Immunohistochemical mapping of nitric oxide synthase in the rat hypothalamus and colocalization with neuropeptides

The localization and distribution of nitric oxide synthase in the hypothalamus have been studied with an immunohistochemical technique using antibodies to neuronal rat nitric oxide synthase. Subsequent double-labeling experiments examined the colocalization patterns of nitric oxide synthase and several peptides. Our results demonstrate a widespread occurrence of nitric oxide synthase-immunoreactive nerve cell bodies and processes throughout the hypothalamus, especially in various parts of the preoptic region, in the supraoptic and paraventricular nuclei, the lateral hypothalamic area, the ventromedial and dorsomedial nuclei, the arcuate nucleus and various parts of the mammillary region. Double labeling experiments showed that nitric oxide synthase-like immunoreactivity coexists with substance P-like immunoreactivity in the medial preoptic area, with oxytocin-, cholecystokinin- and galanin message-associated peptide-like immunoreactivity in the supraoptic nucleus, with enkephalin-, oxytocin- and corticotropin releasing factor-like immunoreactivity in the paraventricular nucleus and with enkephalin-like immunoreactivity in the arcuate nucleus. Furthermore, in the ventromedial nucleus, nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, substance P-, and somatostatin-like immunoreactivity, and in the dorsomedial nucleus with enkephalin-, galanin message-associated peptide- and substance P-like immunoreactivity. In the mammillary region nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, cholecystokinin-, and substance P-like immunoreactivity. Among these neuropeptides, enkephalin and substance P were most frequently found in nitric oxide synthase-immunoreactive neurons. We conclude that nitric oxide synthase-immunoreactive neurons contain neuropeptides in various parts of the hypothalamus, and that nitric oxide in the hypothalamus may be involved in a variety of neuroendocrine and autonomic functions.     

Cholinergic neurons contain Calbindin-D28k in the monkey medial septal nucleus and nucleus of the diagonal band: an immunocytochemical study

The distribution patterns of choline acetyltransferase (CAT), as a marker for cholinergic neurons, and Calbindin-D_28k (CaBP) immunoreactivities in the forebrain basal ganglia of the Japanese monkeyMacaca fuscata were compared. Similar distribution patterns of CAT and CaBP immunoreactivities were found in the medial septal nucleus (MS) and the nucleus of the diagonal band of Broca (DBB). Double-labeling fluorescence immunocytochemistry revealed that most, but not all, cholinergic neurons were CaBP-immunoreactive in the MS and DBB. The results suggest that CaBP may play a role in the septohippocampal cholinergic neuron system of the monkey.     

Somatostatin- and enkephalin-like immunoreactivities are frequently colocalized in neurons in the caudal brain stem of rat

Summary The medulla oblongata and pons of colchicine treated rats were analyzed with a doublestaining technique using mouse monoclonal antibodies to somatostatin and rabbit polyclonal antibodies raised against methionine-enkephalin. Numerous cells reacted with both antisera but cells reacting with only one antiserum were also observed. Double-stained cells were most frequently encountered at all levels of the nucleus tractus solitarii, in a well defined group in the caudal medullary reticular formation, along the lateral ventral surface of the medulla oblongata, dorsolateral to the inferior olive and in the nucleus raphe magnus. These findings provide further examples of coexistence of two peptides and indicate the possibility that somatostatin-and enkephalin-like peptides are co-released.     

脑啡肽与生长抑素在鸡视网膜无长突细胞共存的免疫组织化学研究

本文介绍用免疫组织化学的单标和双标技术研究脑啡肽(ENK)和生长抑素(SOM)在鸡视网膜无长突细胞的定位和共存。单标的实验结果表明,一些SOM免疫反应阳性无长突细胞的形态、胞体在内核层的位置及其突起在内网层的分支式样与某些ENK免疫反应阳性无长突细胞相似,虽然其突起在内网层的第3、4亚层形成的丛网不象ENK免疫反应阳性突起那样丛密,在内网层的第5亚层也未见SOM免疫阳性突起。双标的实验结果表明,一些无长突细胞显示ENK和SOM两种免疫阳性反应,而另一些无长突细胞分别只显示ENK或SOM阳性免疫反应。文中还对视网膜神经多肽间或与经典神经递质的共存进行了讨论。     

Distribution of galanin-binding sites in the monkey and human telencephalon: preliminary observations

Summary Using X-ray film autoradiography the distribution of ¹²⁵I-galanin binding sites was studied in the forebrain of monkey and man. In the monkey a high density was found in all areas of the neocortex, especially layer 4, and in certain subfields in the hippocampal region. Also in the human brain high activity was seen in neocortex, mainly layer 6 and in hippocampal areas, as well as in amygdala, piriform cortex and hypothalamus. These results suggest that the 29-amino acid peptide galanin may be involved in the regulation of higher cortical functions in primates.     

