Haloperidol increases pain behavior following peripheral tissue injury.
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Animals↗
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Tolerance to peripheral tissue is transient and maintained by tissue-specific class I expression.
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Alleles↗
[Effects of dl-tetrahydropalmatine on blood pressure and norepinephrine and epinephrine contents in peripheral tissues].
Administration of dl-tetrahydropalmatine (THP) i.v., ip, and ig lowered the pressure and concurrently slowed the heart rate in anesthetized rats. The hypotensive and bradycardic effects were not produced by injecting THP into the vertebral artery in anesthetized rabbits. These results suggest that the site of hypotensive action of THP may not be a central one. The HPLC coupled with electrochemical detection showed that the contents of norepinephrine (NE) in the heart, aorta, and femoral artery and epinephrine (E) in the adrenal gland were markedly reduced by THP (P < 0.01). A positive correlation was found between the hypotensive effect and the reduction of NE in the aorta and femoral artery (r = 0.97, P < 0.01).
Animals↗
Production of IgE antibody and allergic sensitization of intestinal and peripheral tissues after oral immunization with protein Ag and cholera toxin.
Cholera toxin (CTX) is a potent oral adjuvant for the induction of mucosal IgA Ab responses protein Ags. We examined the Ab responses and allergic sensitization of several strains of mice to protein Ags, administered orally with CTX. The mice made strong IgA and IgG1 serum Ab responses, but little IgG2a Ab to Ags such as hen egg lysozyme (HEL) and OVA. However, when given a subsequent i.p. challenge with Ag alone, the same mice had immediate hypersensitivity reactions that included respiratory distress and death. Within 10 min of i.p. challenge, immunized mice had high levels of plasma histamine and extensive degranulation of mast cells in target tissues. These mice had detectable serum IgE Ab. Ag administered orally with the B subunit (CTB) of CTX did not sensitize mice. Intestinal tissues taken from these mice had Ag-specific ion-secretory responses in vitro, typical of intestinal anaphylaxis. Ag given s.c. without adjuvant could also sensitize for systemic and intestinal anaphylaxis. Sensitization with HEL given s.c. was dose dependent and correlated with a critical amount of HEL in the circulation. HEL was detected in the circulation after oral immunization, but CTX did not increase the uptake of HEL. Thus, oral immunization with a protein Ag in the presence of CTX can sensitize an animal for systemic and intestinal anaphylaxis. These results suggest a cautious approach to the use of CTX as an adjuvant in oral vaccines, and provide a new model to study immediate hypersensitivity reactions to intestinal Ag.
Administration, Oral↗
Binding profile of a selective calcitonin gene-related peptide (CGRP) receptor antagonist ligand, [125I-Tyr]hCGRP8-37, in rat brain and peripheral tissues.
The calcitonin gene-related peptide (CGRP) C-terminal fragment human CGRP8-37 acts as a potent antagonist of various in vitro and in vivo effects of CGRP. Its iodinated counterpart, [125I-Tyr] hCGRP8-37, binds with high affinity (KD values between 7.5 x 10(-11)-2.1 x 10(-10) M) to what is apparently a single class of CGRP receptors in brain, atrium and vas deferens membrane preparations. The relative potencies of various CGRP-related fragments and analogs in competing for [125I-Tyr]hCGRP8-37 binding sites were similar in these three preparations, with hCGRP alpha being the most potent competitor, followed by unlabeled hCGRP8-37, the linear agonist [acetamidomethyl-cysteine2,7] hCGRP alpha, and finally by rat amylin-amide and salmon calcitonin. Competition profiles suggested the existence of a single affinity site (except in the case of hCGRP alpha, for which competition binding data were best fitted to two apparent affinity constants in all three tissues), whereas rat amylin-amide revealed two affinity constants in the rat brain. Guanylylimidodiphosphate (100 microM) failed to alter specific [125I-Tyr]hCGRP8-37 binding in the various tissues studied here. Quantitative receptor autoradiography in the rat brain revealed [125I-Tyr]hCGRP8-37 binding sites mostly concentrated in the nucleus accumbens (shell), caudate putamen (tail), amygdaloid body, pontine nuclei, cerebellum and inferior olive, whereas lower quantities of sites were present in the olfactory tubercle, nucleus accumbens (core), medial geniculate, superior colliculus, temporal cortex, inferior colliculus, lateral lemniscus, vestibular nuclei and principal sensory trigeminal nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Testosterone uptake by the peripheral tissue of the human fetus (author's transl)].
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Brain↗
[Evaluation of blood flow in peripheral tissues in muscular atrophy in the course of nervous system diseases].
