CGRP immunoreactivity and NADPH-diaphorase in afferent nerves of the rat penis

Calcitonin gene-related peptide (CGRP)-immunoreactive afferent nerve fibers are abundant in the rat penis. In addition, NADPH-diaphorase, which stains for nitric oxide synthase, has been localized within both autonomic and sensory dorsal root ganglia (DRG) and may be part of an important biochemical pathway involved in penile tumescence. The purpose of this study was: 1) to examine the circuitry of afferent nerves that are CGRP immunoreactive from the L6 DRG, 2) to examine the possibility that there are NADPH-diaphorase-positive afferent fibers from the L6 DRG to the rat penis, and 3) to examine the localization and colocalization of CGRP and NADPH-diaphorase within L6 DRG afferent perikarya. Calcitonin gene-related peptide immunostaining in the penis was eliminated following a bilateral transection of the pudendal nerves, but was unchanged following a bilateral transection of the pelvic splanchnic or hypogastric nerves. The NADPH-diaphorase staining was not altered by any of the nerve transections. Injection of the retrograde axonal tracer fluorogold (FG) into the dorsum penis labeled perikarya in the L6 DRG. Although the majority of FG-labeled perikarya contained neither CGRP nor NADPH-diaphorase, small subpopulations of perikarya contained either CGRP immunoreactivity, NADPH-diaphorase, or both. A unilateral pudendal nerve transection virtually eliminated (>99%) FG labeling in the ipsilateral L6 DRG. These data suggest that NADPH-diaphorase and CGRP are present, either together or separately, within a subpopulation of penile afferent perikarya. In addition, CGRP-immunoreactive afferent nerve fibers reach the penis primarily via the pudendal nerves. Finally, NADPH-diaphorase-positive penile afferents may be another important source of nitric oxide (NO) for penile tumescence.     

The origin of the luteinizing hormone-releasing hormone (LHRH) neurons in newts (Cynops pyrrhogaster): the effect of olfactory placode ablation

Summary Neurons containing luteinizing hormone-releasing hormone (LHRH) are first detected in newt embryos (Cynops pyrrhogaster) in the olfactory epithelium and ventromedial portion of the olfactory nerve, after which they sequentially appear in the intracerebral course of the terminal nerve at prometamorphosis, and in the septo-preoptic area at postmetamorphosis. In adults, however, LHRH-immunoreactive cells are rarely seen in the nasal region, and their distribution shifts into the brain, suggesting their migration. In order to ascertain the origin and possible migration route of these neurons in newt larvae, the effect of unilateral or bilateral olfactory placodectomy on the LHRH neuronal system has been studied. Removal of the olfactory placode results in the absence of LHRH-immunoreactive cells in the nasal and brain regions of the operated side, whereas the subsequent growth and the LHRH-immunoreactive cellular distribution in the contralateral side are identical to those of normal larvae. Following bilateral placodectomy, no LHRH immunoreactivity is detected on either side of the olfactory-brain axis. These results suggest that LHRH neurons of the newt, Cynops pyrrhogaster, originate in the olfactory placode and then migrate into the brain during embryonic development.     

Reduced neuronal sensitivity to dieldrin and picrotoxinin in a cyclodiene-resistant strain of Drosophila melanogaster (Meigen).

Toxicological and neurophysiological studies were performed to characterize the resistance mechanism in a cyclodiene-resistant strain of Drosophila melanogaster (Maryland strain). Dieldrin had an LC50 of 0.058 ppm against the larvae of susceptible D. melanogaster (Oregon-R wild type) when formulated in the rearing media. The LC50 of the resistant Maryland strain was 10.8 ppm, giving a resistance ratio (LC50-Maryland/LC50-susceptible) of 186-fold. Suction electrode recordings were made from peripheral nerves of the larval central nervous system to test whether reduced nerve sensitivity played any role in the observed resistance. In susceptible preparations (n = 5), inhibition of nerve firing by 1 mM gamma-aminobutyric acid (GABA) was effectively antagonized within 3-10 min by 10 microM dieldrin. In contrast, 30 min incubations with 10 microM dieldrin had no effect on preparations from cyclodiene-resistant individuals (n = 5). Similarly, 10 microM picrotoxinin blocked GABA-dependent inhibition in susceptible nerve preparations (n = 3). In recordings from resistant insects (n = 4), picrotoxinin displayed either weak antagonism of GABA or hyperexcitation indistinguishable from susceptible preparations. These results demonstrate that cyclodiene resistance in the Maryland strain of D. melanogaster 1) is expressed in immature stages, 2) is present at the level of the nerve, and 3) extends to picrotoxinin, albeit at a reduced level compared with dieldrin. The possible role of an altered GABA receptor in this resistance is discussed.     

