Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subependymal giant cell astrocytoma (SEGA) is the most common neoplastic process involving the brain in patients with tuberous sclerosis complex (TSC). Morphologically, these tumors exhibit a wide range of cytoarchitecture with spindle and epithelioid cells resembling astrocytes, and also large, occasionally giant cells, some of which have a distinctly ganglion-like appearance. Unresolved questions regarding SEGAs center on: (a) their cytogenesis, i.e., whether they are derived from single or multiple precursors; and (b) their differentiating capacity along glial or neuronal lines. We sought to determine whether SEGAs represent truly mixed tumors or whether they consist of a single population of cells with a capacity for divergent differentiation. Twenty SEGAs were assessed for immunophenotypic features of either neuronal or glial differentiation or both. Only tumors from patients with a clinically confirmed diagnosis of TSC were included. Immunoreactivity for glial fibrillary acidic protein (GFAP) and/or S-100 protein was considered indicative of a glial phenotype, whereas the presence of neuronal differentiation was assessed by staining for cytoskeletal proteins [neurofilament epitopes, class III Beta-tubulin, microtubule-associated protein 2 (MAP2), synaptophysin], neurosecretory substances [serotonin, cholecystokinin, Beta-endorphin, substance P, somatostatin, metenkephalin, neuropeptide Y, vasoactive intestinal polypeptide (VIP), and for the 28-kDa neuron-associated calcium binding protein calbindin. Of the tumors examined, 18 exhibited both glial and neuronal epitopes, the staining pattern being variable. In 19 tumors, the constituent spindle, polygonal and giant or ganglion-like cells showed variable immunoreactivity for GFAP and S-100 proteins both within the cell body and processes. Neuron-associated cytoskeletal proteins were present in 18 cases. Class III Beta-tubulin immunoreactivity was demonstrated in 17 tumors, both within the bodies of all three cell types and to varying degrees within their processes. Neurofilament protein and calbindin staining was present in 8 tumors, with reactivity for the former being distributed in a phosphorylation-dependent manner. MAP2 was detected in a few cells of two tumors. Immunoreactivity for neuropeptides was observed in 17 lesions. Somatostatin and metenkephalin staining was noted in 10 tumors (50%) being present particularly within polygonal cells. Neuropeptide Y, serotonin and Beta-endorphin reactivity was found in 6 (30%), 5 (25%), and 4 tumors (20%), respectively; Beta-endorphin was lacking in giant cells, whereas neuropeptide Y and serotonin were seen within their cell bodies. Substance P and VIP were evident in only occasional polygonal cells of 2 (10%) and 1 tumor (5%), respectively. Stains for cholecystokinin were negative. The observation of immunoreactivity for both glial- and neuron-associated epitopes within tumor cells of the same morphology suggests that SEGAs represent proliferations of cell lineages with the capacity to undergo divergent glioneuronal as well as neuroendocrine differentiation to a greater extent than do other mixed glial-neuronal neoplasms.
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PMID:Immunohistochemical characterization of subependymal giant cell astrocytomas. 892 13

This study has examined the development of the brainstem in a suboptimal intrauterine environment induced via chronic placental insufficiency in the fetal guinea pig. Placental insufficiency was produced by unilateral ligation of the maternal uterine artery at mid-gestation (term = 66-68 days) resulting in the production of growth-retarded fetuses that are chronically hypoxic and malnourished. The structural and neurochemical development of brainstem nuclei either directly or indirectly related to cardiorespiratory control were analysed by using new stereological methods and immunohistochemistry. A technique was devised to enable the procedures to be performed on alternate frozen sections. There were no significant differences between control and growth-retarded fetuses in the total number of neurons, area of neuronal somata or volume of the hypoglossal nucleus. Quantitative densitometry was used to measure immunohistochemical staining in the brainstem of growth-retarded fetuses compared to controls and revealed a significant (P < 0.02) decrease in substance P(SP)-immunoreactivity in the spinal trigeminal nucleus and a significant (P < 0.05) increase in met-enkephalin-immunoreactivity in the hypoglossal nucleus. Counts of stained neurons demonstrated a significant increase in the density of SP-positive neurons in the nucleus tractus solitarius (P < 0.05) and of met-enkephalin-positive neurons in the ventral medullary reticular formation (P < 0.05). There was also a proliferation of astrocytes, as determined by immunoreactivity to glial fibrillary acidic protein in the dorsal motor nucleus of the vagus, nucleus tractus solitarius and more generally around blood vessels throughout the brainstem. Thus, these results have been shown that although chronic intrauterine deprivation does not alter neuronal numbers, at least in the hypoglossal nucleus, there is a proliferation of astrocytes, and the expression of neurotransmitters/neuromodulators is markedly effected in some of the nuclei involved with cardiorespiratory control.
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PMID:Chronic placental insufficiency in the fetal guinea pig affects neurochemical and neuroglial development but not neuronal numbers in the brainstem: a new method for combined stereology and immunohistochemistry. 905 15

