七星瓢虫成虫下颚须上的化学感受器

七星瓢虫成虫下颚须端节的内侧是一个船背形隆起的平面, 其上着生栓锥形化学感受器约1, 500个, 其中一半左右是味觉感受器, 其余为嗅觉感受器.每一个味觉感受器小体内, 有感受细胞4—8个, 它们的树突远区通过感橛腔时, 或处于同一个感橛腔中, 或在2个感橛腔中, 或在3个感橛腔中.每一个嗅觉感受器小体内, 感受细胞的数目恒为3个, 有限大的感受器淋巴腔.感橛较薄, 终止于栓锥腔的基部.树突在栓锥腔内分枝.栓锥的顶部有许多半球状突起.下颚须内所具有的感受细胞比下唇须内所具有的超百倍之多, 由取食时下颚须的动作来判断, 它们的主要作用在于寻找和试探食物.     

动物的听觉感受器

对声音的感觉是听觉最广义的定义。在生物进化的过程中 ,生物对声波振动的感觉逐步形成了专一的听觉感受器官。动物界中只有昆虫和脊椎动物具有听觉功能。听觉在很多方面都起着重要的作用 ,例如逃避捕食者、寻觅配偶和相互交流等 ,对人类来说听觉是语言发展的关键。现存的感受器官大体上分为以下几种类型。1　感触毛 (听觉毛 )在直翅目昆虫尾须上及鳞翅目幼虫身体上 ,有很多特殊的刚毛———感触毛 ,刚毛基部有关节腹 ,下联感觉细胞及感觉神经元 ,这套装置除了感受机械刺激外 ,还能感受低频率的音波及气流所给予的压力。这类听觉感受器与感…     

中华蜜蜂工蜂触角感受器的扫描电镜观察

对中华蜜蜂(Apis cerana)工蜂触角感受器的扫描电镜观察,见到在触角上有九种类型的感受器,它们是板形感器、腔锥感器、坛形感器、钟形感器、锥形感器、毛形感器A、毛形感器B、毛形感器C和D、缘感器以及各种类型的刚毛等.对于这些感受器的外部形态和分布部位进行了详细地观察和描述,发现中华蜜蜂与西方意蜂(Apis mellifera)有差异.     

小地老虎雄蛾触角感受器的扫描电镜观察

利用扫描电镜观察了小地老虎雄蛾触角感受器的种类、形态和分布.结果表明, 小地老虎雄蛾触角为双栉状(端半部为丝状),由1节柄节、1节梗节和82～92节鞭节组成.在触角上分布有毛形感器、刺形感器、鳞形感器、腔锥感器、腔形感器、 耳形感器、B(o)hm's氏鬃毛7种感受器,其中毛形感器数量最多.     

蜚蠊的感受器及其功能

<正> 蜚蠊,俗称蟑螂,是一种常见的室内卫生害虫。它们有很发达的感觉器官(如触角等),上面有许多感受器。这些感受器具有发现食物、感受外界环境温湿度变化、逃避天敌、寻找配偶     

呼吸道迷走神经感受器概述

肺以及气道与外界环境之间存在着巨大的界面,因此需要有效的防御反射机制。呼吸道感受器是肺部神经反射的起始点,其重要性不言而喻,采用组织,解剖与电生理学方法,经过一个世纪的研究,我们对于呼吸道感受器的认识,特别对其结构的认识,仍然有限,据电生理实验结果,肺部感受器至少可被分为三大类;慢适应感受器,快适应感受器以及C纤维感受器,按血供来源,后者又可分为气道（体循环）与肺（肺循环）两类,近来发现呼吸道中存在着第四类感受器,它们由迷走神经的Aδ传入纤维传递冲动,其放电活动不同于上述各类,对肺充气反应阈值高,故称之为高阈值Aδ感受器,功能上前两类基本属于机械性感受器,而后两类可归为化学敏感性感受器,另外,用组织学方法,观察到气道内有一些神经内分泌细胞,它们可以散在分布,亦可集聚成小体。这些神经上皮小体受多种神经支配,其结构复杂,形态酪似感受器,虽然我们对其形态了解颇深,但对其放电形式一无所知,本文对以上各类感受器进行了评述与探讨。     

北京幽灵蛛体表微感受器的类型、结构和分布

北京幽灵蛛(Pholcus beijingensis)体表的微感受器包括毛状感受器(触毛、听毛、味觉毛和刺)、裂缝状感受器(单个裂缝器、竖琴器)和跗节器等.扫描电镜观察显示,北京幽灵蛛体表的毛状感受器数量最多,分布最广;其次是裂缝感受器;此外,每个跗节末端具有一个跗节器.除触毛在整个身体表面均有分布外,其他毛状感受器(...     