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Female↗
[Manganese-containing superoxide dismutase activity in human lung cancer tissue].
Manganese-containing superoxide dismutase (Mn-SOD) activity in lung cancer tissue from 5 lung cancer patients was measured by nitrite formation method, and lipid peroxide (LPO) was measured spectrophotometrically by thiobarbituric acid reaction. The results showed that Mn-SOD activity was highest in lung cancer tissue, peripheral tissues surrounding the lung cancer stood next and it was lowest in the peripheral normal lung tissue (P less than 0.01). However, LPO value was found to be lower in lung cancer tissues than that in the peripheral normal lung tissues.
Adenocarcinoma↗
Fine needle aspiration of peripheral neuroepithelioma of soft tissues.
Peripheral neuroepithelioma of soft tissue is a malignant primitive neuroectodermal tumor that appears both in children and adults and usually has a poor outcome. Fine needle aspiration on two patients with tumors in the lower limbs showed small round cells with unipolar processes and a tendency to form Homer-Wright rosettes. The cells had a round to oval nucleus with fine chromatin, up to four small, conspicuous nucleoli and vacuolated, periodic acid-Schiff-positive cytoplasm. The diagnosis was supported by electron microscopic study of the aspirate, which showed features of neuroblastic differentiation (i.e., neurosecretory granules), and by histologic, immunohistochemical and cytogenetic study of the resected tumors.
Adolescent↗
Effect of endotoxin on the integrity of the peripheral (soft tissue) microcirculation.
Peripheral edema, hypoproteinemia, and increased fluid requirements are characteristically seen with sepsis. Our purpose was to determine whether the soft tissue edema is caused by a direct vascular injury from sepsis or is secondary to hypoproteinemia. We determined the effect of endotoxin on peripheral (soft tissue) microvascular integrity using lymph flow (QL) and lymph/plasma (L/P) protein ratio to reflect fluid flux and increased permeability. Response was compared with that seen in the lung. Fourteen unanesthetized sheep were given intravenous E. coli endotoxin 2 micrograms/kg. Vascular pressures and cardiac output (CO) were maintained constant with the necessary fluid infusion. Lung QL increased two- to fourfold in all animals with lymph being protein-rich, indicating increased permeability. Peripheral QL increased transiently in response to an initial increase in vascular pressure returning rapidly to baseline except in those animals (N = 5) demonstrating hypoproteinemia where QL remained increased by 50 to 75%. The increased QL was totally explained by the degree of protein depletion, with no evidence of increased permeability. To assure an adequate endotoxin exposure to the peripheral microvessels, endotoxin (2 micrograms/kg) was also directly injected into the tissue drained by the soft tissue lymphatic. We noted a characteristic endotoxin pulmonary hypertension phase but, again, no increase in peripheral microvascular permeability was found. We conclude that endotoxemia does not alter peripheral microvascular permeability if tissue perfusion is maintained, while the lung is clearly a target organ. Hypoproteinemia may be responsible for the early edema in soft tissues with sepsis.
Animals↗
Local production of corticotropin releasing hormone is increased in experimental intestinal inflammation in rats.
BACKGROUND/AIMS: Corticotropin releasing hormone (CRH) suppresses immunological functions via stimulation of the pituitary-adrenal axis, but is also found in peripheral tissues. Peripheral proinflammatory activity of CRH is suggested by increased tissue concentrations in arthritis and in vitro immunostimulatory effects. This study evaluated intestinal CRH concentrations, immunolocalisation, and synthesis in chronic enterocolitis and investigated in vitro responsiveness of lamina propria mononuclear cells to CRH. METHODS: Chronic granulomatous enterocolitis was induced by intramural injection of peptidoglycan-polysaccharide polymers in the ileocaecal region of Lewis rats. CRH protein was measured in caecal specimens by immunohistochemistry and radioimmunoassay and caecal CRH mRNA expression was analysed by reverse transcriptase polymerase chain reaction. RESULTS: In the chronically inflamed caecum abundant immunoreactive CRH was found in inflammatory cells, mesenchymal cells, as well as in myenteric plexi. In contrast, only a few CRH containing cells were detected in normal and HSA injected control caecums. Moreover, caecal CRH protein levels were increased during chronic enterocolitis. Local CRH synthesis as indicated by mRNA expression was considerably increased in chronic enterocolitis whereas it was undetectable or low in uninflamed caecum. In addition, CRH stimulated in vitro proliferation of lamina propria mononuclear cells and inhibited mitogen induced proliferation. CONCLUSION: Increased CRH protein and mRNA expression in chronic enterocolitis and responsiveness of intestinal mononuclear cells to CRH indicate an immunomodulatory role for locally produced CRH in intestinal inflammation.