外周损伤引起成年大鼠体感皮层的功能重组

为了了解外周神经损伤对体感皮层分域组构的影响,在成年大鼠上观察了切断坐骨神经(SC)前、即刻和切断后数周内后爪皮层代表区的改变。在盐酸氯胺酮麻醉下,用微电极记录后爪皮肤轻触刺激在对侧体感皮层工区诱发的多单位反应,得出后爪的皮层代表区图。在16例中,8例大鼠观察了切断SC的即时效应。结果表明,不但SC代表区丧失皮肤反应性,原隐神经(SA)代表区的皮肤反应性也明显下降或消失,同时神经元自发活动也明显减弱。另8例大鼠在切断后数周内做了1～3次重复测定。在最初几天,原SA代表区范围内多数记录点的皮肤反应性仍未恢复,但在原SC代表区内,一些记录点转而对SA皮肤轻触刺激起反应。在随后数周内SA代表区进行性地扩张,占领了大部分原SC代表区。这一结果说明成年大鼠外周神经损伤可导致体感皮层发生显著的重组改变。     

Morphometric investigations of the colon mucosa in chronicTrypanosoma cruzi infected rats

The objective of this investigation was to study the morphometry of the epithelial mucosa in the chronic phase ofT. cruzi infection. Nine young female Wistar rats were inoculated withT. cruzi. Ten months after inoculation the animals were sacrificed and the proximal colon was collected for morphometric measurements of the thickness of the muscle layers, the number of neurons in the myenteric plexus, the crypt cell population (CCP), crypt cell production per crypt (CCPC) and turnover time (TT) of the epithelium. There was no muscle layer hypertrophy but there was significant denervation in the group inoculated withT. cruzi, which also showed hyperplasia of the epithelium. The data suggest that denervation of the myenteric plexus did not induce hypertrophy of the propria muscle layer itself but altered the morphometry of the colonic epithelium inT. crwzi-infected animals, with increased development of CCP and TT. It is possible that this epithelial hyperplasia, as a consequence of a longer crypt cell TT, increased the absorption and secretion activities of the colon, which in turn may participate in the genesis of the enteromegalies observed in the chronic phase of Chagas’ Disease.     

颈动脉内注入腺苷对呼吸,血压和肾交感神经活动的影响

在33只麻醉家兔,观察了颈动脉内注入腺苷所诱发的平均动脉压、心率,呼吸和肾交感神经活动的变化。结果如下:(1)颈动脉内注入腺苷后,平均动脉压呈剂量依赖性下降;呼吸加快,深度变化不明显,剪断窦神经后注入腺苷,仍引起平均动脉压下降,而呼吸变化消失。(2)隔离的颈动脉窦灌流液内加入腺苷后,平均动脉压下降,心率减慢;颈动脉体(CB)失活后反应消失。(3)将腺苷灌注到颈动脉窦区后,平均动脉压下降,肾交感神经传出放电活动增加,CB 失活或剪断窦神经后,反应消失。由此提示:腺苷可作为兴奋 CB 的一种物质,引起平均动脉压降低,心率减慢,呼吸加强和肾交感神经放电活动增加。     

Quantitative gap junction alterations in mammalian heart cells quickly frozen or chemically fixed after electrical uncoupling