The effects of prenatal exposure to carbon monoxide (CO), a major component of cigarette smoke, was studied alone or in combination with postnatal hyperthermia, on the structural and neurochemical development of the postnatal brain at 1 and 8 weeks. Pregnant guinea pigs (n = 11) were exposed to 200 p.p.m CO for 10 h/day from midgestation until term (68 days), whereas control mothers (n = 10) breathed room air. On postnatal day 4, neonates from the control and CO-exposed pregnancies were exposed to hyperthermia (35 degrees C) for 75 min or remained at ambient (23 degrees C) temperature. Using semiquantitative immunohistochemical techniques the following neurotransmitter alterations were found in the medulla at 1 week: a decrease in met-enkephalin-immunoreactivity (IR) following postnatal hyperthermia and an increase in 5-hydroxytryptamine-IR following a combination of CO and hyperthermia. No alterations were observed in substance P- or tyrosine-hydroxylase-IR in any paradigm. At 8 weeks of age the combination of prenatal CO exposure followed by a brief hyperthermic stress postnatally resulted in lesions throughout the brain and an increase in glial fibrillary acidic protein-IR in the medulla. Such effects on brain development could be of relevance in cardiorespiratory control in the neonate and could have implications for the etiology of Sudden Infant Death Syndrome, where smoking and hyperthermia are major risk factors.
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PMID:Exposure to prenatal carbon monoxide and postnatal hyperthermia: short and long-term effects on neurochemicals and neuroglia in the developing brain. 1073 30

Corticotropin releasing factor is a 41 amino acid peptide that is present in afferent systems that project to the cerebellum. In the adult, this peptide modulates the activity of Purkinje cells by enhancing their responsiveness to excitatory amino acids. Two different types of corticotropin releasing factor receptors, designated type 1 and type 2, have been identified. The purpose of this study is to use immunohistochemistry to identify which corticotropin releasing factor receptors are present in the cerebellum of the adult mouse and to determine their cellular distribution. Receptor type 1 immunostaining is present throughout all lobules of the cerebellar cortex. Distinct labeling is present over the somas of most, if not all, Purkinje cells as well as the primary dendrites of Purkinje cells located at the base of vermal folia. In vermal lobules V, VI, VIII and IX numerous glial fibrillary acidic protein immunoreactive processes, oriented radially in the molecular layer, also are immunoreactive for receptor type 1. In the granule cell layer, scattered type 1 immunoreactive puncta are present throughout most cerebellar lobules. Receptor type 2 immunoreactive puncta are present throughout the molecular layer in all lobules. In addition, scattered basket and/or stellate cells, identified with a GABA antibody, are immunopositive for the type 2 receptor. In the Purkinje cell layer, the type 2 receptor immunolabeling is confined to the basal pole of the Purkinje cell including the initial axonal segment. In the granule cell layer, labeling is present over large cell bodies, and their initial axonal segments. These are likely to be Golgi cells, based on their co-staining with GABA. Finally, numerous elongated processes within the white matter, which are likely to be axons, also are type 2 immunoreactive. These data indicate that both types of corticotropin releasing factor receptor are present in the mouse cerebellum. However, the unique distribution of the two types of receptor strongly suggests a differential role for corticotropin releasing factor in modulating the activity of neurons, axons and glial cells via cell-specific ligand-receptor interactions.
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PMID:Cellular localization of corticotropin releasing factor receptors in the adult mouse cerebellum. 1111 57

