A radioimmunoassay for human pro-luteinizing hormone-releasing factor [pro-LRF(14-69)OH]

A radioimmunoassay (RIA) for human pro-LRF(14-69)OH was developed with an antiserum, generated in a rabbit, to [Tyr67]pro-LRF(47-67)NH2 conjugated to BSA. This antiserum bound 28-32% of [125I]pro-LRF(14-69)OH at a final dilution of 1:2500 and the binding was inhibited by pro-LRF(14-69)OH in a dose-dependent manner. The sensitivity of the RIA was 31.2-62.5 pg and the dose that inhibited 50% of the binding to the tracer was 280-320 pg. Intra- and inter-assay coefficients of variation at 50% inhibition were 8 and 12%, respectively. Neither LRF nor pro-LRF(14-37)OH was recognized by the antiserum. The dilution curve generated with human hypothalamic extract was parallel to that of pro-LRF(14-69)OH. In addition the extract yielded a major immunoreactive peak emerging in elution volumes concordant with [125I]pro-LRF(14-69)OH on Sephadex G-50 chromatography.     

刺激杏仁基底外侧核对外侧缰核神经元单位放电的影响

用玻璃微电极细胞外记录大鼠外侧缰核(LHN)神经元的单位放电。共记录了110个神经元。其中痛兴奋神经元(LHPE)75个;痛抑制神经元(LHPI)11个;广动力型神经元2个;无反应神经元17个;此外还有5个对躯体与内脏伤害性刺激反应不同的神经元。电刺激杏仁基底外侧核(以下简称杏仁核,AMG)对LHPE和LHPI的自发放电主要产生抑制作用,分别占总数的81.1％和72.7％,并抑制其对伤害性刺激的反应;对无反应神经元和广动力型神经元无明显影响。AMG内微量注射吗啡能抑制LHPE的伤害性刺激反应,但对其自发放电无明显影响。微量注射纳洛酮则可增加LHPE的自发放电频率,并加强其对伤害性刺激的反应。注射纳洛酮还可以取消电针对LHPE的伤害性刺激反应的抑制作用。     

冷冻或切除小脑蚓部山顶(Culmen)对豚鼠“踏步自动作用”(Stepping automatism)的影响

本研究探讨部分冷冻或切除小脑蚓部(vermis)对整体豚鼠“踏步自动作用”(steppingautomatism)的影响。“踏步自动作用”由我们近年来发现的诱发踏步物质(SIS)(4-R-2,2,5,5-四(三氟甲基)-咪唑啉)所引起。结果表明部分冷冻或切除小脑蚓部的山顶(culmen,Ⅴ和Ⅳ叶)和中央叶(Centralis,Ⅲa,b)明显增强豚鼠的“踏步自动作用”。冷冻小脑不能触发,但仅能调控“踏步自动作用”。这种调控作用对自动化程度差的弱“踏步自动作用”特别显著。蚓部山顶(Ⅴ叶为主)同时调控左右前肢踏步,而一侧蚓部山顶及其半球则主要调控同侧前肢踏步。此外,本研究的结果表明当介面温度(冷冻头和小脑幕间)致冷至5℃—0℃左右,冷冻小脑便可基本模拟部分切除小脑效应。     

Influence of α-interferon therapy on blood lymphoid cells

Summary The influence of natural -interferon (-IFN) therapy (3×10⁶ units i.m. daily) on blood lymphoid cells was studied in 20 patients with gynecological neoplasias (7 patients with condylomata accuminata and 13 patients with ovarian carcinoma). There was a statistically significant increase in the intracellular levels of 2'–5'oligoadenylate synthese 1 day after the first injection of IFN and with few exceptions this activity remained increased during 3 months of treatment. In most of the patients, the capacity of blood lymphoid cells to produce IgA, IgG, and IgM following stimulation with pokeweed mitogen was decreased 1 day after the first injection of IFN and with few exceptions it remained low during 6 months of IFN therapy. In most patients there was a decrease in the capacity of lymphoid cells to act as stimulator or responder cells in a mixed lymphocyte culture during IFN therapy. The -IFN therapy had no major influence on the response of lymphoid cells to mitogens. We conclude, that neither this nor our previous studies on the influence of IFN therapy on immunological functions have given support to the hypothesis that the antitumor action of IFN is mediated by the immune system.     

电刺激兔脑干中缝背核引起呼吸易化效应的观察

本文在30只全麻、制动、断双侧迷走神经的家兔上,记录一侧膈神经放电,观察了电刺激脑干中缝背核(Nucleus Raphe Dorsalis,NRD)所诱发出的呼吸效应。1.施以6—10s 长串电脉冲刺激(波宽0.3ms,频率100Hz,波幅4—6V),诱发出了强的呼吸易化效应,使呼吸加深加快。2.吸气相给予0.4s 短串电脉冲刺激可以明显的延长吸气相,用0.15mA 强度刺激,落位在吸气相的2/3时效应最明显。3.呼气相短串电脉串刺激可规律地使呼气时程缩短,促进呼气向吸气的位相转换,诱发此效应出现的强度阈值在呼气相中逐渐降低。     

