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)

Acrolein was examined as an alternative fixative to formaldehyde for immunocytochemical localization of neuropeptides in the rat brain. A brief (5 min) vascular perfusion with a 5% acrolein solution allowed the identification of thyrotropin-releasing hormone (TRH), vasoactive intestinal peptide (VIP), somatostatin (SRIF), neurotensin (NT), methionine enkephalin (Menk), adrenocorticotropic hormone (ACTH), tyrosine hydroxylase (TH), and luteinizing hormone-releasing hormone (LHRH) in fibers and perikarya within the central nervous system of the rat using the peroxidase-antiperoxidase (PAP) technique. Acrolein appears to be particularly valuable for immunocytochemistry, as it 1) stabilizes heterogeneous peptides and proteins rapidly and effectively, 2) retains antigenicity, and 3) preserves morphological detail.
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PMID:Acrolein: a fixative for immunocytochemical localization of peptides in the central nervous system. 618 5

Considerable evidence has demonstrated an interrelationship between the enkephalinergic and dopaminergic systems in both the mammalian and invertebrate nervous systems. We have described recently the presence of two classes of high affinity opiate binding sites in the nervous tissue of the marine mollusc Mytilus edulis. In order to examine the physiological role of these high affinity opiate sites, M. edulis pedal ganglia (Pg) were treated with the selective neurotoxin 6-hydroxydopamine (1 micrograms/animal, applied topically to the intact Pg); animals were sacrificed 5 days after treatment. The dopamine content of the Pg from lesioned animals was reduced to 33% relative to that of Pg from control animals. Neither serotonin nor norepinephrine levels were reduced. Fluorescent micrographs of formaldehyde-treated Pg from both lesioned and control animals revealed that the neurotoxic substance accumulates in the synaptically rich neuropil and not in the cortex of the Pg. Thus, the partial reduction in dopamine levels may reflect nearly total loss of dopamine in terminals with essentially no change in the nerve cell bodies. High affinity binding of the potent opioid peptide 125I-labeled FK 33-824 (2 nM) was reduced by 81% and low affinity binding (10 nM peptide) by 43% in Pg from lesioned animals relative to that in control tissue. In addition, D-Ala2-Met5-enkephalin, beta-endorphin and etorphine failed to change dopamine levels in lesioned animals. Together, these results suggest that the high affinity opiate binding sites that mediate alteration in dopamine levels are on dopaminergic presynaptic terminals.
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PMID:Evidence for the presynaptic localization of a high affinity opiate binding site on dopamine neurons in the pedal ganglia of Mytilus edulis (Bivalvia). 628 36

Tissue from the pars intermedia of the pituitary from new-born and adult rats was maintained in tissue culture for periods up to 14 days. Both new-born and adult rat pars intermedia cells showed active production of secretory granules during tissue culture, and also showed formaldehyde-chloral induced fluorescence. Immunohistochemically, beta-endorphin could be demonstrated in cultured pars intermedia cells. In contrast to the appearance of the pars intermedia cells in vivo, the granules in the cultured cells were most often seen along the cell membrane, and the cytoplasm was often dominated by clear vacuoles slightly larger than the granules. No exocytotic figures were observed in the cultured cells. The mechanism of hormonal release from the organ, if release does occur, thus remains obscure. In conclusion, cultured cells from the rat pituitary pars intermedia continue their production of hormonal granules in tissue culture, and thus form a valuable tool for further investigations on the complex regulation of hormonal secretion form the organ.
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PMID:Synthesis and storage of hormonal granules in cultured cells of the rat pituitary pars intermedia. 629 1

