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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracellular single-unit recordings were made from dorsal horn neurones in the lumbar spinal cord of cats which were anaesthetized or were anaemically decerebrated. Each neurone was classified functionally as wide dynamic range (WDR), non-nociceptive, nociceptive specific or proprioceptive. Vibration was then applied to the hind limb using a feedback-controlled mechanical stimulator. WDR neurones had 3 distinct types of response to vibration (80 Hz: 0.3-1.0 mm): excitation, depression and a biphasic response consisting of excitation followed by depression. The type of response depended upon the location of the stimulator probe. With the stimulator probe placed inside that part of the receptive field from which low intensity, non-vibrational cutaneous stimuli elicited excitation, 35 neurones were excited by the vibratory stimulation, none was depressed and 4 showed the biphasic response. On the other hand, when the probe was positioned outside the receptive field for low intensity stimuli, 7 WDR neurones were excited, 164 showed depression or the biphasic response and 7 were unaffected. On-going activity and activity evoked by iontophoretic application of glutamate were decreased during the depressant response and during the depressant phase of the biphasic response. In terms of non-nociceptive neurones, all (n = 30) were excited by vibration; depressant or biphasic responses were not observed. Excitation was elicited by placing the probe either inside or outside the receptive field for non-vibrational stimuli. All nociceptive specific neurones (n = 3) were depressed by vibration regardless of the position of the stimulus. All proprioceptive neurones (n = 12) were excited by vibration. The predominantly depressant effect of vibration on nociceptive neurones vs. the predominantly excitatory effect on non-nociceptive neurones prompts us to suggest that the increase in pain threshold and the clinical analgesia elicited by vibration may be mediated at the spinal level by a decrease in the rate of firing of nociceptive neurones and/or by excitation of non-nociceptive neurones.
Pain 1990 Mar
PMID:Differential responses of nociceptive vs. non-nociceptive spinal dorsal horn neurones to cutaneously applied vibration in the cat. 232 96

It has been previously reported that injection of neuroexcitatory compounds into the rostral ventrolateral medulla (RVLM) can produce an inhibition of nociceptive reflexes, often associated with a rise in arterial blood pressure. The aim of this study was to determine whether the subretrofacial (SRF) nucleus, which is a highly circumscribed group of cells within the RVLM known to play a major role in cardiovascular regulation also has an antinociceptive function. In barbiturate-anaesthetised and paralysed cats, unilateral microinjections of the neuroexcitatory compound sodium glutamate (8-20 nl of 0.5 M solution) into the SRF nucleus produced large increases in mean arterial pressure but had only small and inconsistent effects on the simultaneously measured ventral root responses to stimulation of primary afferent C-fibres. On the other hand, glutamate microinjections into RVLM sites closely adjacent to the SRF nucleus, or into the nucleus raphe magnus, produced powerful inhibition of the C-fibre evoked response in the ventral root which was accompanied by no or only small changes in arterial pressure. It is concluded that the SRF pressor cells do not exert any control over nociceptive spinal reflexes, but that such a function may be served by cells in closely adjacent parts of the RVLM. Moreover, the method of recording C-fibre evoked responses in ventral roots as a measure of the magnitude of nociceptive spinal reflexes, combined with the glutamate microinjection procedure, was shown to have a sufficient resolution to allow an accurate mapping of the location of antinociceptive cell groups within the ventrolateral medulla.
Pain 1989 Jun
PMID:Relationship between cardiovascular neurones and descending antinociceptive pathways in the rostral ventrolateral medulla of the cat. 256 78

