Pain-related aversion and Fos expression in the central nervous system in rats

Lei, Liugen; Zhang, Yu‐Qiu; Zhao, Zhi‐Qi

doi:10.1097/00001756-200401190-00014

Cited by 56 publications

(27 citation statements)

References 24 publications

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“…Positron emission tomography studies have revealed increased activation in the ACC following film-and recall-induced emotion and altered states of pain affect by hypnosis (Rainville et al, 1997(Rainville et al, , 1999Lane et al, 1998). Additionally, Fos expression in the ACC is increased following formalin-induced conditioned place avoidance in rodents (Lei et al, 2004). Lesion or stimulation of the ACC or cingulum bundle has been shown to decrease nociceptive responding in the formalin test (Vaccarino and Melzack, 1989;Fuchs et al, 1996;Donahue et al, 2001).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior

LaGraize

Fuchs

2007

Experimental Neurology

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The rostral anterior cingulate cortex (rACC) is involved in supraspinal nociceptive processing. ACC lesions relieve persistent pain, but do not affect the patient's ability to localize a noxious stimulus. Since the rACC has a high density of GABA receptors, it is possible that pain processing is influenced by these receptors in the rACC. The present experiments examined the involvement of rat rACC GABA A and GABA B receptors in regard to sensitivity to mechanical stimulation and escape/ avoidance behavior in response to a noxious stimulus following L5 spinal nerve ligation. Rats were or were not afflicted with a neuropathic pain condition by an L5 spinal nerve ligation. rACC microinjection of 10 μg/μl GABA, a GABA A agonist (0.001 μg/μl, 0.1 μg/μl, or 0.5 μg/μl muscimol), a GABA B agonist (0.1 μg/μl, 1 μg/μl, or 5 μg/μl baclofen), or saline, did not alter mechanical withdrawal thresholds. Importantly, following 10 μg/μl GABA, 0.1 μg/μl, or 0.5 μg/μl muscimol microinjected into the rACC, place escape/avoidance behavior to a noxious mechanical stimulus was attenuated in injured animals. The attenuation was specific to the rACC and was blocked by a preadministered microinjection of the appropriate antagonist(s) into the rACC. In conclusion, microinjection of GABA and higher doses of muscimol did not decrease mechanical hyperalgesia but did attenuate place escape/avoidance behavior that is associated with mechanical stimulation of the ligated paw. These results provide additional support for the role of the rACC in higher order supraspinal processing of noxious events and suggest that rACC GABA A receptors significantly contribute to this processing. KeywordsGABA; Limbic System; Nociception; Escape; Avoidance; Cingulate Cortex Chronic pain conditions affect the lives of millions of individuals every day. Pain is considered to include sensory/discriminative, motivational/affective, and cognitive/evaluative dimensions (Melzack and Casey, 1968). Spinal and supraspinal mechanisms underlying the sensory dimension of pain have received much attention, while the underlying mechanisms of the Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptExp Neurol. Author manuscript; available in PMC 2008 March 1. Published in final edited form as:Exp Neurol. 2007 March ; 204(1): 182-194. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript affective dimension of pain remain unclear. Many structures in the limbic system are involved in affective drives and escape behavior. As a result, these brain regions may be involved in behavior re...

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Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior

LaGraize

Fuchs

2007

Experimental Neurology

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“…Thus, a number of cortical regions have been identified in humans that are activated by nociceptive stimuli but for which there is not much additional data and few animal studies. One such area is the posterior parietal cortex [68], although it has recently been shown that a region designated parietal 2 (called somatosensory cortex 2 in the Paxinos atlas [69]) is activated when a rat is placed in conditioning chamber where it received a nociceptive formalin stimulus two days previously [70]. The SII occupying the superior bank of the lateral fissure and the adjacent insular cortex are also both consistently activated in human imaging studies following nociceptive stimulation.…”

Section: Other Sites For Cortical Modulation Of Painmentioning

confidence: 99%

Cortical modulation of pain

Ohara

Vit

Jasmin

2005

CMLS, Cell. Mol. Life Sci.

122

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The sensation commonly referred to as 'pain' has two components. The first is the sensory-discriminative component and provides information on location, modality and intensity of stimuli. The second is the affective-motivational component and refers to the emotional responses (fear, distress etc.) and the urge to respond evoked by the somatic sensation, and at the cortical level these two components appear to be located in different regions. The cortex probably influences pain by two different mechanisms. There is good evidence that the cortex can reduce pain by interrupting the transmission of noxious information from the spinal cord level by activating descending pain modulatory systems located in the brainstem. Less well established is the idea that modulation can also occur at the cortical level to change the affective-motivational aspects of nociception so that pain is perceived but looses its emotional and aversive component.

