Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

Munn, Elizabeth; Harte, Steven E.; Lagman, Alexander; Borszcz, George S.

doi:10.1016/j.jpain.2008.10.011

Cited by 9 publications

(9 citation statements)

References 56 publications

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“…The dual inhibition of nociceptive processing at medullary and forebrain levels could account for the greater effect of PF administered morphine and rACC administered NMDA on VAD versus VDS thresholds (Borszcz, 1999). Consistent with this interpretation is our recent observation that increases in vocalization thresholds generated by morphine administered into PF is blocked by inactivation of the vPAG (Munn et al, 2009). …”

Section: Discussionsupporting

confidence: 67%

Functional interaction between medial thalamus and rostral anterior cingulate cortex in the suppression of pain affect

Harte¹,

Spuz²,

Borszcz³

2011

Neuroscience

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The medial thalamic parafascicular nucleus (PF) and the rostral anterior cingulate cortex (rACC) are implicated in the processing and suppression of the affective dimension of pain. The present study evaluated the functional interaction between PF and rACC in mediating the suppression of pain affect in rats following administration of morphine or carbachol (acetylcholine agonist) into PF. Vocalizations that occur following a brief noxious tailshock (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed by injection of morphine or carbachol into PF. Vocalizations that occur during tailshock were suppressed to a lesser degree, whereas, spinal motor reflexes (tail flick and hindlimb movements) were only slightly suppressed by injection of carbachol into PF and unaffected by injection of morphine into PF. Blocking glutamate receptors in rACC (NMDA and non-NMDA) by injecting D-2-amino-5-phosphonovalerate (AP-5) or 6-Cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX) produced dose-dependent antagonism of morphine-induced increases in vocalization thresholds. Carbacholinduced increases in vocalization thresholds were not affected by injection of either glutamate receptor antagonist into rACC. The results demonstrate that glutamate receptors in the rACC contribute to the suppression of pain affect produced by injection of morphine into PF, but not to the suppression of pain affect generated by intra-PF injection of carbachol.

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Section: Discussionsupporting

confidence: 67%

Functional interaction between medial thalamus and rostral anterior cingulate cortex in the suppression of pain affect

Harte¹,

Spuz²,

Borszcz³

2011

Neuroscience

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“…‡ p<0.05 as compared with dimaprit (2 μg/site) and morphine (2 μg/site)-treated groups hippocampus, and dentate gyrus produced analgesic effects in the orofacial formalin pain in rats (Rosenfeld and Stocco 1981;Duale et al 2007;Khalilzadeh et al 2010;Tamaddonfard et al 2011;Reisi et al 2014). In the thalamic parafascicular nucleus, microinjection of morphine attenuated the affective reaction to noxious stimulation in rats (Munn et al 2009). Yang et al (2002) reported that morphine microinjection into the Sm depressed nociceptive behavior induced by the formalin injection into the rat hind paw which was reversed by naloxone.…”

Section: Discussionmentioning

confidence: 99%

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

Erfanparast

Tamaddonfard

Taati

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Histamine and opioid systems are involved in supraspinal modulation of pain. In this study, we investigated the effects of separate and combined microinjections of agonists and antagonists of histamine H 1 and H 2 and opioid receptors into the thalamic submedius (Sm) nucleus on the formalin-induced orofacial pain. Two guide cannulas were implanted into the right and left sides of the Sm in ketamineand xylazine-anesthetized rats. Orofacial formalin pain was induced by subcutaneous injection of a diluted formalin solution (50 μl, 1.5 %) into the vibrissa pad. Face rubbing durations were recorded at 3-min blocks for 45 min. Formalin produced a biphasic pain response (first phase: 0-3 min and second phase: 15-33 min). Separate and combined microinjections of histamine H 1 and H 2 receptor agonists, 2-pyridylethylamine (2-PEA) and dimaprit, respectively, and opioid receptor agonist, morphine, attenuated the second phase of pain. The analgesic effects induced by 2-PEA, dimaprit, and morphine were blocked by prior microinjections of fexofenadine (a histamine H 1 receptor antagonist), famotidine (a histamine H 2 receptor antagonist), and naloxone (an opioid receptor antagonist), respectively. Naloxone also prevented 2-PEA-and dimaprit-induced antinociception, and the analgesic effect induced by morphine was inhibited by fexofenadine and famotidine. These results showed the involvement of histamine H 1 and H 2 and opioid receptors in the Sm modulation of orofacial pain. Opioid receptor might be involved in analgesia induced by activation of histamine H 1 and H 2 receptors and vice versa.

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“…Alternately, there is no evidence of involvement of the ventrolateral periaqueductal gray (vPAG) in reward, which receives afferents from VTA (Kirouac et al, 2004) and is a nodal structure in the endogenous antinociceptive circuit (Basbaum and Fields, 1984; Borszcz, 1999). Projections from the vPAG to the medial thalamus and amygdala contribute to suppression of the affective dimension of pain (Borszcz, 1999; Harte et al, 2000) and projections from the medial thalamus (Munn et al, 2009), amygdala (Pavlovic and Bodnar, 1998), and aCC (LaBuda and Fuchs, 2005) to the vPAG also support affective analgesia. The role of cholinergically activated afferents from VTA to vPAG in engaging this endogenous antinociceptive circuit should also be evaluated.…”

Section: Discussionmentioning

confidence: 99%

Separating analgesia from reward within the ventral tegmental area

2014

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Activation of the dopaminergic mesolimbic reward circuit that originates in the ventral tegmental area (VTA) is postulated to preferentially suppress emotional responses to noxious stimuli, and presumably contributes to the addictive liability of strong analgesics. VTA dopamine neurons are activated via cholinergic afferents and microinjection of carbachol (cholinergic agonist) into VTA is rewarding. Here, we evaluated regional differences within VTA in the capacity of carbachol to suppress rats' affective response to pain (vocalization afterdischarges, VADs) and to support conditioned place preference (CPP) learning. As carbachol is a non-specific agonist, muscarinic and nicotinic receptor involvement was assessed by administering atropine (muscarinic antagonist) and mecamylamine (nicotinic antagonist) into VTA prior to carbachol treatment. Unilateral injections of carbachol (4 μg) into anterior VTA (aVTA) and posterior VTA (pVTA) suppressed VADs and supported CPP; whereas, injections into midVTA failed to effect either VADs or CPP. These findings corroborate the hypothesis that the neural substrates underlying affective analgesia and reward overlap. However, the extent of the overlap was only partial. Whereas both nicotinic and muscarinic receptors contributed to carbachol-induced affective analgesia in aVTA, only muscarinic receptors mediated the analgesic action of carbachol in pVTA. The rewarding effects of carbachol are mediated by the activation of both nicotinic and muscarinic receptors in both aVTA and pVTA. The results indicate that analgesia and reward are mediated by separate cholinergic mechanisms within pVTA. Nicotinic receptor antagonism within pVTA failed to attenuate carbachol-induced analgesia, but prevented carbachol-induced reward. As addictive liability of analgesics stem from their rewarding properties, the present findings suggest that these processes can be neuropharmacologically separated within pVTA.

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Contribution of the Periaqueductal Gray to the Suppression of Pain Affect Produced by Administration of Morphine Into the Intralaminar Thalamus of Rat

Cited by 9 publications

References 56 publications

Functional interaction between medial thalamus and rostral anterior cingulate cortex in the suppression of pain affect

Functional interaction between medial thalamus and rostral anterior cingulate cortex in the suppression of pain affect

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

Separating analgesia from reward within the ventral tegmental area

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