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A [14C]iodoantipyrine study of inter-regional correlations of neural substrates following central post-stroke pain in rats.

Lu HC, Chang WJ, Kuan YH, Huang AC, Shyu BC - Mol Pain (2015)

Bottom Line: These results corroborate previous findings that the STT and thalamocingulate pathway are involved in the pathophysiological mechanisms of CPSP symptoms.The mPFC, amygdala, and periaqueductal gray emerged as having important correlations in pain processing in CPSP.The present data provide a basis for a neural correlation hypothesis of CPSP, with implications for CPSP treatment.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. nhnsc@hotmail.com.

ABSTRACT

Background: Central pain syndrome is characterized by a combination of abnormal pain sensations, and pain medications often provide little or no relief. Accumulating animal and clinical studies have shown that impairments of the spinothalamic tract (STT) and thalamocingulate pathway causes somatosensory dysfunction in central post-stroke pain (CPSP), but the involvement of other neuronal circuitries in CPSP has not yet been systematically examined. The aim of the present study was to evaluate changes in brain activity and neuronal circuitry using [(14)C]iodoantipyrine (IAP) in an animal model of CPSP.

Results: Rats were subjected to lateral thalamic hemorrhage to investigate the characteristics of CPSP. Thermal and mechanical hyperalgesia developed in rats that were subjected to thalamic hemorrhagic lesion. The medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), striatum, thalamus, hypothalamus, and amygdala were more active in the CPSP group compared with rats that were not subjected to lateral thalamic hemorrhage. The inter-regional correlation analysis showed that regional cerebral blood flow in the mPFC was highly correlated with the amygdala in the right brain, and the right brain showed complex connections among subregions of the ACC. Rats with CPSP exhibited strong activation of the thalamocingulate and mPFC-amygdala pathways.

Conclusions: These results corroborate previous findings that the STT and thalamocingulate pathway are involved in the pathophysiological mechanisms of CPSP symptoms. The mPFC, amygdala, and periaqueductal gray emerged as having important correlations in pain processing in CPSP. The present data provide a basis for a neural correlation hypothesis of CPSP, with implications for CPSP treatment.

No MeSH data available.


Related in: MedlinePlus

Experimental timeline and example of mechanical and thermal hyperalgesia after lesion of the VPL and VPM. A. Experimental timeline of [14C] experiment. B. Example of collagenase-induced lesion in the VPL and VPM 1 month after injection. C and D. Plantar test and von Frey test on the left hindpaw in the sham and CPSP groups on day 35. p < 0.05 (two-way ANOVA followed by post hoc test). The results showed that the CPSP group had lower pain thresholds than the sham group.
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Fig2: Experimental timeline and example of mechanical and thermal hyperalgesia after lesion of the VPL and VPM. A. Experimental timeline of [14C] experiment. B. Example of collagenase-induced lesion in the VPL and VPM 1 month after injection. C and D. Plantar test and von Frey test on the left hindpaw in the sham and CPSP groups on day 35. p < 0.05 (two-way ANOVA followed by post hoc test). The results showed that the CPSP group had lower pain thresholds than the sham group.

Mentions: The experimental timeline for the brain lesions, behavioral measurements, and brain imaging is illustrated in Figure 2A. A typical collagenase-induced lesion in the VPL and VPM in frozen brain slices is shown in Figure 2B (white arrow). The lesion sites from all of the histological samples are encircled with red lines and overlap in the corresponding brain atlas. The lesion sites were all confirmed and localized in the VB area (Figure 2B).Figure 2


A [14C]iodoantipyrine study of inter-regional correlations of neural substrates following central post-stroke pain in rats.

Lu HC, Chang WJ, Kuan YH, Huang AC, Shyu BC - Mol Pain (2015)

Experimental timeline and example of mechanical and thermal hyperalgesia after lesion of the VPL and VPM. A. Experimental timeline of [14C] experiment. B. Example of collagenase-induced lesion in the VPL and VPM 1 month after injection. C and D. Plantar test and von Frey test on the left hindpaw in the sham and CPSP groups on day 35. p < 0.05 (two-way ANOVA followed by post hoc test). The results showed that the CPSP group had lower pain thresholds than the sham group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4358859&req=5

Fig2: Experimental timeline and example of mechanical and thermal hyperalgesia after lesion of the VPL and VPM. A. Experimental timeline of [14C] experiment. B. Example of collagenase-induced lesion in the VPL and VPM 1 month after injection. C and D. Plantar test and von Frey test on the left hindpaw in the sham and CPSP groups on day 35. p < 0.05 (two-way ANOVA followed by post hoc test). The results showed that the CPSP group had lower pain thresholds than the sham group.
Mentions: The experimental timeline for the brain lesions, behavioral measurements, and brain imaging is illustrated in Figure 2A. A typical collagenase-induced lesion in the VPL and VPM in frozen brain slices is shown in Figure 2B (white arrow). The lesion sites from all of the histological samples are encircled with red lines and overlap in the corresponding brain atlas. The lesion sites were all confirmed and localized in the VB area (Figure 2B).Figure 2

Bottom Line: These results corroborate previous findings that the STT and thalamocingulate pathway are involved in the pathophysiological mechanisms of CPSP symptoms.The mPFC, amygdala, and periaqueductal gray emerged as having important correlations in pain processing in CPSP.The present data provide a basis for a neural correlation hypothesis of CPSP, with implications for CPSP treatment.

View Article: PubMed Central - PubMed

Affiliation: Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan. nhnsc@hotmail.com.

ABSTRACT

Background: Central pain syndrome is characterized by a combination of abnormal pain sensations, and pain medications often provide little or no relief. Accumulating animal and clinical studies have shown that impairments of the spinothalamic tract (STT) and thalamocingulate pathway causes somatosensory dysfunction in central post-stroke pain (CPSP), but the involvement of other neuronal circuitries in CPSP has not yet been systematically examined. The aim of the present study was to evaluate changes in brain activity and neuronal circuitry using [(14)C]iodoantipyrine (IAP) in an animal model of CPSP.

Results: Rats were subjected to lateral thalamic hemorrhage to investigate the characteristics of CPSP. Thermal and mechanical hyperalgesia developed in rats that were subjected to thalamic hemorrhagic lesion. The medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), striatum, thalamus, hypothalamus, and amygdala were more active in the CPSP group compared with rats that were not subjected to lateral thalamic hemorrhage. The inter-regional correlation analysis showed that regional cerebral blood flow in the mPFC was highly correlated with the amygdala in the right brain, and the right brain showed complex connections among subregions of the ACC. Rats with CPSP exhibited strong activation of the thalamocingulate and mPFC-amygdala pathways.

Conclusions: These results corroborate previous findings that the STT and thalamocingulate pathway are involved in the pathophysiological mechanisms of CPSP symptoms. The mPFC, amygdala, and periaqueductal gray emerged as having important correlations in pain processing in CPSP. The present data provide a basis for a neural correlation hypothesis of CPSP, with implications for CPSP treatment.

No MeSH data available.


Related in: MedlinePlus