The purpose of this study was to determine the effects of prenatal growth restriction on the ventilatory and thermoregulatory responses to asphyxia and hypercapnia in the newborn guinea-pig. Spontaneously growth-restricted (SGR) animals born to unoperated dams, and growth-retarded (GR) neonates born to dams in which a uterine artery had been ligated at mid gestation, were studied and compared with control neonates. Ventilatory responses to progressive asphyxia and steady-state hypercapnia were tested at 3-6 days of age using a barometric plethysmograph. The animals were then killed and the brains prepared for histological and immunohistochemical analysis. During progressive asphyxia, SGR neonates (n = 5) had a significantly increased minute ventilation compared with both control (n = 6) and GR (n = 5) neonates. Rectal temperature fell significantly in GR and SGR neonates after progressive asphyxia, but was unchanged in control neonates. The ventilatory responses to steady-state hypercapnia were not different in the GR, SGR and control neonates. The immunoreactive expression of glial fibrillary acidic protein, tyrosine hydroxylase, substance P and met-enkephalin in the medulla was also not different between the three groups. It was concluded that prenatal growth restriction is associated with alterations in the respiratory and thermoregulatory responses to asphyxia and hypercapnia, with greater effects observed when in utero growth restriction arises spontaneously, compared with that produced experimentally over approximately the last half of gestation.
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PMID:Consequences of intrauterine growth restriction on ventilatory and thermoregulatory responses to asphyxia and hypercapnia in the newborn guinea-pig. 1205 28

Adenosine can reduce pain and allodynia in animals and man, probably via spinal adenosine A1 receptors. In the present study, we investigate the distribution of the adenosine A1 receptor in the rat spinal cord dorsal horn using immunohistochemistry, in situ hybridization, radioligand binding, and confocal microscopy. In the lumbar cord dorsal horn, dense immunoreactivity was seen in the inner part of lamina II. This was unaltered by dorsal root section or thoracic cord hemisection. Confocal microscopy of the dorsal horn revealed close anatomical relationships but no or only minor overlap between A1 receptors and immunoreactivity for markers associated with primary afferent central endings: calcitonin gene-related peptide, or isolectin B4, or with neuronal subpopulations: mu-opioid receptor, neuronal nitric oxide synthase, met-enkephalin, parvalbumin, or protein kinase Cgamma, or with glial cells: glial fibrillary acidic protein. A few adenosine A1 receptor positive structures were double-labeled with alpha-amino-3-hydroxy-5-methyl-4-isoaxolepropionic acid glutamate receptor subunits 1 and 2/3. The results indicate that most of the adenosine A1 receptors in the dorsal horn are located in inner lamina II postsynaptic neuronal cell bodies and processes whose functional and neurochemical identity is so far unknown. Many adenosine A1 receptor positive structures are in close contact with isolectin B4 positive C-fiber primary afferents and/or postsynaptic structures containing components of importance for the modulation of nociceptive information.
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PMID:Distribution of antinociceptive adenosine A1 receptors in the spinal cord dorsal horn, and relationship to primary afferents and neuronal subpopulations. 1458 Sep 41

Corticotropin releasing factor (CRF) and its cognate receptors, defined as Type 1 and Type 2 have been localized within the cerebellum. The Type 2 CRF receptor (CRF-R2) is known to have both a full length (CRF-R2alpha) and a truncated (CRF-R2alpha-tr) isoform. A recent study documented CRF-R2alpha primarily in Bergann glia and astrocytes, as well as in populations of Purkinje cells in the adult cerebellum. The goal of the present study is to determine if CRF-R2alpha is present in the postnatal cerebellum, and if so to describe its cellular distribution. RT-PCR data showed that CRF-R2alpha is expressed in the mouse cerebellum from birth through postnatal day 21. Between birth and P14, CRF-R2alpha-immunoreactivity was localized within the somata of Purkinje cells, and migrating GABAergic interneurons. GFAP-immunoreactive astrocytes, including Bergmann glia, also expressed CRF-R2alpha-immunoreactivity from P3-P14. There is a change, however, in CRF-R2alpha immunolabeling within neurons as the cerebellum matures. Compared to its expression in the adult cerebellum, Purkinje cells, and GABAergic interneurons showed more extensive CRF-R2alpha immunolabeling during early postnatal development. We postulate that CRF-R2alpha could be involved in developmental events related to the survival and differentiation of Purkinje cells and GABAergic neurons, whereas in the adult, this isoform of the CRF receptor family is likely involved in modulating Bergmann glia that have been shown to play a role in regulating the synaptic environment around Purkinje neurons.
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PMID:Cellular localization of the full-length isoform of the type 2 corticotropin releasing factor receptor in the postnatal mouse cerebellar cortex. 1747 57