辣椒素引起脊髓P物质释放及其对血压的影响

为进一步研究脊髓 P 物质(SP)在调节心血管活动中的作用,在大鼠脊髓蛛网膜下腔注射(ith)辣淑素(cap),以刺激脊髓 SP 能神经末梢释放 SP,结果引起血浆去甲肾上腺素(NA)和肾上腺素(AD)含量增高,及具有剂量依赖性的动脉血压上升,心率升高。ith 具有高度特异性的 SP 受体拮抗剂或 SP 抗血清均可阻断 cap 引起的升压效应,免疫组化测定也观察到注入的cap 剂量越大,脊髓胸段 SP 样免疫阳性反应物的致密度越低,这些观察结果支持 cap 可以引起脊髓内 SP 的释放的说法。在第一颈段(C_1)横断脊髓后 ith cap 所引起的升压效应与完整动物 ith cap 的升压效应无显著差异。以上结果提示脊髓 SP 能神经末梢释放的 SP 可以通过交感肾上腺髓质系统引起心血管兴奋效应,SP 可能是引起交感节前神经元兴奋的神经递质。     

Modulation of phosphoinositide metabolism in rat brain slices by excitatory amino acids,arachidonic acid,and GABA

In rat brain slices the synthesis of [³H]phosphoinositides and the production of [³H]inositol monophosphate (IP₁) induced by norepinephrine (NE) were inhibited by glutamate. Calcium concentrations were varied to test if these inhibitory effects of glutamate were mediated by a calcium-dependent process. Although reducing calcium or addition of the calcium antagonist verpamil reduced the inhibitory effects of glutamate, these results were equivocal because reduced calcium directly decreased agonist-induced [³H]phosphoinositide synthesis. The inhibitory effects of glutamate were mimicked by quisqualate in a dose-dependent manner, but none of a variety of excitatory amino acid receptor antagonists modified the inhibition caused by quisqualate. It is suggested that glutamate activates a quisqualate-sensitive receptor (for which an antagonist is not available) and causes inhibition of phosphoinositide hydrolysis mediated in part by a direct or indirect inhibitory effect of calcium on phosphoinositide synthesis. Modulatory effects of arachidonic acid were examined because glutamate and calcium can activate phospholipase A₂. Arachidonic acid caused a rapid and dose-dependent inhibition of [³H]phosphoinositide synthesis and of NE-stimulated [³H]IP₁ production. A similar inhibition of the response to carbachol also occurred. The inhibition caused by arachidonic acid was unchanged by addition of inhibitors of cyclooxygenase or lipoxygenase. Activation of phospholipase A₂ with melittin caused inhibitory effects similar to those of arachidonic acid. Inhibitors of phospholipase A₂ were found to impair phosphoinositide metabolism, likely due to their lack of specificity for phospholipase A₂. Further studies were carried out in slices that were prelabelled with [³H]inositol in an attempt to separate modulatory effects on [³H]phosphoinositide synthesis and agonist-stimulated [³H]IP₁ production. Several excitatory amino acid agonists inhibited NE-stimulated [³H]IP₁ production. This inhibitory inter-action could be due to impaired synthesis of [³H]phosphoinositides because, even though the slices were prelabeled, addition of unlabelled inositol reduced NE-stimulated [³H]IP₁ production, indicating that continuous regeneration of [³H]phosphoinositides is required. In contrast to the inhibitory effects of the excitatory amino acids, gamma-aminobutyric acid (GABA) enhanced the response to NE in cortical and hippocampal slices. GABA also enhanced the response to carbachol in hippocampal and striatal slices and to ibotenic acid in hippocampal slices. Baclofen potentiated the response to NE similarly to the effect of GABA and baclofen partially blocked the inhibitory effect of arachidonic acid but did not alter that of quisqualate.Abbreviations AMPA -amino-3-hydroxy-5-methyl-4-isoxazolepropionic - acid AP₄ dl-2-amino-4-phosphonobutyric acid - BPB bromphenacyl bromide - BSA bovine serum albumin - CNQX 6-cyano-7-nitroquinoxaline-2,3-dione - DFMO -difluoromethylornithine - DIDS diisothiocyanotostilbene-2,2-disulfonic acid - EGTA ethyleneglycol-bis-N - N, N N-tetraacetic acid - GABA -aminobutyric acid - GDEE glutamate diethyl ether - -GG -glutamylglycine - IP₁ inositol monophosphate - IP₂ inositol bisphosphate - IP₃ inositol trisphosphate - NDGA nordihydroguaiaretic acid - NE norepinephrine - NMDA N-methyl-d-aspartate     

大鼠隔—海马通路损伤对海马内递质含量及酶活力的影响

单侧切断大鼠海马缴和部分穹窿可使海马部分去神经。损伤后7d,海马内胆碱能系统中乙酰胆碱(ACh)含量下降72.5%,胆碱乙酰基转移酶(ChAT)活力下降45.7%,胆碱酯酶活力下降52.2%,在单胺能系统中,去甲肾上腺素(NA)含量下降16.3%,多巴胺(DA)含量下降31.3%,5-羟色胺含量下降30.3%。在损伤过程中,海马内氨基酸含量没有改变。实验结果表明,海马缴和穹窿是脑内胆碱能和单胺能传入神经到达海马靶区的部分共同通路。     

去甲肾上腺素、乙酰胆碱对绵羊心肌浦肯野纤维瞬时性内向离子流的影响

用电压箝制术观察了去甲肾上腺素、乙酰胆碱对绵羊浦肯野纤维由乙酰毒毛旋花子甙元诱发的瞬时性内向离子流(I_Ti)的效应。当乙酰毒毛旋花子甙元浓度为4.5×10~(-8)mol/L 时,诱发出的I_(T1)稳定并能维持约1.5h。去甲肾上腺素1.5×10~(-6)mol/L,可使I_(Ti)的峰值由11.4±2.5nA 增加到14.5±4.1nA(n=11,P相似文献