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Robert C Coghill - One of the best experts on this subject based on the ideXlab platform.
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distinct temporal filtering mechanisms are engaged during dynamic increases and decreases of Noxious Stimulus intensity
Pain, 2015Co-Authors: Carsten Dahl Morch, Ken Steffen Frahm, Robert C Coghill, Lars Arendtnielsen, Ole Kaeseler AndersenAbstract:Physical stimuli are subject to pronounced temporal filtering during afferent processing such that changes occurring at certain rates are amplified and others are diminished. Temporal filtering of nociceptive information remains poorly understood. However, the phenomenon of offset analgesia, where a disproportional drop in perceived pain intensity is caused by a slight drop in Noxious heat stimulation, indicates potent temporal filtering in the pain pathways. To develop a better understanding of how dynamic changes in a physical Stimulus are constructed into an experience of pain, a transfer function between the skin temperature and the perceived pain intensity was modeled. Ten seconds of temperature-controlled near-infrared (970 nm) laser stimulations above the pain threshold with a 1°C increment, decrement, or constant temperature were applied to the dorsum of the hand of healthy human volunteers. The skin temperature was assessed by an infrared camera. Offset analgesia was evoked by laser heat stimulation. The estimated transfer functions showed shorter latencies when the temperature was increased by 1°C (0.53 seconds [0.52-0.54 seconds]) than when decreased by 1°C (1.15 seconds [1.12-1.18 seconds]) and smaller gains (increase: 0.89 [0.82-0.97]; decrease: 2.61 [1.91-3.31]). The maximal gain was observed at rates around 0.06 Hz. These results show that temperature changes occurring around 0.06 Hz are best perceived and that a temperature decrease is associated with a larger but slower change in pain perception than a comparable temperature increase. These psychophysical findings confirm the existence of differential mechanisms involved in temporal filtering of dynamic increases and decreases in Noxious Stimulus intensity.
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OFFSET ANALGESIA: A TEMPORAL CONTRAST MECHANISM FOR NOCICEPTIVE INFORMATION
Pain, 2008Co-Authors: Marc D. Yelle, June M. Rogers, Robert C CoghillAbstract:Temporal filtering of afferent information is an intrinsic component of the processing of numerous types of sensory information. To date, no temporal filtering mechanism has been identified for nociceptive information. The phenomenon of offset analgesia, the disproportionately large decrease in perceived pain following slight decreases in Noxious thermal intensity, however, suggests the existence of such a mechanism. To test the hypothesis that a temporal filtering mechanism is engaged during Noxious Stimulus offset, subjects rated heat pain intensity while Stimulus fall rates were varied from -0.5 to -5.0 degrees C/s. In the absence of a temporal filtering mechanism, pain intensity would be expected to decrease in direct proportion to the Stimulus fall rate. However, psychophysical fall rates were considerably faster than Stimulus fall rates, such that subjects reported no pain while Stimulus temperatures were clearly within the Noxious range (47.2 degrees C). In addition, paired Noxious stimuli were presented simultaneously to determine if offset analgesia evoked by one Stimulus could inhibit pain arising from a separate population of primary afferent neurons. Pain ratings were significantly lower than those reported from two constant 49 degrees C stimuli when offset analgesia was induced proximal to, but not distal to, a second Noxious Stimulus. These asymmetric spatial interactions are not readily explained by peripheral mechanisms. Taken together, these findings indicate that offset analgesia is mediated in part by central mechanisms and reflect a temporal filtering of the sensory information that enhances the contrast of dynamic decreases in Noxious Stimulus intensity.
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Transient Analgesia Evoked by Noxious Stimulus Offset
Journal of neurophysiology, 2002Co-Authors: Joshua D. Grill, Robert C CoghillAbstract:Pain has long been thought to wax and wane in relative proportion to fluctuations in the intensity of Noxious stimuli. Dynamic aspects of nociceptive processing, however, remain poorly characterize...