Animals↗
Hormonal regulation of peripheral-type benzodiazepine receptors.
Central benzodiazepine (BZ) receptors are located only in the central nervous system and mediate the clinical effects obtained by various BZs. In addition, there is another receptor that binds BZs with different drug specificities, which is located mainly on the outer mitochondrial membrane of various peripheral tissues. Peripheral BZ receptors (PBR) are composed of three subunits: an isoquinoline binding site, a voltage-dependent anion channel, and an adenine nucleotide carrier, with molecular weights of 18, 32, and 30 kDa, respectively. Complementary DNA of the isoquinoline binding subunit has been cloned in rat, calf, and human. The major role of PBR is in the regulation of steroid biosynthesis. Various PBR ligands stimulate the conversion of cholesterol into pregnenolone and the production of steroid hormones. The naturally occurring diazepam-binding inhibitor stimulates in vivo steroidogenesis via binding to PBR. In the female, PBR density is increased in rat and human ovary proportional with greater cell maturation and differentiation. In the male, testosterone modulates PBR density in the genital tract. These results show the strong relationship between PBR and the endocrine system.
Animals↗
Striatal implants of fetal striatum or gelfoam protect against quinolinic acid lesions of the striatum.
Previous studies in our laboratory have shown that intrastriatal implants of fetal striatum significantly attenuate excitotoxic damage resulting from a 240 nmol quinolinic acid (QA) challenge delivered 7 days later. In contrast, animals with intrastriatal implants of other tissue types (adipose tissue, peripheral nerve or adrenal medulla) demonstrate a more limited, but consistent trend in protection from QA excitotoxicity. The present study was designed to test the hypothesis that partial striatal protection found in animals receiving peripheral tissue grafts is due to the transplantation procedure eliciting a host response which attenuates excitotoxicity. Adult female Long-Evans rats received either cellular (fetal striatum) or acellular (gelfoam) implants followed 1 week later by a unilateral injection of 240 nmol QA into the grafted striatum. Animals were tested for rotational asymmetries before grafting, post-implantation, and after lesioning. Compared to baseline rotational behavior, rats which received implants did not show changes in ipsilateral turning after QA lesions. This protective effect was not limited to rotational behavior since improvements in spontaneous locomotor activity were evident. In addition, the adipsia and aphagia often associated with striatal lesions were ameliorated in both groups of grafted animals. Morphometric analysis demonstrated that endogenous dopaminergic, cholinergic and enkephalinergic systems in the two transplanted groups sustained less excitotoxic damage than in the QA lesioned, non-grafted animals. These results are consistent with the hypothesis that a host generated response activated by the implantation procedure provides a protective effect against QA excitotoxicity.
Animals↗
VP-RBP, a protein enriched in brain tissue, specifically interacts with the dendritic localizer sequence of rat vasopressin mRNA.
The concept of mRNA localization suggests that this process is mediated by sequences residing in the transcript to which proteins specifically bind and ultimately deliver the mRNA along cytoskeletal elements to specific intracellular destinations. The mRNA encoding the vasopressin (VP) precursor protein is localized to the nerve cell processes both in hypothalamic magnocellular neurons and in primary cultured neurons derived from embryonic rat superior cervical ganglia microinjected with a corresponding eukaryotic expression vector. The last 395 nucleotides of the VP mRNA encompassing part of the coding region, as well as the complete 3'-untranslated region, are sufficient to confer dendritic targeting to a normally nonlocalized reporter transcript. Here we report that, by employing in vitro crosslinking analyses with rat brain proteins and radiolabelled VP transcripts, an RNA-binding protein specifically interacts with the dendritic localizer sequence of the VP mRNA. This protein is enriched in nerve cell tissues. Peripheral tissues and various cell lines contain only low amounts of the binding activity. It therefore represents a candidate protein that may be involved in any aspect related to subcellular VP mRNA sorting in nerve cells, including transport and anchoring of the mRNA and possibly its translational control.
Animals↗
Colloid and elastic fibre: ultrastructural study on the histogenesis of colloid milium.
