Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoradiographic analyses of salmon calcitonin (sCT) binding in the rat mesencephalon revealed an exceptionally high concentration of receptors in the ventral and ventrolateral segments of the periaqueductal gray matter (PAG) extending along the entire rostral-caudal axis. Relatively heavy labeling was also seen along a band extending ventrolaterally through the mesencephalic reticular formation. Other receptor-rich areas include the nucleus linearis, pars compacta and lateralis of the substantia nigra, locus coeruleus, parabrachial nuclei and nucleus raphe pontis of the pontine reticular formation. Injections of sCT into the PAG induced a dose-dependent increase in hot-plate latencies. All rostral-caudal levels of these brain regions appeared to be equally responsive. Injections into the midline pontine reticular formation were also effective in increasing response latencies. Unilateral injections into the hypothalamus, medial thalamus, ventral thalamus and mesencephalic reticular formation proved to be ineffective. Human calcitonin (hCT) was considerably less potent. These biological effects are consistent with the potencies of both peptides in displacing 125I-sCT from slide-mounted sections of rat PAG. Naloxone failed to antagonize sCT-induced analgesia, suggesting an opiate independent mechanism for this peptide in eliciting analgesia.
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PMID:Calcitonin receptors in the rat mesencephalon mediate its analgesic actions: autoradiographic and behavioral analyses. 299 94

The observation that the narcotic antagonist naloxone could inhibit analgesia produced by electrical stimulation of the brain indicated the involvement of an endogenous chemical in the relief of pain. Multiple endogenous opioid peptides have been identified that have similar pharmacological properties to known narcotic analgesics. The biosynthesis, release, and degradation of opioid peptides have been studied in order to better understand how the manipulation of endogenous opioid systems can be used to produce or augment analgesia. The results of our studies reveal that various conditions and manipulations, such as electrical brain stimulation, acupuncture, stress, and the administration of opioid analgesics, can cause the release of endogenous opioid peptides and possibly endogenous nonpeptide substances. It has also been discovered that nonopioid peptides, such as cholecystokinin, calcitonin, and angiotensin II, can alter the action of opioid analgesics by antagonizing or potentiating their effects. An understanding of the role of endogenous peptides in endogenous opioid mechanisms is necessary for the development of new ways to treat pain and such other disorders as sleep apnea in children (sudden infant death syndrome), head injury, and opioid addiction that involve the activation or alteration of endogenous opioid systems.
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PMID:The role of endogenous peptides in the action of opioid analgesics. 352 91

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

Intracisternal injection of calcitonin (0.01-5 micrograms) dose dependently prevented the development of duodenal ulcers induced by cysteamine in female rats. By contrast, intravenous infusion of the peptide at a dose 50 times higher than an effective intracisternal dose, had no effect. Intracisternal injection of calcitonin increased by three fold the generation of 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2, in the duodenal mucosa. These studies demonstrated that calcitonin acts within the brain to potently suppress duodenal ulcers induced by cysteamine. The mechanisms of the antiulcer effect may involve changes in prostaglandin generation along with alterations of gastrointestinal secretion and motility associated the central injection of calcitonin. Growing evidence suggests that salmon calcitonin may act as a neuromodulator or neurotransmitter in the central nervous system. Specific binding sites have been demonstrated for calcitonin in the hypothalamus, brain stem and dorsal horn of the spinal cord using homogenate and membrane preparations or in vitro autoradiography methods. The peptide injected into the cerebrospinal fluid (CSF) produces a wide spectrum of biological effects including analgesia, hyperthermia, changes in pituitary hormone release, decrease in food and water intake, locomotor activity, and blood pressure. Numerous studies also demonstrated that calcitonin acts within the brain to markedly influence gastrointestinal secretory and motor function in rats and dogs and gastric ulceration in rats. In particular, intracisternal injection of salmon calcitonin was found very potent to selectively inhibit gastric ulcers elicited by stress, aspirin and central thyrotropin-releasing factor but not by necrotizing agents. In the present study, we further investigated the antiulcer effect of salmon calcitonin using the well established cysteamine experimental model to induce duodenal ulcers in rats. Part of this work has been reported in abstract form.
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PMID:Potent CNS action of calcitonin to inhibit cysteamine-induced duodenal ulcers in rat. 360 Jan 97

The possibility that the catecholaminergic (CA) system might be involved in calcitonin (CT)-induced analgesia was examined. The administration of the neurotoxin for CA neurons, 6-hydroxydopamine (6-OHDA) significantly reduced salmon CT (sCT) analgesia as measured in rats by the hot-plate test. Pretreatment with an alpha- and beta-blocker (phentolamine and propranolol) was also effective in lowering significantly the activity of sCT. When the two drugs were administered alone, propranolol, but not phentolamine, reduced the analgesic effect of sCT. A more pronounced and long-lasting inhibitory effect on sCT-analgesia was obtained using atenolol (selective beta 1-receptor blocker). The present data support the role of the CA system in sCT-induced analgesic activity.
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PMID:Role of catecholamines in calcitonin-induced analgesia. 393 65