Allan I. Basbaum - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of Noxious Stimulus-evoked pain behaviors and neuronal fos-like immunoreactiivity in the spinal cord of the rat by supraspinal morphine
Pain, 1996Co-Authors: K.r. Gogas, Jon D. Levine, H.j. Cho, G.i. Botchkina, Allan I. BasbaumAbstract:In previous studies, we reported that supraspinally administered DAMGO, a mu-opioid agonist, produces a dose-related, naloxone-reversible inhibition of formalin-evoked pain behaviors and spinal cord Fos-like immunoreactivity (FLI) in the rat spinal cord. Although these results support the hypothesis that activation of supraspinal mu-opioid receptors produces antinociception by increasing the activity of bulbospinal inhibitory pathways, other studies suggest that supraspinal morphine decreases rather than increases descending inhibitory control. In the present study, we specifically examined the effect of intracerebroventricular (i.c.v.) injection of morphine in the rat. Supraspinal morphine produced a dose-related, naloxone-reversible inhibition of both formalin-evoked behaviors and spinal cord FLI. Although the magnitude of the antinociception produced by i.c.v. morphine in the formalin test was significantly correlated with the numbers of FLI neurons in the spinal cord, the lowest dose of i.c.v. morphine tested (0.70 nmol) produced a significant reduction of FLI in the superficial laminae without producing behavioral antinociception, which is consistent with our hypothesis that Noxious Stimulus-evoked Fos expression in the superficial laminae is a poor predictor of the magnitude of pain behavior. These data support the hypothesis that the antinociceptive effects of supraspinally administered morphine result from an increase in descending inhibitory control.
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Differential effects of morphine on Noxious Stimulus-evoked fos-like immunoreactivity in subpopulations of spinoparabrachial neurons
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1994Co-Authors: Luc Jasmin, Hao Wang, K Tarczy-hornoch, Jon D. Levine, Allan I. BasbaumAbstract:In previous studies we reported that although morphine dose dependently inhibits Noxious Stimulus-evoked expression of the c-fos proto-oncogene in the rat spinal cord, morphine was without effect in certain populations of presumed nociresponsive neurons, even under conditions of complete behavioral analgesia. To determine whether the neurons that continue to express the c-fos gene include projection neurons, we evaluated the effect of morphine on Noxious Stimulus-evoked c-fos expression in spinoparabrachial neurons retrogradely labeled with Fluoro-gold. In the formalin test, we found that morphine analgesia was associated with a significant reduction in the number of Fos-like- immunoreactive spinoparabrachial projection neurons in the lateral reticulated area of the neck of the dorsal horn. Morphine, however, did not reduce the number of Fos-like-immunoreactive spinoparabrachial projection neurons either in the superficial dorsal horn or in the area around the central canal. These results indicate that under conditions of morphine analgesia two distinct populations of spinoparabrachial neurons can be recognized on the basis of their expression of the c-fos gene in response to Noxious stimulation. Since the expression of the c- fos gene has been correlated with neuronal activity, these data suggest that activity, and central transmission of nociceptive information, persists in certain nociresponsive projection neurons during morphine analgesia. Alternatively, if activity has, in fact, been blocked in these neurons, our results indicate that injury can produce significant molecular changes in neurons even though the neuronal activity and pain associated with the injury is blocked by morphine.
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Diffuse Noxious inhibitory controls reduce the expression of Noxious Stimulus-evoked Fos-like immunoreactivity in the superficial and deep laminae of the rat spinal cord.
Pain, 1994Co-Authors: Michael M. Morgan, K.r. Gogas, Allan I. BasbaumAbstract:Behavioral and electrophysiological studies have shown that a Noxious Stimulus applied to one part of the body can reduce the response to a subsequent Noxious Stimulus elsewhere on the body. This phenomenon is referred to as diffuse Noxious inhibitory controls (DNIC). In the present study we used immunocytochemical labeling for the Fos protein product of the c-fos proto-oncogene to determine the location of lumbar spinal nociresponsive neurons that are inhibited by a spatially remote Noxious Stimulus. Repetitive hindpaw pinch evoked pronounced Fos-like immunoreactivity in the superficial and deep laminae of the lumbar spinal cord. Placing the tail in 50 degrees C water before each hindpaw pinch significantly reduced Fos-like immunoreactivity in these regions. These data demonstrate that nociresponsive neurons in both the superficial and deep laminae of the spinal cord are sensitive to inhibition by a spatially remote Noxious conditioning Stimulus.
