INT1562
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
To reveal secretory, activational and transcriptional changes in the hypothalamus of morphine-dependent rats during naloxone precipitated opioid withdrawal, we measured corticosterone secretion, c-Fos induction and heteronuclear (hn)RNA levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in naïve and morphine dependent animals injected with saline or 5 mg/kg naloxone. | |||||||||||||||
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There is evidence that suggests that increased corticotropin-releasing hormone (CRH) release in the central nucleus of the amygdala underlies the anxiogenic and stress-like consequences of withdrawal that are common in phenomenology to all drugs of abuse. | |||||||||||||||
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Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism reduces gastric tone and contractility, in part by vagal pathways. | |||||||||||||||
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Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism reduces gastric tone and contractility, in part by vagal pathways. | |||||||||||||||
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We have previously shown that procaine and lidocaine stimulate corticotropin-releasing hormone (CRH) secretion by explanted rat hypothalami. | |||||||||||||||
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Because a prominent effect of the local anesthetics is to decrease neuronal firing by blocking sodium conductance, we were surprised by the capacity of these agents to cause CRH secretion and pituitary-adrenal activation and wished to further elucidate the possible mechanism(s) of these effects. | |||||||||||||||
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We have previously shown that procaine and lidocaine stimulate corticotropin-releasing hormone (CRH) secretion by explanted rat hypothalami. | |||||||||||||||
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To accomplish this, we first explored the effect of the sodium channel blocker tetrodotoxin (TTX) on basal and stimulated immunoreactive CRH (iCRH) secretion by explanted rat hypothalami. | |||||||||||||||
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Corticotropin-releasing factor release from the mediobasal hypothalamus of the rat as measured by microdialysis. | |||||||||||||||
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Also we observed a high degree of co-localization of CRH R1 and CRH R2 receptors on circulating and resident immune cells. | |||||||||||||||
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In painful inflammation, exogenous as well as endogenous corticotropin-releasing hormone (CRH) can release opioid peptides (mainly beta-endorphin) from various types of immune cells and produce antinociception by activating opioid receptors on peripheral sensory nerve endings. | |||||||||||||||
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Also we observed a high degree of co-localization of CRH R1 and CRH R2 receptors on circulating and resident immune cells. | |||||||||||||||
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In painful inflammation, exogenous as well as endogenous corticotropin-releasing hormone (CRH) can release opioid peptides (mainly beta-endorphin) from various types of immune cells and produce antinociception by activating opioid receptors on peripheral sensory nerve endings. | |||||||||||||||
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Inhibition of corticotrophin releasing factor secretion in the pentobarbitone-morphine-treated rat. | |||||||||||||||
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In early-life psychological stress such as maternal separation, chronic pain occurs later in life due to dysregulation of the hypothalamic-pituitary-adrenal axis and significant increase in corticotrophin releasing factor (CRF) secretion. | |||||||||||||||
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In early-life psychological stress such as maternal separation, chronic pain occurs later in life due to dysregulation of the hypothalamic-pituitary-adrenal axis and significant increase in corticotrophin releasing factor (CRF) secretion. | |||||||||||||||
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The corticotrophin-releasing factor (CRF) is shown to be released during stress suggesting that CRF has a physiological role in the mediation of central nervous system (CNS) response to stress, including an inhibitory effect on gastric emptying. | |||||||||||||||
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The diurnal response to ovine corticotropin-releasing factor (CRF-41), arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) was studied in rats in which the endogenous release of CRF was blocked by chlorpromazine, morphine sulfate, and pentobarbital sodium. | |||||||||||||||
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Activation of the HPA axis in vivo depends on the secretion of CRH, an intact pituitary and the ventral adrenergic bundle innervating the hypothalamic paraventricular nucleus. | |||||||||||||||
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The influence of beta-endorphin on the secretion of corticotrophin releasing factor (CRF) by isolated rat hypothalami in vitro was studied. beta-Endorphin (10(-11)-10(-10) M) caused dose-related increases in the CRF contents of the hypothalami and of the medium in which they were incubated. | |||||||||||||||
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