The acetylcholine writhing test and the hot plate test were used in mice to evaluate peripheral and central analgesia after porcine, salmon and human calcitonin administrations. ICV and IV injection of calcitonins caused a peripheral analgesia that persisted for at least 2 hr. SC injection of calcitonins did not produce peripheral analgesia. However, when administered by IP route, an increasing peripheral analgesia was observed. Although it had a slow onset, it was as powerful as after ICV or IV administration. Employing the hot plate test to determine the entity of a central analgesic response, the IP administration of calcitonin surprisingly revealed a hyperalgesic effect. It started soon after the injection, reaching its maximum after about 2 hr. At this point the hyperalgesic effects were fully antagonized by EDTA.2 Na ICV, or by Ca++ICV. Moreover only the latter produced a strong and long acting analgesia. Applying a central or peripheral test, calcium seems to play different roles on the algesia variations induced by calcitonins.
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PMID:Are calcitonins analgesic and/or hyperalgesic? 393 32

Intracerebroventricular (i.c.v.) injection of 19 pmol/rat or more of salmon calcitonin (sCT) or iodinated sCT suppressed spontaneous intake of food and water in a dose-dependent manner. Tail-whipping was a peculiar behavior which concomitantly developed, but no analgesia ensued from the doses tested (up to 62 pmol/rat). It was examined how the rise and fall pattern of these behavioral effects would correlate with the dispositional pattern of 125I-sCT. When the radioactive peptide was injected in anorectic doses via the i.c.v. route, the radioactivity was found to distribute throughout the brain, but not uniformly. In rats which showed a marked anorexia and tail-whipping behavior, distribution occurred in such a manner that it could be interpreted to reflect the regional and subcellular distribution pattern of sCT-specific binding sites. Even 3 hr after injection, the hypothalamus, the smallest region, retained the highest radioactivity corresponding to about 1% of the dose and at least one half of which was identified as the intact iodo-sCT. To be noted is the finding that sCT injected centrally will quickly enter the systemic circulation and peripherally induced long-lasting hypocalcemia, since the anorectic dose of sCT is considerably higher than the dose needed for the peripheral effect. It is concluded that most of the sCT after i.c.v. injection leaks into the systemic circulation, but the rest is retained rather selectively around the receptor in hypothalamic nuclei for a long time, leading to day-long suppression of feeding and drinking behavior.
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PMID:Intracerebroventricular injection of 125I-salmon calcitonin in rats: fate, anorexia and hypocalcemia. 399 41

Animal experiments demonstrate that the intracerebro-ventricular administration of calcitonin induces analgesia. During the treatment of such diseases as osteitis deformans Paget and acute pancreatitis with calcitonin no spectacular pain-relieving effect was evident, but the application of calcitonin in hypercalcemic patients with bone tumors led to considerable pain relief. Recent double-blind studies document the analgesic effectiveness of calcitonin in malignant diseases, but also against postoperative pains in nontumor patients. Calcitonin as an analgesic drug deserves further investigation.
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PMID:Calcitonin: analgesic effects. 636 72

It has been proposed that the polypeptide calcitonin (CT) occurs in the central nervous system and may have a neuromodulatory role in endogenous pain relief pathways. However, recent results suggest that CT is not present in the central nervous system. Intrathecal (IT) injection of CT on the lumbar enlargement of rats caused a reversible increase of the hindpaw lick latency in the hot plate test. No analgesia was observed with the vocalization test to electrical stimulation of the tail. In contrast 10 micrograms morphine hydrochloride IT caused analgesia in both tests. It is concluded that IT CT does not cause analgesia, but has a reversible blocking effect on motor responses.
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PMID:Subarachnoid injection of salmon calcitonin does not induce analgesia in rats. 649 28

Human and salmon synthetic calcitonins were employed by the epidural or subarachnoid routes of administration in nine patients suffering from chronic, intractable oncological pain. The aim of the study was to investigate the analgesic effect of the hormone by the above-mentioned routes when a lower amount than that commonly used in the normal parenteral route is injected. Both calcitonins produced an effective analgesia, the difference between human and salmon calcitonin seeming to be mainly concerned with the duration of the action, which is short for human and more prolonged (up to 12 hours) for salmon calcitonin. No irritating meningeal phenomena and no respiratory difficulties were observed during the treatment. Our results suggest that epidural administration of synthetic salmon calcitonin may be considered a practical solution in the management of intractable oncological pain.
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PMID:Antalgic activity of calcitonin: effectiveness of the epidural and subarachnoid routes in man. 668 94


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