The histological distribution of met-enkephalin-like immunoreactivity was studied in the forebrain (particularly the striatum) and the spinal cord of the rat using the indirect peroxidase-labelled antibody method. In most experiments, vibratome sections of formaldehyde-fixed tissues and purified antibodies were used. The search for optimal conditions for the immunohistochemical reaction lead us to establish that met-enkephalin-containing perikarya of both untreated and colchicinized animals were better demonstrated when tissue were pre-treated with diluted hydrogen peroxide only. The additional treatment of these sections with Triton X-100 (or some other detergents) resulted in the near disappearance of the perikaryal immunoreactivity; on the contrary, numerous met-enkephalin containing nerve fibres and varicosities were then demonstrated in the same region. Using only the hydrogen peroxide treatment, we found numerous met-enkephalin-containing perikarya in the medial and ventral regions of the neostriatum. This distribution was prolonged caudally by the existence of a prominent group of stained somata in the ventral putamen-central nucleus of the amygdala. When intraventricular injections of colchicine were used, positive perikarya were more numerous within the striatum (the globus pallidus excepted) but their distribution was largely the same as in non injected animals. However, some new groups of somata were stained in this case in the forebrain (in the lateral septum, the olfactory tubercle and the hypothalamus particularly). In control animals only few met-enkephalin-containing perikarya were observed in the dorsal horn of the spinal cord when H2O2 pretreatment was used alone and they were numerous only when intraspinal injections of colchicine were performed. Met-enkephalin-containing fibres and varicosities, which were scattered in the whole neostriatum in the conditions used above, became very numerous when the tissue sections were incubated in the presence of Triton X-100. Their density increased markedly from the latero-dorsal to the medio-ventral regions but, in addition, an organization under the form of islands of stronger immunoreactivity was also evidenced. These islands were more numerous ventrally in the anterior neostriatum and in the central region of the "putamen." The dense plexus of immunoreactive nerve fibers forming "tube-like structures" which was always observed in the paleostriatum and in the cranial medial forebrain bundle (islands of Calleja) appeared more diffuse when detergents were used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Different localizations of Met-enkephalin-like immunoreactivity in rat forebrain and spinal cord using hydrogen peroxide and Triton X-100. Light microscopic study. 636 51

By means of immunohistochemistry combined with formaldehyde-induced fluorescence microscopy, met-enkephalin-like immunoreactivity was found to occur in the adrenalin -cells of frog adrenal glands. Immunoelectron microscopy demonstrated that the immunoreactive material is confined to the secretory granules. These findings suggest the concomitant release of enkephalin and adrenalin by exocytosis.
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PMID:Co-existence of enkephalin and adrenalin in the frog adrenal gland. 637 81

The formaldehyde method was used to examine the interaction of PGE1 with morphine, beta-endorphin and Met-enkephalin on rat mast cells by their effects on IgE-mediated 14C-serotonin release. PGE1 (2x10(-8) -2x10(-5) M) caused a dose-related inhibition of the mediator release 1 min after an antigen challenge, and morphine (3x10(-7) -3x10(-5) M) reversed this PGE1 effect dose-dependently and stereospecifically; naloxone (2x10(-4) M) antagonized this action of morphine. Beta-Endorphin (3x10(-7) -10(-5) M) and Met-enkephalin (3x10(-6) -10(-4) M) mimicked this morphine action dose-dependently and were antagonized by naloxone (2x10(-4) M). These results suggest that morphine and endorphins modulate immunological mediator release from rat mast cells through opioid receptors.
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PMID:IgE-mediated 14C-serotonin release from rat mast cells modulated by morphine and endorphins. 689 Jan 33

When samples of the ventricle surfaces of human post-mortem brain were examined by scanning- and transmission electron microscopy, varicose nerve fibres could be seen traversing among the cilia and microvilli of ependymal cells. The varicosities contained numerous small electron-lucent vesicles and frequent large electron-dense vesicles, and were usually nonsynaptic but occasionally anchored to the surface by desmosome-like junctions. Supra-ependymal nerve fibres were observed in the lateral ventricles (e.g., n. caudatus), foramen of Monro (stria medullaris), third ventricle (habenula) and floor of the fourth ventricle in brains of the five cases examined. However, only in one of these was a yellow formaldehyde-induced fluorescence observed (on the fourth ventricle floor). Its discrete granular appearance, rapid fading and colour were typical of supra-ependymal 5-HT nerve fibres observed in rat brain. Very recent investigations on serial cryostat sections of rat brain ventricle regions revealed the absence of an immunohistochemical reaction with antisera to substance P, leu- and met-enkephalin and glutamic acid decarboxylase, but the presence of a reaction with 5-HT antiserum. The target for impulse-released 5-HT from this nonsynaptic 5-HT nerve plexus, bathed in cerebrospinal fluid, is not yet known.
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PMID:Demonstration of supra-ependymal 5-HT nerve fibres in human brain and their immunohistochemical identification in rat brain. 702 69