Effects of coexisting neurochemicals on the release of serotonin from the intermediate area of rat thoracic spinal cord

Serotonin (5-HT), substance P (SP), neurokinin A (NKA), and thyrotropin-releasing hormone (TRH) coexist in the nerve terminals of the intermediolateral cell column (IML) of the thoracic spinal cord. The Ca2⁺-dependent release of 5-HT from the microdissected intermediate area (including the IML) of the rat thoracic spinal cord, and the 5-HT_1B autoreceptor regulator of 5-HT release, were previously demonstrated. In this paper, the effects of SP, NKA, TRH, and/or their analogs on the release of [³H]5-HT from the intermediate area were investigated using an in vitro superfusion system. Both SP (the endogenous ligand for neurokinin-1 (NK₁) receptor) and an NK₁, agonist (GR 73632) significantly increased the basal release of [³3H]5-HT. SP and GR 73632 did not change the K⁺-stimulated release of [³H]5-HT. The effect of the NK₁ agonist on the basal release of [³H]5-HT was dose-dependent, was reduced by an NK₁ antagonist (GR 82334), and was not dependent on extracellular Ca²⁺. Neither NKA, an NK₂, agonist (GR 64349), nor a TRH analog (MK-771) altered the basal or stimulated release of [³H]5-HT. These data suggest that basal release of 5-HT from the intermediate area of the rat thoracic spinal cord is regulated by SP (acting through an NK₁ receptor), but not by NKA or TRH. These results provide evidence for the role of SP as a modulator of serotoninergic neurons in the intermediate area of the thoracic spinal cord, and may help to clarify the role of coexisting neurochemicals in the spinal regulation of the sympathetic nervous system. © 1995 Wiley-Liss, Inc.

1 This article is a US Government work and, as such, is in the public domain in the United States of America.

     

1例小脑幕硬脑膜动静脉瘘合并运动神经元病

1病例介绍 患者,女性,47岁。主因进行性四肢无力11个月,声音嘶哑、吞咽困难3个月就诊。患者11个月前（2009年6月）无明显诱因出现左下肢无力,迈步费力,逐渐加重。10个月前开始出现右上肢无力,写字和端碗费力,无肢体麻木、头痛及二便障碍,外院行头、颈段MRI（一）。     

Association of polymyositis with rheumatoid arthritis

The association of polymyositis (PM) and rheumatoid arthritis (RA) is described in a 40-year-old female Mexican patient who was studied for a long period of time. The characteristic changes of PM that preceded the onset of RA for 7 years included proximal symmetrical muscle weakness, increased creatine kinase activity, and distinctive electromyography and muscle biopsy results. The occurrence of RA during the final 4 years of the 11-year period was characterized by long-lasting deforming and symmetric polyarthritis, high positive rheumatoid factor, subcutaneous nodules, and erosive joint changes. Through observation, myopathic changes other than those from PM were excluded. Joint changes other than from RA were also ruled out. A review of the literature revealed few specific reports of the coexistence of both diseases.     

CGRP-like immunoreactivity in A11 dopamine neurons projecting to the spinal cord and a note on CGRP-CCK cross-reactivity

Using the indirect immunofluorescence technique and double labelling procedures combined awith retrograde tracing it could be demonstrated that the A11 dopamine cell group, located at the border between the diencephalon and mesencephalon of the rat brain and some of which project to the spinal cord, contains calcitonin gene-related peptide (CGRP)-like immunoreactivity. Thus, another catecholamine group in the rat brain has been shown to have a coexisting peptide. One of the CGRP antisera used in the present study also stained cholecystokinin (CCK) containing neurons in various brain areas. Absorption and displacement experiments using immunohistochemistry and radioimmunoassay showed that this cross-reactivity was confined to the C-terminal portion of the peptide molecule. Therefore, the present results suggest that CGRP antisera used for immunohistochemistry and radioimmunoassay should be tested for possible cross-reactivity with CCK.     

Chronic myelomonocytic leukemia coexisting with B-cell chronic lymphocytic leukemia

Coexistence of B-cell chronic lymphocytic leukemia (B-CLL) and chronic myelomonocytic leukemia (CMML) is an unusal event, and to our knowledge, only four such cases have been reported in the literature. We report a 68-year-old white woman in whom these two diseases were diagnosed concomitantly. The diagnosis was made on the basis of peripheral blood count, morphology and immunophenotyping, and bone marrow cytology and histology. Interphase FISH analysis detected a 13q14.3 deletion in lymphocytes nuclei and no such abnormality in monocytes nuclei. The PCR analysis of IgH gene rearrangement in the bone marrow, as well as the peripheral blood lymphocytes, showed two different monoclonal IgH configurations as the result of biallelic clonal rearrangement of IgH genes suggesting an origin of lymphocytes from B-cell progenitors. The patient was originally treated with prednisone 1 mg/kg/day because of progressive significant thrombocytopenia, without improvement. Subsequently, she received one course of cladribine (2-CdA). Significant reduction of lymphocytes in the peripheral blood was observed. However, rapid increase of monocytes was seen shortly after the 2-CdA treatment. Subsequently, she received hydroxyurea (1.5 g/day) without hematological improvement. The patient died in January 2003, three months after diagnosis because of progression of both leukemias and associated pneumonia. Possible etiopathogenic relationship between both disorders is discussed.