Tissues peripheral to well-developed papules of colloid milium were chosen for biopsy and electron microscopy examination. Evidence was presented that colloid is derived from elastic fibres through sequential degenerative change. In the upper to middle dermis of the peripheral tissue, a number of abnormal masses in the vicinity of small colloid depositions were observed. Ultrastructurally, those abnormal masses were degenerating elastic fibres in which "electron-dense layers" of normal elastic fibre increased in amount, although their electron density diminished. Electron-light layers were gradually diminished in quantity. Degenerated elastic fibres finally became granulo-fibrillar and were indistinguishable from colloid. Many fibrils which closely resembled 10 nm tubular microfibrils of normal elastic fibre were observed in the granulo-fibrillar substance. Since one stage of the degeneration of elastic fibre which eventually leads to the formation of colloid milium was very similar to that of actinic elastosis, a direct role of sunlight in the formation of colloid milium is suggested.
Aged↗
Melatonin plays a crucial role in the regulation of rhythmic clock gene expression in the mouse pars tuberalis.
Circadian rhythms in physiology and behavior are driven by a central clock residing within the hypothalamic suprachiasmatic nucleus (SCN). Molecularly, the biological clock is based on the transcriptional/translational feedback loop of clock genes (mPer, mCry, Clock, and Bmal1). Circadian expression of clock genes is not limited to the SCN, but is found in many peripheral tissues. Peripheral rhythms depend on neuroendocrine/neuronal output from the SCN. Melatonin, the hormone of darkness, represents an important neuroendocrine output of the circadian clock. The hypophyseal pars tuberalis (PT) is one of the main target regions for melatonin. The aim of the study was to test whether mPer, mCry, Clock, and Bmal1 are rhythmically expressed in the mouse PT and how the absence of melatonin receptors affects clock gene expression. We analyzed clock gene expression by in situ hybridization and compared wild-type (WT), melatonin 1 receptor knockout (MT1 ko), and melatonin 2 receptor knockout (MT2 ko) mice. mPer1, mCry1, Clock, and Bmal1, but not mPer2 and mCry2, were rhythmically expressed in the PT of WT and MT2 ko mice. In the PT of MT1 ko mice, expression of mPer1, mCry1, Clock, and Bmal1 was dramatically reduced. We conclude that melatonin, acting through the MT1 receptor, is an important regulator of rhythmic clock gene expression in the mouse PT.
Animals↗
Differential regulation of the growth hormone receptor gene: effects of dexamethasone and estradiol.
GH receptor (GHR) expression differs during development between central and peripheral tissues. Peripheral GHR expression is known to be sensitive to gonadal and adrenal steroids, but little is known about their effects on GHR in the central nervous system. We have now studied the effects of estradiol (E2) or dexamethasone on GHR expression in rat arcuate nucleus (ARC) and hippocampus, using quantitative in situ hybridization. Dexamethasone, which strongly down-regulates hepatic GHR expression, had no effect on central GHR transcript abundance, whereas E2 treatment, which stimulates hepatic GHR expression, significantly reduced ARC GHR messenger RNA (mRNA) levels. E2 also increased somatostatin (SS) expression significantly in both ARC and periventricular nuclei but did not reduce ARC GH-releasing hormone (GHRH) mRNA levels. Ovariectomy stimulated GHR and GHRH mRNA levels in the ARC, whereas it lowered ARC SS expression. E2 replacement in ovariectomized animals restored GHRH and SS mRNA levels to control values. Hippocampal GHR mRNA transcripts showed the same response to these endocrine manipulations as seen in the ARC. The induction of hepatic GHR expression by E2 is known to involve the transcription of an alternate 5' untranslated first exon, GHR1. This was readily detectable in the liver using a specific GHR1 probe but could not be detected in any CNS area. Our results show that GHR expression in the CNS is sensitive to regulation by peripheral steroids but that CNS and hepatic expression of GHR is differentially regulated by the same treatments.
Animals↗
Probenecid increases dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in rat adrenal gland.
Although norepinephrine and epinephrine are the predominant catecholamines (CAs) in peripheral tissues, peripheral dopamine (DA) systems are also physiologically significant. The DA is present both in the sympathetic ganglia and in the adrenal gland. We attempted to determine the possible presence of it in individual adrenal cells. We found increments in adrenal 3,4-dihydroxyphenylacetic acid (DOPAC) levels produced by probenecid, an inhibitor of anionic secretory mechanisms. Small amounts of DA and DOPAC were detected in the rat adrenal gland by using the high-performance liquid chromatographic electrochemical detection method. Two hr after probenecid treatment (200 mg/kg, i.p.), the concentration of striatal homovanillic acid approximately doubled compared with those of control rats, and the levels of striatal DOPAC remained much the same. Conversely, the adrenal DOPAC was markedly increased with no change in the levels of CAs. The existence of DOPAC and the increase of DOPAC by probenecid indicate that the adrenal DA may be independently granulated.
3,4-Dihydroxyphenylacetic Acid↗