This paper summarizes theory and evidence for a neural sensitization model of hyperresponsivity to low-level chemical exposures in multiple chemical sensitivity (MCS). MCS is a chronic polysymptomatic condition in which patients report illness from low levels of many different, structurally unrelated environmental chemicals (chemical intolerance, CI). Neural sensitization is the progressive host amplification of a response over time from repeated, intermittent exposures to a stimulus. Drugs, chemicals, endogenous mediators, and exogenous stressors can all initiate sensitization and can exhibit cross-sensitization between different classes of stimuli. The properties of sensitization overlap much of the clinical phenomenology of MCS. Animal studies have demonstrated sensitization to toluene, formaldehyde, and certain pesticides, as well as cross-sensitization, e.g., formaldehyde and cocaine. Controlled human studies in persons with self-reported CI have shown heightened sensitizability in the laboratory to nonspecific experimental factors and to specific chemical exposures. Useful outcome measures include spectral electroencephalography, blood pressure, heart rate, and plasma beta-endorphin. Findings implicate, in part, dopaminergic mesolimbic pathways and limbic structures. A convergence of evidence suggests that persons with MCS or with low-level CI may share some characteristics with individuals genetically vulnerable to substance abuse: (a) elevated family histories of alcohol or drug problems; (b) heightened capacity for sensitization of autonomic variables in the laboratory; (c) increased amounts of electroencephalographic alpha activity at rest and under challenge conditions over time. Sensitization is compatible with other models for MCS as well. The neural sensitization model provides a direction for further systematic human and animal research on the physiological bases of MCS and CI.
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PMID:Neural sensitization model for multiple chemical sensitivity: overview of theory and empirical evidence. 1041 81

We examine the effect on the hypothalamus-pituitary-adrenal gland (HPA) axis of prolonged exposure to low levels of formaldehyde in female C3H/He mice, using immunocytochemical and RT-PCR methods. Two groups of female mice were exposed to differing concentrations (0, 80, 400, 2000 ppb) of formaldehyde inhalation for 16 h/day, 5 days/week, for 12 weeks. The corticotropin releasing hormone (CRH)-immunoreactive (ir) neurons in the hypothalamus were then examined, together with the adrenocorticotropin hormone (ACTH)-ir cells and ACTH mRNA in the pituitary. One group comprised sham control mice. The other group was made allergic by injection of ovalbumin (OVA) and alum prior to exposure to formaldehyde, since most sick building syndrome (SBS) sufferers are women with allergic disease. These animals were further exposed to aerosolized OVA as a booster four times during the exposure period. Our results showed a dose-dependent increase in the number of CRH-ir neurons in the non-allergy (NAG) group. A similar pattern was found in ACTH-ir cells and ACTH mRNA. The allergy (AG) model group showed an increase in basal levels of all markers of HPA activity. Moreover, the AG mice appeared to respond to the lowest concentration of formaldehyde, and all indices of HPA activity were reduced at the highest concentrations of formaldehyde. These results relate to an important clinical issue and also have implications in the broader area of HPA regulation. We conclude that our experimental system may be a suitable animal model for SBS and/or multiple chemical sensitivity (MCS).
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PMID:Effect of prolonged exposure to low concentrations of formaldehyde on the corticotropin releasing hormone neurons in the hypothalamus and adrenocorticotropic hormone cells in the pituitary gland in female mice. 1519 73

We studied the change in the hypothalamo-pituitary-adrenal gland (HPA) axis upon adding prior toluene inhalation to our previous formaldehyde inhalation experiments to determine whether short term exposure to relatively high levels of toluene triggers multiple chemical sensitivity (MCS). Data come from immunocytochemical, morphometrical and RT-PCR measurements. Four groups of adult female mice were exposed to differing concentrations (0, 80, 400, and 2,000 ppb) of formaldehyde for 16 hr/day, 5 days/week for twelve weeks, after the mice were exposed intranasally to 500 ppm toluene per mouse for 6 hr/day, for 3 days. We found that the number of corticotropin releasing hormone (CRH)-immunoreactive (ir) neurons was up-regulated according to the amount of formaldehyde as well as inhalation of formaldehyde alone in our previous experiment. The proportion of adrenocorticotropin hormone (ACTH)-ir cells increased according to the formaldehyde concentration, though there was no significant difference between the 400 and 2,000 groups. The number of ACTH-ir cells was higher in the 400 group than in the other groups (0, 80, and 2,000). Expression of ACTH-mRNA was also up-regulated according to the quantity of formaldehyde. The sinusoid in the anterior pituitary showed more dilatation in the 400 and 2,000 groups than in the control group, especially in the 2,000 group. We propose that exposure to toluene prior to inhalation of formaldehyde has no effect on the HPA axis and as a trigger of MCS, although greater sinusoid dilatation was found in the anterior pituitary gland at higher concentrations of formaldehyde.
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PMID:Hypothalamo-pituitary-adrenal gland axis in mice inhaling toluene prior to low-level long-term exposure to formaldehyde. 1580 35


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