垂体在刺激脑内渗透压感受器引起的肾脏反应中的作用

实验在α氯醛糖和氨基甲酸乙酯混合麻醉的大鼠中进行。脑室内注射高张盐水(icv.HS)后,肾血浆流量、肾小球滤过率、尿量、尿钠排出量、尿钾排出量和渗透物质清除率均增加,游离水清除率下降。去除垂体后,icv.HS不再能引起上述肾脏反应。另外给大鼠静脉注射血管升压素(VP)拮抗剂(V_1和V_2受体拮抗剂),并不能削弱上述icv.HS引起的肾脏反应。脑室内注射高张盐水后,尿中多巴胺(DA)排出量无显著增多;给予多巴脱羧酶抑制剂苄丝肼也不能削弱icv.HS引起的肾脏反应。上述实验结果表明,在本实验条件下刺激脑内渗透压感受器引起的肾脏反应依赖于垂体的完整性,但看来并不依赖于外周的VP和DA,故垂体通过何种机制介导icv.HS引起上述肾脏反应,有待于进一步的研究。     

瞬时感受器电位Ⅴ亚家族离子通道——温度感受器

生物体可以感受广泛的温度范围,其中温度超过43℃或低于15℃还可引起伤害性痛觉。近年来在哺乳动物中已经发现6个与温度有关的通道,其中4个属于瞬时感受器电位（transient receptor potential,TRP）Ⅴ亚家族成员。这些通道组织分布非常广泛,功能上属于钙渗透性通道,可被多种理化刺激激活。它们具有不同的温度阈值,并受一些理化因素的调节。     

刺激脑内渗透压感受器能降低大鼠管球反馈的敏感性

在麻醉大鼠肾脏近曲小管和远曲小管分别进行微穿刺,采集小管液。测定单个肾单位肾小球滤过率(SNGFR)。由于微穿刺部位对管球反馈造成的影响,在同一肾单位,采集近曲小管末段小管液测出的SNGFR值(SNGFR_p)比在远曲小管起始段测出的SNGFR值(SNG-FR_d)高,故可将在这两个部位测得的SNGFR值的差(SNGFR_(p-d))用作衡量管球反馈(TGF)敏感性的间接指标。脑室内注射高张盐水(icv.HS)后,SNGFR_(p-d)减小,表明脑内渗透压感受器受刺激可使TGF的敏感性降低。静脉注射速尿后,icv.HS不再引起肾血浆流量和肾小球滤过率的增加,但仍能引起尿钠排出增多。上述结果表明,刺激脑内渗透压感受器可通过减弱TGF导致肾脏血流动力学的改变,而其增加尿钠排出的效应则是通过抑制肾小管的重吸收实现的。     

Naturally occurring and synthetic constitutive-active cytokine receptors in disease and therapy

Cytokines control immune related events and are critically involved in a plethora of patho-physiological processes including autoimmunity and cancer development. Mutations which cause ligand-independent, constitutive activation of cytokine receptors are quite frequently found in diseases. Many constitutive-active cytokine receptor variants have been directly connected to disease development and mechanistically analyzed. Nature’s solutions to generate constitutive cytokine receptors has been recently adopted by synthetic cytokine receptor biology, with the goal to optimize immune therapeutics. Here, CAR T cell immmunotherapy represents the first example to combine synthetic biology with genetic engineering during therapy. Hence, constitutive-active cytokine receptors are therapeutic targets, but also emerging tools to improve or modulate immunotherapeutic strategies. This review gives a comprehensive insight into the field of naturally occurring and synthetic constitutive-active cytokine receptors.     