Michael M. Morgan - One of the best experts on this subject based on the ideXlab platform.
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Paradoxical inhibition of nociceptive neurons in the dorsal horn of the rat spinal cord during a nociceptive hindlimb reflex.
Neuroscience, 1999Co-Authors: Michael M. MorganAbstract:Abstract Nociceptive-specific and multireceptive neurons in the lumbar dorsal horn are excited by Noxious stimuli applied to the hindpaw and inhibited by Noxious stimuli applied to distant body regions. Given that at least a subset of these neurons are part of the circuit for nociceptive reflexes, inhibition of nociceptive-specific and multireceptive neurons should inhibit nociceptive reflexes. Unfortunately, previous attempts to test this hypothesis have been inconclusive because of methodological differences between electrophysiological and behavioral experiments. The present study overcame this problem by recording neural and reflex activity simultaneously. Rats were anesthetized with halothane and surgically prepared for single-unit recording from the lumbar dorsal horn. Hindpaw heat caused a burst of activity that reliably preceded hindpaw withdrawal in 10 nociceptive-specific and 17 multireceptive neurons. A distant Noxious Stimulus (tail in 50°C water or ear pinch) inhibited the evoked activity of both nociceptive-specific and multireceptive neurons and simultaneously changed the topography of the hindpaw reflex from flexion to extension without altering reflex latency. The present data are consistent with previous reports of inhibition of nociceptive-specific and multireceptive neurons during application of a distant Noxious Stimulus. However, inhibition of nociceptive-specific and multireceptive neurons concomitant with a shift in the hindlimb reflex from flexion to extension suggests that these neurons are part of the circuit for flexor reflexes specifically. Presumably, lateral inhibition from the flexor to extensor circuit allows for the release of hindlimb extension when neurons in the flexion circuit are inhibited by a distant Noxious Stimulus. Such a system reduces the chance of injury by allowing for withdrawal reflexes to a single Noxious Stimulus and escape reactions, such as running and jumping, to multiple Noxious stimuli.
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Inhibition and facilitation of different nocifensor reflexes by spatially remote Noxious stimuli
Journal of neurophysiology, 1994Co-Authors: Michael M. Morgan, Mary M. Heinricher, Howard L. FieldsAbstract:1. Noxious stimuli have been shown to produce a diffuse inhibition of nociresponsive neurons in the spinal and trigeminal dorsal horns. The present study sought to extend these electrophysiological studies of diffuse Noxious inhibitory controls (DNIC) by determining the effect of a spatially remote Noxious Stimulus on behavioral measures of nociception. Changes in latency for hindpaw withdrawal and tail flick reflexes were measured in lightly halothane-anesthetized or awake, spinally transected rats before, during, and after application of a spatially remote Noxious Stimulus. 2. Surprisingly, in no case did application of a spatially remote Noxious Stimulus inhibit the hindpaw withdrawal reflex. The latency for this reflex was either reduced or did not change when the tail or contralateral hindpaw was placed in hot water (50 degrees C) or when a Noxious pinch was applied to the ear. In contrast, the latency for the tail flick reflex was consistently increased when the hindpaw was placed in hot water. Both the hindpaw reflex facilitation and the tail flick reflex inhibition produced by a Noxious conditioning Stimulus were attenuated in spinally transected rats indicating supraspinal modulation of both reflexes. 3. In addition, and consistent with the work of others, placing the tail in hot water reduced the evoked activity of convergent neurons in both the trigeminal and lumbar spinal dorsal horns. Thus inhibition of the activity of nociresponsive neurons in the dorsal horn is consistent with inhibition of the tail flick reflex, but not with facilitation of the hindpaw withdrawal reflex.(ABSTRACT TRUNCATED AT 250 WORDS)
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Diffuse Noxious inhibitory controls reduce the expression of Noxious Stimulus-evoked Fos-like immunoreactivity in the superficial and deep laminae of the rat spinal cord.
