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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal administration of monosodium glutamate (MSG: 2-4 mg/g, SC) selectively destroys circumventricular organs, especially the arcuate nucleus and median eminence of the hypothalamus, and also attenuates both nonopioid (continuous cold-water swim: CCWS) and opioid (morphine) analgesia when rats are tested as adults. The present study evaluated whether administration of MSG (1-6 g/kg, SC) or its equiosmotic control (2.37 M NaCl) to adult rats altered either basal nociception on the tail-flick and jump tests or analgesia following morphine (5 mg/kg, SC) or CCWS (2 degrees C for 3.5 min). MSG treatment dose-dependently produced small but significant increases in basal nociceptive thresholds in adult rats. Morphine analgesia was significantly reduced on both tests following pretreatment with MSG (30-32%) and hypertonic NaCl (17-25%). In contrast, MSG (55-247%), but not NaCl pretreatment potentiated both nonopioid CCWS analgesia on both tests and CCWS hypothermia. These data are discussed in terms of differential neonatal and adult MSG effects, dissociations between opioid and nonopioid pain-inhibition, and the role of MSG in altering adaptive mechanisms to environmental stressors.
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PMID:Dissociation of opioid and nonopioid analgesic responses following adult monosodium glutamate pretreatment. 260 62

It is generally believed that morphine activates a descending system(s) of inhibition, an effect contributing significantly to the analgesia produced. There has arisen, however, considerable controversy on this point. To address whether morphine inhibits spinal nociceptive transmission when given into the brainstem, the effects of focal electrical stimulation and monosodium S-glutamate (Glu) given in the periaqueductal gray (PAG), the locus coeruleus/subcoeruleus (LC/SC) and/or the nucleus raphe magnus (NRM) on spinal unit responses to noxious heating (50 degrees C) of the skin were examined and compared with effects produced by morphine (Mor). Focal electrical stimulation in 46 sites in the midbrain, dorsolateral pons and ventromedial medulla reliably inhibited unit responses to noxious heating of the skin (mean 34% of control). Microinjections of Glu (50 nmol, 0.5 microliter) were made into 17 sites in the midbrain, 10 sites in the LC/SC and 11 sites in the NRM, inhibiting unit responses to a mean 57% at 22 of the 38 sites of microinjection. Mor (10-20 micrograms, 0.5 microliter) was microinjected into 15 sites in the midbrain, 13 sites in the LC/SC and 11 sites in the NRM, inhibiting unit responses to heat to 63% of control at 24 sites of microinjection. The effects of morphine were shown to be receptor specific by antagonism with naloxone administered either intravenously or into the brainstem at the same site of microinjection as morphine. In 31 sites in the midbrain, dorsolateral pons and ventromedial medulla, microinjections of both Mor and Glu into the same sites attenuated unit responses to heating of the skin to a mean 77% and 71% of control, respectively. The results support the hypothesis that Mor acts supraspinally to modulate spinal nociceptive transmission by activating an endogenous descending inhibitory system(s). Focal electrical stimulation, glutamate and morphine modulated spinal nociceptive transmission by activation of descending inhibitory systems whose cell bodies of origin are in the PAG, the LC/SC or the NRM.
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PMID:Inhibition of spinal nociceptive transmission from the midbrain, pons and medulla in the rat: activation of descending inhibition by morphine, glutamate and electrical stimulation. 285 46

The antinociceptive role of spinal serotonin (5-HT) neurons descending from 5-HT cells near the ventrolateral surface of the medulla oblongata was investigated by stimulating these cells in normal rats, in rats with generalized or selective chemical ablation of 5-HT nerves, and in rats with postsynaptic blockade of 5-HT receptors. Electrical stimulation of the lateral medulla elicited analgesia in normal rats; the increase in pain threshold was proportional to the intensity and to the frequency of stimulation. In addition, microinjection of kainic acid or L-glutamate at the same sites also produced analgesia. However, generalized destruction of CNS 5-HT nerves produced by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-DHT reduced the magnitude of the antinociceptive responses to electrical stimulation. Postsynaptic blockade of CNS 5-HT receptors produced by intraventricular injection of cyproheptadine also reduced the stimulation-produced analgesia. The specificity of the lesions for 5-HT nerves is demonstrated by the lack of effect on the levels of noradrenaline in the same brain regions. The results indicate that the activity of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord serves to elevate pain threshold.
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PMID:The antinociceptive role of a bulbospinal serotonergic pathway in the rat brain. 289 26