Chronic Effects of Xanthines on Levels of Central Receptors in Mice

1.Chronic ingestion of caffeine causes a significant increase in levels of A₁-adenosine, nicotinic and muscarinic receptors, serotonergic receptors, GABA_A receptors and L-type calcium channels in cerebral cortical membranes from mice NIH Swiss strain mice.2.Chronic theophylline and paraxanthine had effects similar to those of caffeine except that levels of L-type channels were unchanged. Chronic theobromine, a weak adenosine antagonist, and 1-isobutyl-3-methylxanthine (IBMX), a potent adenosine antagonist and phosphodiesterase inhibitor, caused only an increase in levels of A₁-adenosine receptors. A combination of chronic caffeine and IBMX had the same effects on receptors as caffeine alone. Chronic 3,7-dimethyl-1-propargylxanthine (DMPX), a somewhat selective A_2A-antagonist, caused only an increase in levels of A₁-adenosine receptors. Pentoxyfylline, an adenosine-uptake inhibitor inactive at adenosine receptors, had no effect on receptor levels or calcium channels.3.A comparison of plasma and brain levels of xanthines indicated that caffeine penetrated more readily and attained somewhat higher brain levels than theophylline or theobromine. Penetration and levels were even lower for IBMX, paraxanthine, DMPX, and pentoxyfylline.4.The results suggest that effective blockade of both A₁ and A_2A-adenosine receptors is necessary for the full spectrum of biochemical changes elicited by chronic ingestion of xanthines, such as caffeine, theophylline, and paraxanthine.     

Quantitative Relationships of Five Putative Neurotransmitter Receptor Sites in Rat Hippocampal Formation

The hippocampus is well suited for studies of the interrelationships of various neurotransmitter systems in the CNS by reason of its simple laminated organization, defined connections, and variety of identified neurotransmitters. We have studied the biochemical and pharmacological properties of five radiolabeled ligand binding sites in a membrane fraction prepared from rat hippocampal formation. These binding sites are thought to identify recognition sites for neurotransmitter receptors. The rank order of ligand binding sites is [³H]muscimol > [³H]quinuclidinyl benzilate > [³Hdihydroergocryptine > [³H]dihydroalprenolol > ¹²⁵I-labeled α-bungarotoxin. All ligands have a single, saturable, high-affinity binding site. Pharmacological characterization of the ligand binding sites indicates properties consistent with the identification of these sites as neurotransmitter receptors.     

Electrically evoked release of [(3)H]noradrenaline from mouse cultured sympathetic neurons: release-modulating heteroreceptors

Cultured neurons from the thoracolumbar sympathetic chain of newborn mice are known to possess release-inhibiting alpha(2)-autoreceptors. The present study was carried out in a search for release-modulating heteroreceptors on these neurons. Primary cultures were preincubated with [(3)H]noradrenaline and then superfused and stimulated by single pulses, trains of 8 pulses at 100 Hz, or trains of 36 pulses at 3 Hz. The cholinergic agonist carbachol reduced the evoked overflow of tritium. Experiments with antagonists indicated that the inhibition was mediated by M(2) muscarinic receptors. The cannabinoid agonist WIN 55,212-2 reduced the evoked overflow of tritium through CB(1) receptors. Prostaglandin E(2), sulprostone, and somatostatin also caused presynaptic inhibition. The inhibitory effects of carbachol, WIN 55,212-2, prostaglandin E(2), and somatostatin were abolished (at the highest concentration of WIN 55, 212-2 almost abolished) by pretreatment of the cultures with pertussis toxin (250 ng/ml). Several drugs, including the beta(2)-adrenoceptor agonist salbutamol, opioid receptor agonists, neuropeptide Y, angiotensin II, and bradykinin, failed to change the evoked overflow of tritium. These results demonstrate a distinct pattern of presynaptic inhibitory heteroreceptors, all coupled to pertussis toxin-sensitive G proteins. The lack of operation of several presynaptic receptors known to exist in adult mice in situ may be due to the age of the (newborn) donor animals or to the culture conditions.     