In order to gain insights on the function of the cellular prion protein (PrP(C)) sleep and the levels of the stress hormones corticosterone (CORT) and the adrenocorticotropic hormone (ACTH) before and after sleep deprivation (SD) were compared in two wild type (WT) mice strains and the following three PrP(C) transgenic lines: mice null for PrP(C) (mPrP(0/0)) and mice with specific and central expression of PrP in neurons (NSE-HPrP/mPrP(0/0)) or in glia cells (GFAP-HPrP/mPrP(0/0)). After SD mPrP(0/0) mice showed a larger degree of sleep fragmentation and of latency to enter rapid eye movement (REM) and non-REM sleep (NREM) than WT. During sleep recovery, the amount of NREM sleep and the slow-wave activity (SWA) were reduced in mPrP(0/0) mice. After SD, CORT and ACTH levels have distinct patterns in WT and mPrP(0/0). The NREM and SWA deficit was restored in NSE-HPrP/mPrP(0/0) mice but not in GFAP-HPrP/mPrP(0/0). Hormonal profile was only partially restored in NSE-HPrP/mPrP(0/0) mice and was similar to that of mPrP(0/0) and GFAP-HPrP/mPrP(0/0) mice. These findings demonstrate that neuronal, but not non-neuronal, PrP(C) is involved in sleep homeostasis and sleep continuity. They also suggest that neuronal PrP(c)-dependent hormonal regulation of HPA axis may contribute to the sleep homeostasis.
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PMID:Contributions of neuronal prion protein on sleep recovery and stress response following sleep deprivation. 1757 Mar 49

Pituitary adenoma is a rare neoplasm in childhood, with prolactin and adrenocorticotropic hormone (ACTH)-secreting adenomas predominating in this age group. Herein is reported a case of an ACTH-producing macroadenoma with an unusual histology that occurred in a 2-year-old girl. Because of the patient's age and the macroadenoma's suprasellar location and large size (up to 4 cm in diameter), radical surgery was performed under the suspicion of craniopharyngioma or germ-cell tumor. Pathologically, it was a unique pituitary adenoma composed of monotonous ACTH-producing cells, smaller folliculo-stellate cells (FSC), and mucin-producing cells. The FSC, non-hormone-secreting pituitary cells of uncertain function, were confirmed by their S-100 protein, glial fibrillary acidic protein and cytokeratin expression immunoprofiles. The abrupt transition between the prominent gland-forming mucin-producing epithelia and the FSC component suggested that the mucin-producing epithelia might be derived from the FSC. This association might represent so-called 'retrodifferentiation' of adenoma cells to the FSC and the precursor cells of Rathke's pouch.
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PMID:Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl. 1768 32

Apolipoprotein A-IV (apo A-IV) is a satiation protein synthesized in the small intestine and hypothalamus. To further understand its anorectic mechanisms, we used immunohistochemical techniques to characterize the distribution of apo A-IV in brain areas involved in energy homeostasis. Dense apo A-IV staining was detected in the arcuate (ARC) and ventromedial hypothalamic nuclei with less staining in cells in the paraventricular and dorsomedial nuclei. In the brainstem, apo A-IV staining was found in the nucleus of the solitary tract. Double-staining immunohistochemistry revealed co-existence of apo A-IV with neuronal nuclei (a neuronal marker), but less with glial fibrillary acidic protein (a glial marker), in ARC, suggesting that apo A-IV is largely present in neurons. In the ARC, apo A-IV was co-localized with pro-opiomelanocortin (POMC), and apo A-IV administration stimulated hypothalamic POMC gene expression, suggesting that the brain apo A-IV system suppresses food intake by stimulating the ARC POMC system. To ascertain whether the apo A-IV detected in the brain is derived from the circulation, (125)I-labeled recombinant rat apo A-IV was intravenously injected into mice. No increase of radioactive apo A-IV was found in the brain, consistent with a lack of uptake of co-injected (99m)Tc-labeled albumin, indicating that circulating apo A-IV is unable to cross the blood brain barrier. These data collectively support the hypothesis that apo A-IV, produced by neuronal cells, may exert its anorectic action by interacting with catabolic regulatory neuropeptides.
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PMID:Characterization of apolipoprotein A-IV in brain areas involved in energy homeostasis. 1857 93


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