western blotting and image analysis. The number of the pinealocytes and the volume of pineal were also estimated using stereologic quantification including the optical fractionator and Cavalieri's method. It has also shown a progressive reduction of the total area of the pineal gland and the nuclear size of pinealocytes beginning at 4 weeks of induced diabetes. Surprisingly, the immunoreactive intensities and protein amounts of serotonin (5-HT) and protein gene product (PGP) 9.5 in the pineal gland were progressively increased from 4 weeks of diabetes. Meanwhile, nerve fibers immunoreactive for PGP 9.5 had disappeared. Diabetes-induced neuropathy was observed in nerve fibers containing tyrosine hydroxylase (TH). The affected nerve fibers appeared swollen and smooth in outline but they showed a distribution pattern, packing density and protein levels comparable to those of the age-matched control animals. Ultrastructural observations have revealed diabetes-induced deformity of Schwann cells and basal lamina, accumulation of synaptic vesicles and deprivation of the dense-core vesicles in the axon terminals and varicosities. The increase in immunoreactivities in 5-HT and PGP 9.5 and shrinkage of pineal gland in the diabetic rats suggest an inefficient enzyme activity of the pinealocytes. This coupled with the occurrence of anomalous TH nerve fibers, may lead to an ineffective sympathetic innervation of the pinealocytes resulting in reduced melatonin production in STZ-induced diabetes.     

Involvement of alpha-adrenoceptors in norepinephrine-induced prostaglandin E2 release by rat pineal gland in vitro

Rat pineal glands incubated in vitro with 10 or 100 microM norepinephrine (NE) released 51% and 415% more prostaglandin E2 (PGE2) to the medium than in the absence of NE. Phentolamine (10 microM) prevented fully the effect of NE at both concentrations, whereas propranolol failed to affect it significantly. After superior cervical ganglionectomy (SCGx), NE-induced PGE2 release was significantly higher than in sham-operated controls--an effect also blocked by phentolamine but not by propranolol. These results suggest that NE releases PGE2 in rat pineals via alpha-adrenoceptors, acting at a post-synaptic site, and that SCGx induces alpha-adrenergic supersensitivity in the pinealocytes.     

Reinnervation of Müller's smooth muscle by atypical sympathetic pathways following neonatal ganglionectomy in the rat: structural and functional investigations of enhanced neuroplasticity

Müller's extraocular smooth muscle is reinnervated by sympathetic nerves following denervation by ipsilateral superior cervical ganglionectomy in neonates but not in older animals. Experiments were performed to determine: (1) the source and extent of reinnervation, (2) the role of impulse activity in sympathetic outgrowth and (3) the effects of reinnervation on smooth muscle maturation. Müller's muscles were evaluated structurally (muscle volume, catecholamine histochemistry, retrograde labeling of sympathetic neurons) and functionally (contractile responses to electrical stimulation of postganglionic innervation and adrenoceptor agonist) in control preparations and in muscles following neonatal ipsilateral superior ganglionectomy, ipsilateral decentralization, ipsilateral superior ganglionectomy combined with contralateral decentralization of chemical (guanethidine) sympathectomy. Fluorescent tracer injections of muscles in adult control rats labeled cells in the ipsilateral superior (98%) and middle cervical ganglia. Acute ipsilateral superior ganglionectomy produced complete degeneration of sympathetic innervation of Müller's muscle in neonatal and adult rats. In preparations denervated neonatally and maintained chronically, muscles were reinnervated by neurons in both the contralateral superior and ipsilateral middle cervical ganglia. The total number of neurons reinnervating the muscle was one half that of controls. Sectional density of innervation was 45% of control. Electrical stimulation of postganglionic axons in the contralateral pathway produced muscle contractions with a prolonged time course. Reinnervation alleviated, in part, deficits in muscle volume and contraction which occurred following sustained denervation by chemical sympathectomy. Decentralization decreased ipsilateral muscle volume but did not affect numbers of neurons projecting to or nerve density within the muscle. Stimulation frequencies required to produce a 50% maximum contraction were reduced in these preparations. Decentralization of the contralateral ganglion did not impede sprouting into the denervated muscle, as nerve density and number of labeled cells were comparable to muscles reinnervated by contralateral ganglia with intact preganglionic innervation. However, maximum contraction to electrical stimulation was reduced. Comparisons with ipsilaterally decentralized muscles revealed that increased stimulation frequencies were required for 50% maximum contraction.(ABSTRACT TRUNCATED AT 400 WORDS)