A population of neurons localized to a small region of the brain stem reticular formation, the rostral ventrolateral reticular nucleus (RVL), is the principal area of the brainstem regulating resting, reflex, and probably behaviorally coupled control of arterial pressure. The critical area of the RVL reticular nucleus engaged in cardiovascular control surrounds a cluster of adrenergic neurons of the C1 group, and is therefore designated the C1 area. C1 area neurons have a direct and extremely potent synaptic relationship with preganglionic sympathetic neurons of the intermediolateral (IML) nucleus of the spinal cord. Neurons in the C1 area are tonically active and fire in relationship to the cardiac cycle, a rhythm imposed by baroreceptors. They thereby provide the background of excitation to preganglionic neurons to maintain normal resting arterial pressure. Which transmitter released by C1 area neurons produces sympathetic excitation is uncertain, but it may be glutamate. C1 area neurons are critical to the integration of a wide range of cardiovascular reflexes, including the arterial pressure responses to arterial baroreceptor, chemoreceptor, and other cardiopulmonary receptor stimulation, to pain and possibly to exercise, to brain stem ischemia and distortion, and probably to the arterial pressure elevations associated with emotional behavior. The cardiovascular neurons of the C1 area are responsive to the actions of a number of neurotransmitters, many of which are confined to local circuit neurons in the region, including gamma-aminobutyric acid (GABA), catecholamines, acetylcholine, and several opiates. They also appear to be the site of action upon arterial pressure of a number of drugs--including clonidine and possibly the beta-blockers. Neurons of the C1 area of the RVL reticular nucleus, therefore, appear to function as one of the most critical output systems of the brain for regulating arterial pressure in health and sickness.
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PMID:The C1 area of the rostral ventrolateral medulla oblongata. A critical brainstem region for control of resting and reflex integration of arterial pressure. 257 88

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

Concentrations of glutamate and aspartate have been measured in 45 microdissected brain areas and nuclei in rat. Both amino acids are ubiquitously present and distributed unevenly in the central nervous system. Very high glutamate levels were found in the cerebellum and the insular cortex, high levels in neocortical and limbic cortical areas, and in the nuclei of the medial hypothalamus. Aspartate is distributed rather uniformly with the highest concentration in the hypothalamic arcuate nucleus and the lowest in the midbrain central gray matter and the cerebellum. Acute formalin (pain) stress elevated glutamate and aspartate levels in the cortical areas and substantia nigra significantly, but had minor or no effects on other brain nuclei. Increased locomotor and behavioral activities due to a high dose of amphetamine resulted in a 2-5-fold increase of glutamate and aspartate concentrations, particularly in the biogenic amine-containing brain nuclei.
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PMID:Distribution and stress-induced increase of glutamate and aspartate levels in discrete brain nuclei of rats. 287 35

Trigeminothalamic projection neurons are important components of the pathways for conscious perception of pain, temperature, and tactile sensation from the orofacial region. The neurotransmitters utilized by trigeminal neurons projecting to the thalamus are unknown. By use of a monoclonal antibody specific for fixative-modified glutamate and a polyclonal antiserum against glutaminase, we recently identified neurons in the trigeminal sensory complex that contain glutamate-like immunoreactivity (Glu-LI) and glutaminase-like immunoreactivity. In the present study, we utilized combined retrograde transport-immunohistochemical techniques to localize putative glutamatergic trigeminothalamic neurons. Following injection of the retrograde tracer, wheatgerm agglutinin conjugated to horseradish peroxidase (WGA:HRP), into the ventroposterior medial thalamus (VPM), the number of neuronal profiles that were double-labeled with WGA:HRP and Glu-LI was greatest in principal sensory nucleus (Pr5), followed by subnuclei interpolaris (Sp5I) and caudalis (Sp5C). The average percentages of projection neurons double-labeled with Glu-LI were approximately 60-70% in Pr5 and Sp5I and 40% in Sp5C. The majority of double-labeled profiles in Sp5C were located in the magnocellular layer, as opposed to the marginal and substantia gelatinosa layers. A large injection site that spread into the intralaminar thalamic nuclei and nucleus submedius--areas implicated in the processing of nociceptive information--resulted in an increase in the ratio of single-labeled to double-labeled projection profiles in Sp5C. These results suggest that glutamate may be the neurotransmitter for a majority of trigeminothalamic projection neurons located in Sp5I and Pr5. However, on the basis of anatomical association, glutamate does not appear to be the major transmitter for neurons in Sp5C that forward nociceptive information to the thalamus.
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PMID:Localization of glutamate in trigeminothalamic projection neurons: a combined retrograde transport-immunohistochemical study. 288 92