Neonatal administration of monosodium glutamate (MSG) produces necrosis of circumventricular structures, including perikarya in the medial-basal hypothalamus that contain beta-endorphin (BEND) and met-enkephalin. Since neonatal MSG treatment alters morphine analgesia, the present study examined neonatal MSG effects upon opioid analgesia observed following either BEND or d-ala d-leu enkephalin (DADL). Rats treated with either MSG or vehicle over the first ten post-natal days, were surgically prepared with a lateral ventricle cannula at 100 days of age. Respective groups received central injections of either BEND (0, 0.1, 0.5 or 1.0 microgram) or DADL (0, 4, 20 or 40 micrograms), and jump thresholds were assessed 15, 30, 45 and 60 min thereafter. Following testing, selected MSG-treated and control animals were prepared for BEND immunocytochemistry. While the magnitude, duration and sensitivity of BEND analgesia on the jump test failed to differ between groups, MSG-treated rats displayed a 10-fold leftward shift in sensitivity and a 200-300% increase in the magnitude of DADL analgesia. Immunocytochemical analysis indicated that MSG treatment depleted perikarya in the medial-basal hypothalamus, periventricular thalamic fibers and periaqueductal gray terminal fields that contained BEND. The differential effects of MSG treatment upon opiate and opioid analgesia are discussed in terms of possible alterations in opiate receptor subpopulations.
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PMID:Differential alterations in opioid analgesia following neonatal monosodium glutamate treatment. 293 2

The analgesic response elicited by central administration of arginine vasopressin (AVP) appears to be dependent upon the integrity of the hypothalamic paraventricular nucleus (PVN), since lesions placed in the PVN eliminate AVP analgesia. A projection to the zona externa of the median eminence constitutes one of the VP-containing efferents of the PVN. Neonatal treatment with monosodium glutamate (MSG) destroys perikarya of the arcuate nucleus and median eminence. The present study examined whether AVP analgesia was affected in the MSG-treated rat and whether these alterations were accompanied by specific changes in VP immunoreactivity in the zona externa of the median eminence. Female rats, neonatally treated with either MSG or a saline control, were tested as adults on the tail-flick test following intracerebroventricular injections of 0, 75, 150 and 500 ng doses of AVP. After testing, selected animals were prepared for AVP and oxytocin immunocytochemistry of the median eminence. Significant potentiations in the magnitude of AVP analgesia were observed in MSG-treated rats. AVP and oxytocin immunoreactivity in the zona interna and oxytocin immunoreactivity in the zona externa of the median eminence were similar in MSG-treated and control rats. In contrast, AVP immunoreactivity in the zona externa of the median eminence was markedly reduced in the MSG-treated rat. These data suggest that VP analgesia may normally be inhibited by those medial-basal hypothalamic neurons affected by neonatal MSG treatment.
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PMID:Potentiation of vasopressin analgesia in rats treated neonatally with monosodium glutamate. 407 21

Definite and dose-dependent analgesia followed microinjection of L-glutamate into the nucleus reticularis paragigantocellularis (NRPG) of rats. This analgesic effect was inhibited by lumbar intrathecal pretreatment with phenoxybenzamine and phentolamine but not by propranolol, methysergide or naloxone. Microinjection of L-glutamate into the nucleus raphe magnus (NRM) also produced an analgesic effect which was reduced by intrathecal pretreatment with methysergide but not by phentolamine. These findings provide direct evidence that the NRPG and NRM function separately in descending pain-suppression systems of the spinal cord.
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PMID:Analgesia produced by microinjection of L-glutamate into the rostral ventromedial bulbar nuclei of the rat and its inhibition by intrathecal alpha-adrenergic blocking agents. 613 29

Neonatal administration of monosodium glutamate (MSG) produces neurotoxic degeneration of the retina and medial-basal hypothalamus, including the arcuate nucleus. Since this hypothalamic area contains the only neuronal cell bodies in brain which contain adrenocorticotrophic hormone (ACTH) and beta-lipotropin (beta-LPH) and beta-endorphin, destruction of these cells by MSG may interfere with pain responses mediated by nerve fibers arising from these perikarya. The present study examined whether MSG-treated rats, as compared to littermate controls, exhibited concomitant changes in the immunocytochemical distribution of ACTH and beta-LPH, and their reactivity to several analgesia-inducing manipulations. Although MSG-treated rats did not differ from control rats in their baseline reactivity to electric shock, they displayed an inability to exhibit analgesia following acute exposure to cold-water swim stress. In addition, MSG-treated rats showed an attenuated analgesic response following morphine administration. However, the analgesia elicited by either abrupt food deprivation, or the glucoprivic stress of 2-deoxy-D-glucose, was unaffected by neonatal MSG treatment. Concomitant with these selective analgesic deficits, MSG-treated rats displayed a marked immunocytochemical reduction in ACTH/beta-LPH perikarya and terminals in brain, but not pituitary. These data indicate that multiple pain-inhibitory systems exist, and that some rely upon an intact medial-basal hypothalamus to produce analgesia.
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PMID:Neonatal monosodium glutamate. Effects upon analgesic responsivity and immunocytochemical ACTH/beta-lipotropin. 624 67