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“…In the rostral ventromedial medulla, ON, OFF and neutral cells projecting to the spinal and trigeminal dorsal horn modulate pain processing; manipulations of these neurons produce bidirectional, pro-and hypoalgesic actions the sensory and affective qualities of which seem to be closely matched (Hirakawa et al, 2000). Such modulation can be reinstated by re-exposure to the environment to which pain-induced aversion had previously been conditioned (Lei et al, 2004). The amydgala is involved in the formation of affective memories (Richardson et al, 2004).…”

Section: -Htmentioning

confidence: 99%

High-Efficacy 5-Hydroxytryptamine 1A Receptor Activation Counteracts Opioid Hyperallodynia and Affective Conditioning

Colpaert

Deseure²,

Stinus³

et al. 2005

J Pharmacol Exp Ther

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Pain may become intractable as tolerance develops to opioids and the opioids, paradoxically, induce pain. We examined the hypothesis that the analgesia produced by the novel analgesic and high-efficacy 5-hydroxytryptamine (5-HT) 1A receptor agonist (3-chloro-4-fluoro-phenyl)-[4-fluoro-4-{[(5-methyl-pyridin-2-ylmethyl)-amino]methyl}piperidin-1-yl]methanone, fumaric acid salt (F 13640) may counteract opioid-induced pain. In studies of the somatosensory quality of pain in infraorbital nerve-injured rats, morphine infusion (5 mg/day) by means of osmotic pumps initially caused analgesia (i.e., decreased the behavioral response to von Frey filament stimulation), followed by hyperallodynia and analgesic tolerance. Infusion of F 13640 (0.63 mg/day) prevented the development of opioid hyperallodynia and reversed opioid hyperallodynia once established. In studies of the affective/motivational quality of pain, F 13640 both prevented and reversed the conditioned place aversion induced by naloxone (0.04 mg/kg i.p.) in morphine-infused rats; F 13640 also prevented and reversed the conditioned place preference induced by morphine injections (7.5 mg/kg i.p.). The data confirm that opioids produce bidirectional hypo-and proalgesic actions, and offer initial evidence that high-efficacy 5-HT 1A receptor activation counteracts both the sensory and the affective/motivational qualities of opioid-induced pain. The data also indicate that F 13640 may be effective with opioidresistant pain. It further is suggested that opioid addiction may represent self-therapy of opioid-induced pathological pain.Although opioids produce powerful pain relief, pain may become intractable as tolerance develops to opioid analgesia; it has been proposed that this is because opioids may, paradoxically, induce pain. Indeed, a concept of signal transduction in central pain-processing systems (Colpaert, 1996) specifies that any input to such systems causes not a single effect but two dual effects that are bidirectional, or opposite in sign. Thus, morphine eventually causes not only analgesia as a "first order" effect but also a "second order" hyperalgesia that outlasts opioid receptor activation for some time. Upon chronic opioid exposure, the second order pain, or sensitization to nociceptive input, grows and neutralizes the first order analgesia. Considerable evidence now indicates that tolerance to opioid analgesia results from opioid-induced pain ("opioid pain"; here used to refer to hyperalgesia, allodynia, and hyperallodynia; Colpaert, 1996;Mao, 2002;Ossipov et al., 2003).Opioid pain is comprehensive, encompassing both the "physiological" (e.g., nociceptive) and the more recently identified (Scholz and Woolf, 2002) "pathological" (e.g., neuropathic) types of pain. Indeed, opioids not only produce hyperalgesia (i.e., an enhanced response to nociceptive stimulation; Colpaert, 1996) but also neuropathic-like allodynia (i.e., pain behaviors in response to innocuous stimuli; Ossipov et al., 2003). In human, opioid pain occurs after the intraoperative ...

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Pain-related aversion and Fos expression in the central nervous system in rats

Cited by 56 publications

References 24 publications

GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior

GABAA but not GABAB receptors in the rostral anterior cingulate cortex selectively modulate pain-induced escape/avoidance behavior

Cortical modulation of pain

High-Efficacy 5-Hydroxytryptamine 1A Receptor Activation Counteracts Opioid Hyperallodynia and Affective Conditioning

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