Angiotensin II vascular receptors in fetal and neonatal rats

Specific binding sites for angiotensin II in aorta and renal arteries have been studied in rat fetuses (18th day of pregnancy) and 1-day-old newborn rats by binding studies in arterial membranes using [125I] ileu-5-angiotensin II. One type of angiotensin receptor was found both in fetuses and in the newborns; the capacity of this (RT) decreased immediately after birth (from 0.06 +/- 0.01 nM to 0.02 +/- 0.005 nM; +/- SEM) and the affinity (Kd) increased at birth (from 3.5 +/- 0.6 nM to 19.5 +/- 1.2 nM; +/- SEM). Localization of the specific binding sites was studied by autoradiography on arteries from fetal and newborn rats either perfused with iodinated angiotensin II by cannulation of the aorta or in vitro on cryostat sections incubated with the radioactive angiotensin II. Both in fetuses and in the newborn the binding sites were located in the tunica media of the arteries.     

Somatotropic and lactotropic receptors in transgenic mice expressing human or bovine growth hormone genes

The somatotropic and lactotropic receptors were studied in liver microsomal preparations from transgenic mice carrying the human growth hormone (hGH) or bovine growth hormone (bGH) gene fused to mouse metallothionein-I (MT) or phosphoenolpyruvate carboxykinase promoter/regulator (PEPCK). Specificity studies indicated that, similarly to normal mice, liver microsomes from the transgenic animals possess a mixed population of somatotropic and lactotropic binding sites. In transgenic animals of both sexes, the binding capacity of somatotropic receptors was significantly increased without corresponding changes in affinity. Expression of the MT-hGH hybrid gene was associated with the induction of somatotropic receptors which was approximately twice as great as that measured in animals expressing the MT-bGH hybrid gene. The binding capacity of lactotropic receptors in liver microsomes (quantitated, by the use, of labelled ovine prolactin) was increased 2–3 fold in transgenic females and approximately 10-fold in transgenic males as compared to the respective normal controls. We conclude that lifelong excess of GH up-regulates hepatic GH and prolactin receptors, and that lactogenic activity of GH is not essential for induction of prolactin receptors in the liver of transgenic mice.     

γ-Aminobutyric Acid and Benzodiazepine Receptor Changes Induced by Unilateral 6-Hydroxydopamine Lesions of the Medial Forebrain Bundle

Quantitative autoradiography was used to ascertain alterations in [3H]muscimol, [3H]flunitrazepam (FLU), [3H]naloxone, [3H]D-alanine-D-leucine-enkephalin (DADL), and [3H]spiroperidol binding in basal ganglia 1 week, 4 weeks, and 5 months after unilateral 6-hydroxydopamine lesions of the medial forebrain bundle (MFB) in the rat. At 1 and 4 weeks following lesions, [3H]spiroperidol binding increased 33% in striatum. At 5 months, [3H]spiroperidol was only nonsignificantly increased above control. At 1 week, [3H]muscimol binding decreased 39% in ipsilateral globus pallidus (GP), but increased 41% and 11% in entopeduncular nucleus (EPN) and substantia nigra pars reticulata (SNr), respectively. At 4 weeks, [3H]muscimol binding was reduced 19% in striatum and 44% in GP and remained enhanced by 32% in both EPN and SNr. These changes in [3H]muscimol binding persisted at 5 months. [3H]FLU binding was altered in the same direction as [3H]muscimol binding; however, changes were slower in onset and became significant (and remained so) only at 4 weeks after lesions. Decreases in [3H]naloxone and [3H]DADL binding were seen in striatum, GP, EPN, and SNr. Scatchard analyses revealed that only receptor numbers were altered. This study provides biochemical evidence for differential regulation of striatal GABAergic output to GP and EPN/SNr.     