Concentrations of putative neuroactive substances glutamate, aspartate, gamma-aminobutyric acid, glycine, proline and ethanolamine were determined in ventricular cerebrospinal fluid collected in patients suffering from Parkinson's disease, pain syndromes or cerebellar tremor. Values are similar to those given in the literature for lumbar cerebrospinal fluid. A decrease in gamma-aminobutyric acid in Parkinson patients, as reported in lumbar cerebrospinal fluid, could not be observed. Further evidence for a rostro-caudal gradient for gamma-aminobutyric acid is supplied. New insights into pathophysiological mechanisms in any of the investigated syndromes may not be derived.
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PMID:Ventricular cerebrospinal fluid concentrations of putative amino acid transmitters in Parkinson's disease and other disorders. 289 52

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.
Pain 1988 Apr
PMID:The antinociceptive role of a bulbospinal serotonergic pathway in the rat brain. 289 26

The role of trigeminal nucleus caudalis (Vc) in control of the autonomic and endocrine correlates of nociception was assessed in chloralose-anesthetized cats. Microinjections of the neuroexcitatory agent, L-glutamate (0.5 M), were directed at the marginal layers, at the central magnocellular portion, and at the deep magnocellular portion of Vc. Changes in the plasma concentration of adrenocorticotropin (ACTH), in mean arterial pressure, and in heart rate were examined. Glutamate excitation of neurons within the marginal layers of Vc evoked a significant (+143 +/- 52 pg/ml, P less than 0.01) increase in plasma ACTH during the 10 min postinjection sampling period. Glutamate injections into the deep magnocellular portion of Vc also increased plasma ACTH (+97 +/- 28 pg/ml, P less than 0.05), whereas activation of neurons in the central magnocellular portion of Vc had no consistent effect on plasma ACTH (-25 +/- 29 pg/ml, P greater than 0.10). Arterial pressure increased transiently after glutamate injections into the marginal layers or central magnocellular portion of Vc, whereas injections into the deep magnocellular portion of Vc did not affect arterial pressure. Heart rate increased transiently regardless of the laminar site of injection within Vc. These data indicate that activation of neurons in laminar regions of Vc that process nociceptive information cause an increase in plasma ACTH, whereas activation of neurons in laminae of Vc that process mainly non-nociceptive input have no significant influence on plasma ACTH.
Pain 1988 Jun
PMID:Glutamate activation of neurons within trigeminal nucleus caudalis increases adrenocorticotropin in the cat. 290 7

In urethane-anesthetized male rats, injection of 5 nmol clonidine into the nucleus of the solitary tract (NTS) causes hypotension and bradycardia. These effects are greater in spontaneously hypertensive rats (SHR) and normotensive Sprague-Dawley (SD) rats than in normotensive Wistar-Kyoto (WKY) rats. The effects of clonidine are stereoselectively inhibited by 100 ng intra-NTS naloxone in SHR and SD but not in WKY rats. In SHR, the effects of clonidine are also inhibited by intra-NTS administration of ICI 174864 (a delta-receptor antagonist) but not by beta-funaltrexamine (a mu-receptor antagonist), while in SD rats only the mu- and not the delta-antagonist was effective. Neonatal treatment of SHR with monosodium glutamate (MSG) reduced the beta-endorphin content of the arcuate nucleus and the NTS, reduced the cardiovascular effects of clonidine, and abolished their naloxone sensitivity. MSG treatment of newborn WKY reduced the beta-endorphin content of the arcuate nucleus but not the NTS and did not affect the responses to clonidine. Measurement of pain sensitivity by the formalin test indicated that clonidine was more potent as an analgesic in SHR and SD than in WKY rats, and its effect was inhibited by naloxone (2 mg/kg i.p.) in the former two strains but not in WKY. It is proposed that a naloxone-sensitive component of the cardiovascular effects of clonidine is due to release of a beta-endorphin-like opioid from the NTS, and that this mechanism is present in SHR and SD but not in WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endorphinergic mechanism in the central cardiovascular and analgesic effects of clonidine. 369 Mar 93


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