Pain, 1994Co-Authors: Michael M. Morgan, K.r. Gogas, Allan I. BasbaumAbstract:Behavioral and electrophysiological studies have shown that a Noxious Stimulus applied to one part of the body can reduce the response to a subsequent Noxious Stimulus elsewhere on the body. This phenomenon is referred to as diffuse Noxious inhibitory controls (DNIC). In the present study we used immunocytochemical labeling for the Fos protein product of the c-fos proto-oncogene to determine the location of lumbar spinal nociresponsive neurons that are inhibited by a spatially remote Noxious Stimulus. Repetitive hindpaw pinch evoked pronounced Fos-like immunoreactivity in the superficial and deep laminae of the lumbar spinal cord. Placing the tail in 50 degrees C water before each hindpaw pinch significantly reduced Fos-like immunoreactivity in these regions. These data demonstrate that nociresponsive neurons in both the superficial and deep laminae of the spinal cord are sensitive to inhibition by a spatially remote Noxious conditioning Stimulus.
Jon D. Levine - One of the best experts on this subject based on the ideXlab platform.
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centralization of Noxious Stimulus induced analgesia nsia is related to activity at inhibitory synapses in the spinal cord
Pain, 2009Co-Authors: Jon D. Levine, Claudia Herrera Tambeli, Robert W GearAbstract:Abstract The duration of Noxious Stimulus-induced antinociception (NSIA) has been shown to outlast the pain Stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by Noxious stimulation is maintained by activity in spinal inhibitory receptors.
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Adaptations in nucleus accumbens circuitry during opioid withdrawal associated with persistence of Noxious Stimulus-induced antinociception in the rat☆
The journal of pain : official journal of the American Pain Society, 2003Co-Authors: Brian L. Schmidt, Jon D. Levine, Claudia Herrera Tambeli, Robert W GearAbstract:We studied adaptations in nucleus accumbens opioidergic circuitry mediating Noxious Stimulus-induced antinociception (NSIA) in rats withdrawing from chronic morphine administration. Although the magnitude of NSIA in withdrawing rats was similar to that observed in naive rats despite the tolerance of withdrawing rats to the antinociceptive effects of acutely administered morphine, the involvement of nucleus accumbens opioid receptors in NSIA in withdrawing rats was different from previous observations in both naive and tolerant rats. In withdrawing rats intra-accumbens administration of the mu-opioid receptor antagonist Cys2, Tyr3, Orn5, Pen7 amide (CTOP), but not the delta-receptor antagonist naltrindole, blocked NSIA. Both antagonists blocked NSIA in the naive state, but neither was effective in tolerant rats. Also, intra-accumbens administration of the mu-agonist [D-Ala2, N-Me-Phe(4,) Gly5-ol]-enkephalin (DAMGO) alone was sufficient to induce antinociception in withdrawing rats, whereas a combination of both mu- and delta-receptor agonists (ie, DAMGO and D-Pen(2,5)-enkephalin [DPDPE], respectively) is required to induce antinociception in naive rats. The delta- agonist DPDPE was without effect in the withdrawing rat, alone or when combined with DAMGO. Thus, although the magnitude of NSIA does not differ significantly among the 3 states, it is mediated by both mu- and delta-receptors in the naive rat, mu- but not delta-receptors in the withdrawing rat, and neither receptor type in the morphine tolerant rat. These changes may result from different degrees of tolerance, with delta-receptors being the most sensitive; however, it is not known how these changes occur without affecting the magnitude of the resultant antinociception.