Intrinsic and synaptic properties of neurons in the vocal-control nucleus lMAN from in vitro slice preparations of juvenile and adult zebra finches

A common theme of diverse neural systems is that circuits that are important for initial acquisition of learning do not necessarily serve as a substrate for the long-term storage of that memory. The neural basis of vocal learning in songbirds provides an example of this phenomenon, since a circuit that is necessary for vocal production during initial stages of vocal development apparently plays no subsequent role in controlling learned vocalizations. This striking functional change suggests the possibility of marked physiological changes in synaptic transmission within this circuit. We therefore examined intrinsic and synaptic properties of neurons in the cortical nucleus lMAN (lateral magnocellular nucleus of the anterior neostriatum), which forms part of this developmentally regulated circuit, in an in vitro preparation of the zebra finch forebrain. Although both functional and morphological characteristics of these neurons change substantially during vocal development, we did not observe widespread, substantive changes in the electrophysiological characteristics of juvenile versus adult lMAN neurons examined in vitro. Overall, both the intrinsic properties and synaptic responses of lMAN neurons were similar in slices from juvenile birds (at ages when lesions of lMAN disrupt vocal production) and in slices from adult birds (when lMAN lesions have no effect on song production). However, one intrinsic property that did vary between juvenile and adult cells was spike duration, which was longer in juvenile cells, suggesting the potential for activation of second-messenger cascades and/or enhanced synaptic transmission onto target cells of lMAN neurons. The pattern of synaptic response observed in both juvenile and adult cells suggests that lMAN projection neurons receive direct excitatory afferent inputs, as well as disynaptic inhibitory inputs from interneurons within lMAN. Activation of inhibitory interneurons rapidly curtails the excitatory response seen in projection neurons. This inhibition was abolished by bicuculline, indicating that the inhibitory interneurons normally exert their postsynaptic response via GABA_A receptors on projection neurons. The inhibitory response could also be blocked by CNQX (6-cyano-7-nitroquinoxaline-2,3-dione), suggesting that the activation of inhibitory interneurons within lMAN may be governed primarily by AMPA receptors. © 1998 John Wiley & Sons, Inc. J Neurobiol 37: 642–658, 1998     

The amphiphilic peptide adenoregulin enhances agonist binding to A1-adenosine receptors and [35S]GTPγS to brain membranes

Summary 1. Adenoregulin is an amphilic peptide isolated from skin mucus of the tree frog,Phyllomedusa bicolor. Synthetic adenoregulin enhanced the binding of agonists to several G-protein-coupled receptors in rat brain membranes.2. The maximal enhancement of agonist binding, and in parentheses, the concentration of adenoregulin affording maximal enhancement were as follows: 60% (20 µM) for A₁-adenosine receptors, 30% (100 µM) for A_2a-adenosine receptors, 20% (2 µM) for ₂-adrenergic receptors, and 30% (100 µM) for 5HT_1A receptors. High affinity agonist binding for A_1-, _2-, and 5HT_1A-receptors was virtually abolished by GTPS in the presence of adenoregulin, but was only partially abolished in its absence. Magnesium ions increased the binding of agonists to receptors and reduced the enhancement elicited by adenoregulin.3. The effect of adenoregulin on binding of N⁶-cyclohexyladenosine ([³H]CHA) to A₁-receptors was relatively slow and was irreversible. Adenoregulin increased the B_max value for [³H]CHA binding sites, and the proportion of high affinity states, and slowed the rate of [³H]CHA dissociation. Binding of the A₁-selective antagonist, [³H]DPCPX, was maximally enhanced by only 13% at 2 µM adenoregulin. Basal and A₁-adenosine receptor-stimulated binding of [³⁵S]GTPS were maximally enhanced 45% and 23%, respectively, by 50 µM adenoregulin. In CHAPS-solubilized membranes from rat cortex, the binding of both [³H]CHA and [³H]DPCPX were enhanced by adenoregulin. Binding of [³H]CHA to membranes from DDT₁ MF-2 cells was maximally enhanced 17% at 20 µM adenoregulin. In intact DDT₁ MF-2 cells, 20 µM adenoregulin did not potentiate the inhibition of cyclic AMP accumulation mediatedvia the adenosine A₁ receptor.4. It is proposed that adenoregulin enhances agonist binding through a mechanism involving enhancement of guanyl nucleotide exchange at G-proteins, resulting in a conversion of receptors into a high affinity state complexed with guanyl nucleotide-free G-protein.