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

Abstract

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.

Endogenous opioidergic dysregulation of pain in fibromyalgia: a PET and fMRI study

“…In particular, we observed a strong coupling of evoked-pain brain activity and MOR availability in two regions – the DLPFC and rACC – known to play an important role in anti-nociception. 7; 32; 43 These findings extend to the clinical pain experience, as increased brain activation and MOR availability was also associated with lower ratings of pain affect. These findings may therefore contribute to the mechanistic understanding of experimental pain sensitivity and clinical pain report in FM.…”

Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: An 11C-(R)-PK11195 PET Study

“…In addition, region-of-interest-based correlation analysis revealed that pain score was positively correlated with averaged BP ND values of the cingulate cortex (r 5 0.73, P 5 0.0254) and thalamus (r 5 0.78, P 5 0.0126). Functional interaction between the anterior part of the cingulate cortex and thalamus has been reported to suppress pain (35); therefore, inflammation in the cingulate cortex and thalamus may decrease pain suppression in CFS/ME patients. Our previous PET study showed that impaired serotonin dynamics in the anterior cingulate cortex were associated with the severity of pain in CFS/ME patients (3), suggesting that serotonergic dysfunction is also related to pain in these patients.…”

Separating analgesia from reward within the ventral tegmental area

“…Systemically administered drug treatments that preferentially suppress the affective response of humans to pain (Gracely et al, 1978; Price et al, 1985) also preferentially suppress production of VADs (Borszcz et al, 1994). Generation of VADs is suppressed by damage of or drug treatments into forebrain sites known to contribute to production of the affective response of humans to clinical and experimental pain (Mark et al, 1961; Hoffmeister, 1968; Sweet, 1980; Borszcz, 1999; Harte et al, 2000; Zubieta et al, 2001; Borszcz and Leaton, 2003; Nandigama and Borszcz, 2003; Harte et al, 2004; Harte et al, 2011). Additionally, the capacity of noxious tailshock to support fear conditioning is directly related to its production of VADs (Borszcz, 1993, 1995, 2006; Borszcz and Leaton, 2003).…”