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Neural and Endocrine Mechanisms Mediating Noxious Stimulus-Induced Inhibition of Bradykinin Plasma Extravasation in the Rat
The Journal of pharmacology and experimental therapeutics, 1999Co-Authors: Frederick Jia-pei Miao, Jon D. LevineAbstract:We studied the mechanisms by which activation of primary afferent nociceptors inhibits bradykinin-induced plasma extravasation in the rat. First, capsaicin, administered into the plantar surface of the hindpaw, dose-dependently inhibited bradykinin-induced plasma extravasation in the knee joint, a site distant from the Noxious Stimulus. The inhibitory effect of capsaicin was markedly attenuated after T12/L1 spinal transection combined with lumbar preganglionic sympathectomy, which interrupts ascending spinal tracts to rostral sites and to spinal sympathetic and sympathoadrenal outflow. Second, interruption of the sympathetics (cutting the L1-3 white rami) or surgical adrenal denervation significantly attenuated capsaicin-induced inhibition of bradykinin-induced plasma extravasation. Interruption of the sympathoadrenal pathway produced the largest attenuation. Lesioning of the hypothalamic-pituitary-adrenal axis did not affect the inhibitory action of capsaicin. Third, intra-articular perfusion with phentolamine (10−5 M, an α-adrenoceptor antagonist), propranolol (10−5 M, a β-adrenoceptor antagonist), and naloxone (10−5 M, an opioidergic receptor antagonist) each attenuated the inhibitory action of capsaicin. Propranolol and naloxone produced the largest attenuation. Blocking glucocorticoid receptors (RU-38,486, 30 mg/kg s.c.) did not affect the inhibitory action of intraplantar capsaicin. Fourth, the magnitude of the attenuation of capsaicin-induced inhibition of bradykinin-induced plasma extravasation after a combined treatment of surgical lumbar sympathetic decentralization with intra-articular phentolamine or surgical adrenal denervation with intra-articular propranolol or naloxone was similar to each of the surgical or pharmacological treatments of the same axis alone. These results support the suggestion that two neural/endocrine circuits, sympathoadrenal and sympathetic, account for most, if not all, of nociceptor activity-induced inhibition of bradykinin-induced plasma extravasation produced by capsaicin.
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Inhibition of Noxious Stimulus-evoked pain behaviors and neuronal fos-like immunoreactiivity in the spinal cord of the rat by supraspinal morphine
Pain, 1996Co-Authors: K.r. Gogas, Jon D. Levine, H.j. Cho, G.i. Botchkina, Allan I. BasbaumAbstract:In previous studies, we reported that supraspinally administered DAMGO, a mu-opioid agonist, produces a dose-related, naloxone-reversible inhibition of formalin-evoked pain behaviors and spinal cord Fos-like immunoreactivity (FLI) in the rat spinal cord. Although these results support the hypothesis that activation of supraspinal mu-opioid receptors produces antinociception by increasing the activity of bulbospinal inhibitory pathways, other studies suggest that supraspinal morphine decreases rather than increases descending inhibitory control. In the present study, we specifically examined the effect of intracerebroventricular (i.c.v.) injection of morphine in the rat. Supraspinal morphine produced a dose-related, naloxone-reversible inhibition of both formalin-evoked behaviors and spinal cord FLI. Although the magnitude of the antinociception produced by i.c.v. morphine in the formalin test was significantly correlated with the numbers of FLI neurons in the spinal cord, the lowest dose of i.c.v. morphine tested (0.70 nmol) produced a significant reduction of FLI in the superficial laminae without producing behavioral antinociception, which is consistent with our hypothesis that Noxious Stimulus-evoked Fos expression in the superficial laminae is a poor predictor of the magnitude of pain behavior. These data support the hypothesis that the antinociceptive effects of supraspinally administered morphine result from an increase in descending inhibitory control.
