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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

Standard curves of autoradiography. A. Correlations between pixel intensity and pixel count. The pixel intensity was highly correlated with pixel count. B. Pixel intensity increased with increasing exposure time. The optimal resolution appeared on day 4.
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Fig1: Standard curves of autoradiography. A. Correlations between pixel intensity and pixel count. The pixel intensity was highly correlated with pixel count. B. Pixel intensity increased with increasing exposure time. The optimal resolution appeared on day 4.

Mentions: Brain activity was correlated with [14C]IAP signal intensity in brain images. The pixel intensity of brain images using the [14C]IAP method can elucidate metabolism in the brain and allow quantitative analyses. To quantify the pixel intensity of images of different brain slices, image normalization is very important. We first defined the range of signal intensities to be included in the image analysis. The range of the environmental background signal was 25.811-46.979 counts per minute (CPM), and the signal of the [14C]IAP 0.001 μCi filter paper was 42 CPM. Therefore, pixels with a signal intensity < 0.001 μCi were considered background. Five dose ranges (0.001-10 μCi 14C) could be displayed as gray-scale pixels on the images. The doses of [14C]IAP radioactivity were positively correlated with the pixel intensity and radioactivity count on a logarithmic scale. The pixel intensity was also shown to be positively correlated with radioactivity count (r = 0.94, p < 0.05), with a linear regression equation was obtained between the pixel intensity and radioactivity count, (Equation 1, Figure 1A).1\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ \left(Y = 824.48\ \mathrm{X} - 23020\right) $$\end{document}Y=824.48X−23020Figure 1


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)

Standard curves of autoradiography. A. Correlations between pixel intensity and pixel count. The pixel intensity was highly correlated with pixel count. B. Pixel intensity increased with increasing exposure time. The optimal resolution appeared on day 4.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Fig1: Standard curves of autoradiography. A. Correlations between pixel intensity and pixel count. The pixel intensity was highly correlated with pixel count. B. Pixel intensity increased with increasing exposure time. The optimal resolution appeared on day 4.
Mentions: Brain activity was correlated with [14C]IAP signal intensity in brain images. The pixel intensity of brain images using the [14C]IAP method can elucidate metabolism in the brain and allow quantitative analyses. To quantify the pixel intensity of images of different brain slices, image normalization is very important. We first defined the range of signal intensities to be included in the image analysis. The range of the environmental background signal was 25.811-46.979 counts per minute (CPM), and the signal of the [14C]IAP 0.001 μCi filter paper was 42 CPM. Therefore, pixels with a signal intensity < 0.001 μCi were considered background. Five dose ranges (0.001-10 μCi 14C) could be displayed as gray-scale pixels on the images. The doses of [14C]IAP radioactivity were positively correlated with the pixel intensity and radioactivity count on a logarithmic scale. The pixel intensity was also shown to be positively correlated with radioactivity count (r = 0.94, p < 0.05), with a linear regression equation was obtained between the pixel intensity and radioactivity count, (Equation 1, Figure 1A).1\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ \left(Y = 824.48\ \mathrm{X} - 23020\right) $$\end{document}Y=824.48X−23020Figure 1

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