Summary The gap junction morphology was quantified in freeze-fracture replicas prepared from rat auricles that had been either quickly frozen at 6 K or chemically fixed by glutaraldehyde, in a state of normal cell-to-cell conduction or in a state of electrical uncoupling. The general appearance of the gap junctions was similar after both preparative procedures. A quantitative analysis of three gap junctional dimensions provided the following measurements in the quickly frozen conducting auricles (mean±sd): (a) P-face particles' diameter 8.27±0.74 nm (n =5709), (b) P-face particles' center-to-center distance 10.78±2.12 nm (n=4800), and (c) E-face pits' distance 9.99±2.19 nm (n=1600). Corresponding values obtained from chemically fixed tissues were decreased by about 3% for the particle's diameter and about 5% for the particles' and pits' distances. Electrical uncoupling by the action of either 1 mM 2–4-dinitrophenol (DNP), or 3.5 mMn-Heptan-1-ol (heptanol), induced a decrease of the particle's diameter, which amounted to –0.69±0.01 nm (mean ±se) in the quickly frozen preparations and –0.71±0.01 nm in the chemically fixed ones. The particles' distance was decreased by –0.96±0.04 nm in the quickly frozen samples and by –0.90 ±0.03 nm in the chemically fixed ones and the E-face pits' distance was similarly reduced. All differences were statistically significant (P<0.001 for all dimensions). Electrical recoupling after the heptanol effect promoted a return of these gap junctional dimensions towards normal values, which was about 50% complete within 20 min. It is concluded that very similar morphological alterations of the gap junctional structure are induced in the mammalian heart by different treatments promoting electrical uncoupling and that these conformational changes appear independently of the preparative procedure. The suggestion that the observed decrease of the particles' diameter is genuinely related to the closing mechanism of the unit cell-to-cell channel set in thei centers is thus confirmed.     

Leukotriene C4 Transport and Metabolism in the Central Nervous System

The transport and metabolism of radiolabeled leukotriene (LT) C4 in the CNS were investigated after intraventricular injection. Under thiopental (Pentothal) anesthesia, New Zealand white rabbits were injected intracerebroventricularly with 0.2 ml of artificial CSF containing 2.5 microCi of [3H]LTC4 (36 Ci/mmol), 0.3 microCi of [14C]mannitol, and, in some cases, 0.9 mg of probenecid, 1.8 mg of cysteine, 1.4 micrograms of unlabeled LTC4, or 2 mg of tolazoline HCl. After 2 h, the conscious rabbits were killed, and the quantity and nature of the 3H and 14C were determined in CSF, choroid plexus, and brain. The [3H]LTC4 recovered in CSF and brain was not extensively metabolized, as greater than 70% of the 3H remained [3H]LTC4, although some spontaneous conversion to 11-trans-[3H]LTC4 occurred. Oxidized forms of [3H]LTC4, [3H]LTD4, and [3H]LTE4 did not exceed 18% in CSF and brain. After intraventricular injection of [3H]LTC4, 3H was transferred from the CSF to blood by a probenecid-sensitive, but tolazoline-insensitive, transport system in the CNS much more rapidly than mannitol. Cysteine decreased the retention of [3H]LTC4 in brain. These results are consistent with previous in vitro observations that [3H]LTC4 is transferred from CSF into blood by an efficient transport system for LTC4 in choroid plexus.     

电离辐射引起胃排空延迟机理的初步探讨

本文观察了800rad照射后胃肠肌电的变化及切斷内脏神经与电刺激迷走神经对官的影响,初步分析了电离辐射引起胃排空延迟的机理。结果是:800rad照后大鼠胃肠肌电的峰波平均振幅胃幽部窦部照后1小时至第4天明显降低(P<0.05);幽门括约肌政变不大;十二指肠球部照后第3～7天明显下降(P<0.01)。切断内脏神经后照射大鼠胃肠肌电的峰波平均振幅胃幽门窦部变化不大,幽门括约肌照后1小时至第5天明显升高(P<0.05),十二指肠球部照后第3～7天明显下降(P<0.05)。800rad照后第4天大鼠胃对电刺激迷走神经的反应性明显降低(P<0.01)。上述结果表明:照后胃排空延迟的原因不仅与神经-体液调节紊乱有关,而且与射线损伤了平滑肌,使其兴奋性暂时的功能性降低有关。此外照后由于十二指肠球部运动的变化而使内感受器对胃运动的调节发生紊乱也是值得重视的因素。     

延髓中缝核区注射谷氨酸钠降低大鼠动脉血压的作用

本工作研究了大鼠延髓中缝核在心血管活动调整中的作用。通过埋植套管向大鼠延髓中缝核区注射神经元兴奋剂谷氨酸钠5-μg可明显降低血压,抑制交感神经传出活动,心率无显著改变。降血压效应可被脊髓蛛网膜下腔注射5-HT受体阻断剂肉桂硫胺50μg,或腹腔注射赛庚啶15mg/kg所部分对抗;并可被皮下注射阿片受体阻断剂纳洛酮1mc/kg所削弱。结果提示:延髓中缝核-脊髓5-HT下行通路对脊髓的血管调节功能起抑制性影响,内源性阿片样物质可能参与该机制。