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Differential effects of morphine on Noxious Stimulus-evoked fos-like immunoreactivity in subpopulations of spinoparabrachial neurons
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1994Co-Authors: Luc Jasmin, Hao Wang, K Tarczy-hornoch, Jon D. Levine, Allan I. BasbaumAbstract:In previous studies we reported that although morphine dose dependently inhibits Noxious Stimulus-evoked expression of the c-fos proto-oncogene in the rat spinal cord, morphine was without effect in certain populations of presumed nociresponsive neurons, even under conditions of complete behavioral analgesia. To determine whether the neurons that continue to express the c-fos gene include projection neurons, we evaluated the effect of morphine on Noxious Stimulus-evoked c-fos expression in spinoparabrachial neurons retrogradely labeled with Fluoro-gold. In the formalin test, we found that morphine analgesia was associated with a significant reduction in the number of Fos-like- immunoreactive spinoparabrachial projection neurons in the lateral reticulated area of the neck of the dorsal horn. Morphine, however, did not reduce the number of Fos-like-immunoreactive spinoparabrachial projection neurons either in the superficial dorsal horn or in the area around the central canal. These results indicate that under conditions of morphine analgesia two distinct populations of spinoparabrachial neurons can be recognized on the basis of their expression of the c-fos gene in response to Noxious stimulation. Since the expression of the c- fos gene has been correlated with neuronal activity, these data suggest that activity, and central transmission of nociceptive information, persists in certain nociresponsive projection neurons during morphine analgesia. Alternatively, if activity has, in fact, been blocked in these neurons, our results indicate that injury can produce significant molecular changes in neurons even though the neuronal activity and pain associated with the injury is blocked by morphine.
Earl Carstens - One of the best experts on this subject based on the ideXlab platform.
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Isoflurane depresses diffuse Noxious inhibitory controls in rats between 0.8 and 1.2 minimum alveolar anesthetic concentration.
Anesthesia and analgesia, 2003Co-Authors: Steven L. Jinks, Joseph F. Antognini, Earl CarstensAbstract:UNLABELLED Diffuse Noxious inhibitory control (DNIC) occurs when the response to a Noxious Stimulus is inhibited by a second, spatially remote Noxious Stimulus. The minimum alveolar anesthetic concentration (MAC) to suppress movement is not altered by a second remote Noxious Stimulus. We hypothesized that DNIC would be depressed in the peri-MAC range. Rats were anesthetized with isoflurane, and MAC was measured. We recorded dorsal horn neuronal responses to Noxious thermal stimulation of the hindpaw, with or without concomitant supramaximal Noxious mechanical stimulation of the tail or contralateral hindpaw. At 0.8 MAC, the tail clamp decreased neuronal responses 70% compared with control heat-evoked responses (from 1032 +/- 178 impulses per minute to 301 +/- 135 impulses per minute; P 0.05). Similarly, 1.2 MAC isoflurane significantly depressed DNIC elicited by hindpaw clamping. In another group, the cervical spinal cord was reversibly blocked by cooling to determine whether the inhibition was mediated supraspinally. With spinal cord cooling, the counterStimulus-evoked inhibition was not observed at 0.8 MAC. These results suggest that DNIC involves supraspinal structures and is present at sub-MAC isoflurane concentrations but is depressed at more than 1 MAC. IMPLICATIONS Diffuse Noxious inhibitory control (DNIC) occurs when a Noxious Stimulus is perceived as being less painful when a second Noxious Stimulus is applied elsewhere on the body. DNIC is present in anesthetized animals, although how anesthesia affects it is unknown. We found that isoflurane depressed DNIC in the transition from 0.8 to 1.2 minimum alveolar anesthetic concentration, suggesting that DNIC is depressed in the anesthetic range needed to suppress movement.
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isoflurane blunts electroencephalographic and thalamic reticular formation responses to Noxious stimulation in goats
Anesthesiology, 1999Co-Authors: Joseph F. Antognini, Earl CarstensAbstract:BACKGROUND: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to Noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to Noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. METHODS: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a Noxious mechanical Stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The Noxious Stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. RESULTS: At an isoflurane concentration of 0.6 MAC, the Noxious Stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the Noxious Stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the Noxious Stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the Noxious Stimulus. CONCLUSIONS: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to Noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after Noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.
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Increasing Isoflurane from 0.9 to 1.1 Minimum Alveolar Concentration Minimally Affects Dorsal Horn Cell Responses to Noxious Stimulation
Anesthesiology, 1999Co-Authors: Joseph F. Antognini, Earl CarstensAbstract:BackgroundThe spinal cord appears to be the site at which isoflurane suppresses movement that occurs in response to a Noxious Stimulus. In an attempt to localize its site of suppressant action, the authors determined the effect of isoflurane on dorsal horn neuronal responses to supramaximal Noxious