Neonatal administration of monosodium glutamate (MSG) destroyed perikarya in the arcuate nucleus and median eminence, including those that contain met-enkephalin and beta-endorphin and it increased the density of opiate receptors in the midbrain. Treatment with glutamate decreased the analgesic response on the jump test following a 10 mg/kg dose of morphine, yet increased the analgesic response on the hot-plate test following 1 mg/kg dose of morphine. The present study demonstrated that changes in morphine-induced analgesia induced by glutamate varied as functions of the pain test and of gender. While males treated with glutamate displayed attenuated analgesia induced by morphine (2.5-15 mg/kg) on the jump test, jump thresholds of females treated with glutamate were potentiated after a 10 mg/kg dose of morphine and attenuated after a 15 mg/kg dose of morphine, relative to controls. In contrast, analgesia on the hot-plate test was potentiated in animals of both genders treated with glutamate after all doses of morphine. Changes in tolerance to morphine induced by glutamate also depended on the pain test and gender. While the peak analgesic response on the jump test did not occur until the fifth injection of morphine in all rats treated with glutamate, tolerance on the jump test was subsequently retarded in males treated with glutamate and accelerated in glutamate-treated females. Tolerance on the hot-palate test appeared not to be consistently affected by treatment with glutamate. Morphine-induced hyperthermia was initially decreased in rats treated with glutamate, but subsequently decreased in glutamate-treated males and increased in glutamate-treated females.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monosodium glutamate and analgesia induced by morphine. Test-specific effects. 652 50

Injection of 2-deoxy-D-glucose (2DG) elicits both analgesic and hyperphagic responses in rats. While pituitary dysfunction, decreased dopamine availability, or neonatal monosodium glutamate treatment decreases 2DG hyperphagia, they increase 2DG analgesia. In contrast, 2-DG analgesia alone is decreased by repeated 2-DG injections, while 2-DG hyperphagia alone is decreased following naloxone pretreatment. The present four experiments examined further mechanisms subserving these two induced responses. In the first experiment, rats were deprived of food for 6 h following 2-DG (600 mg/kg). While 2-DG hyperphagia persisted in the absence of glucoprivation, 2-DG analgesia failed to occur after this delay. In the second experiment, acute exposure to inescapable foot shock (4 mA, 0.5 s/5 s for 1 h) preceded administration of 2-DG (600 mg/kg). While 2-DG hyperphagia was eliminated by this procedure, 2-DG analgesia was significantly potentiated. In the third experiment, repeated morphine (10 mg/kg) injections over 14 days eliminated 2-DG analgesia on the fifteenth day, but failed to affect 2-DG hyperphagia. In the fourth experiment, lesions placed in either the lateral hypothalamus or zona incerta decreased 2-DG hyperphagia, but failed to affect 2-DG analgesia. These results are discussed in terms of common and dissociative mechanisms mediating both responses.
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PMID:Dissociation of analgesic and hyperphagic responses following 2-deoxy-D-glucose. 658 11

Neonatal administration of monosodium glutamate (MSG) produces in rats neurotoxic degeneration of the circumventricular system, including the medial-basal hypothalamus, depleting several neuropeptides and neurotransmitters in this area. In addition, a number of behavioral and neuroendocrine responses are impaired, including a significant decrease in the analgesic response to cold-water swims (CWS). The present study examined whether the alterations in the analgesic responses following CWS and 2-deoxy-D-glucose (2-DG) induced by neonatal MSG treatment were due either to direct alterations in a pain-inhibitory system, or alternatively, to alterations in a system that processes the stressful consequences or properties of a stimulus. To accomplish this, the analgesic, hypothermic, and locomotor responses following CWS and the analgesic, hyperphagic, and locomotor responses following 2-DG were assessed in rats treated neonatally (days 2, 4, 6, 8, and 10) with either MSG or a vehicle solution. MSG-treated rats displayed significant reductions in both their analgesic and hypothermic responses following CWS, suggesting that MSG treatment impairs an animal's ability to process sufficiently the stimulus properties of the swim as stressful. While MSG treatment potentiated 2-DG analgesia, it reduced 2-DG hyperphagia, suggesting that MSG treatment also impairs coping responses to glucoprivation. These data indicate the importance of the circumventricular system in the coding of stimuli as potential stressors and in the subsequent activation of requisite systems necessary to provide a sustained, coordinated, and synchronous coping response.
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PMID:Impairments in analgesic, hypothermic, and glucoprivic stress responses following neonatal monosodium glutamate. 673 8


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