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The anterior cingulate cortex and pain processing.

Fuchs PN, Peng YB, Boyette-Davis JA, Uhelski ML - Front Integr Neurosci (2014)

Bottom Line: Of primary interest is the contribution of the cingulate cortex in processing the affective component of pain.The purpose of this review is to summarize recent data obtained using novel behavioral paradigms in animals based on measuring escape and/or avoidance of a noxious stimulus.These paradigms have successfully been used to study the nature of the neuroanatomical and neurochemical contributions of the anterior cingulate cortex (ACC) to higher order pain processing in rodents.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, University of Texas at Arlington, Arlington TX, USA ; Department of Biology, University of Texas at Arlington, Arlington TX, USA.

ABSTRACT
The neural network that contributes to the suffering which accompanies persistent pain states involves a number of brain regions. Of primary interest is the contribution of the cingulate cortex in processing the affective component of pain. The purpose of this review is to summarize recent data obtained using novel behavioral paradigms in animals based on measuring escape and/or avoidance of a noxious stimulus. These paradigms have successfully been used to study the nature of the neuroanatomical and neurochemical contributions of the anterior cingulate cortex (ACC) to higher order pain processing in rodents.

No MeSH data available.


Related in: MedlinePlus

(A) Mean (± SEM) time spent in the light side of the PEAP chamber in sham vlPAG lesioned animals. L5 SNL, Sham ACC stimulated animals avoided noxious hindpaw stimulation significantly more than sham ligated, sham ACC stimulated animals. ACC stimulation did not have an effect in sham ligated animals, but significantly attenuated the avoidance behavioral response in L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals. (B) Mean (± SEM) time spent in the light side of the PEAP chamber in L5 SNL animals with vlPAG lesions or incomplete vlPAG lesions. L5 SNL, Sham ACC stimulated animals with an incomplete lesion of the vlPAG avoided noxious hindpaw stimulation significantly more than L5 SNL, ACC stimulated animals with an incomplete vlPAG lesion. There was not a significant avoidance response following vlPAG lesions in ACC stimulated, L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals (Reprint from LaBuda and Fuchs, 2005).
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Figure 4: (A) Mean (± SEM) time spent in the light side of the PEAP chamber in sham vlPAG lesioned animals. L5 SNL, Sham ACC stimulated animals avoided noxious hindpaw stimulation significantly more than sham ligated, sham ACC stimulated animals. ACC stimulation did not have an effect in sham ligated animals, but significantly attenuated the avoidance behavioral response in L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals. (B) Mean (± SEM) time spent in the light side of the PEAP chamber in L5 SNL animals with vlPAG lesions or incomplete vlPAG lesions. L5 SNL, Sham ACC stimulated animals with an incomplete lesion of the vlPAG avoided noxious hindpaw stimulation significantly more than L5 SNL, ACC stimulated animals with an incomplete vlPAG lesion. There was not a significant avoidance response following vlPAG lesions in ACC stimulated, L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals (Reprint from LaBuda and Fuchs, 2005).

Mentions: Data from neuroanatomical and behavioral pharmacological studies strongly suggest the existence of a supraspinal pain suppression system at the level of the periaqueductal gray (PAG). Research investigating this system indicates that activation of the ACC might recruit the pain suppression system at the level of the PAG. Indeed, focal brain stimulation of the ACC has been shown to inhibit the response of dorsal horn neurons to mechanical stimulation (Figure 3; Senapati et al., 2005; Ma et al., 2011), although evidence for facilitation of a nociceptive behavioral response has also been reported (Calejesan et al., 2000). We conducted an experiment to determine whether the effect of ACC activation was due to the activation of an endogenous pain suppression system at the level of the PAG (LaBuda and Fuchs, 2005). As seen in Figure 4, focal electrical stimulation of the ACC significantly reduced escape/avoidance behavior as revealed by animals spending less time in the light side of the chamber. Of additional interest is the finding that lesions of the vlPAG significantly attenuated the effect of ACC activation. Animals with lesions of the vlPAG and stimulation of the ACC spent more time in the light side of the chamber compared to animals that had no lesions (or incomplete lesions) of the vlPAG and received stimulation of the ACC. In no instance was there a change in the mechanical paw withdrawal threshold. The results of this study further support the notion that sensory and affective pain processing can be differentiated using the PEAP.


The anterior cingulate cortex and pain processing.

Fuchs PN, Peng YB, Boyette-Davis JA, Uhelski ML - Front Integr Neurosci (2014)

(A) Mean (± SEM) time spent in the light side of the PEAP chamber in sham vlPAG lesioned animals. L5 SNL, Sham ACC stimulated animals avoided noxious hindpaw stimulation significantly more than sham ligated, sham ACC stimulated animals. ACC stimulation did not have an effect in sham ligated animals, but significantly attenuated the avoidance behavioral response in L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals. (B) Mean (± SEM) time spent in the light side of the PEAP chamber in L5 SNL animals with vlPAG lesions or incomplete vlPAG lesions. L5 SNL, Sham ACC stimulated animals with an incomplete lesion of the vlPAG avoided noxious hindpaw stimulation significantly more than L5 SNL, ACC stimulated animals with an incomplete vlPAG lesion. There was not a significant avoidance response following vlPAG lesions in ACC stimulated, L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals (Reprint from LaBuda and Fuchs, 2005).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4017137&req=5

Figure 4: (A) Mean (± SEM) time spent in the light side of the PEAP chamber in sham vlPAG lesioned animals. L5 SNL, Sham ACC stimulated animals avoided noxious hindpaw stimulation significantly more than sham ligated, sham ACC stimulated animals. ACC stimulation did not have an effect in sham ligated animals, but significantly attenuated the avoidance behavioral response in L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals. (B) Mean (± SEM) time spent in the light side of the PEAP chamber in L5 SNL animals with vlPAG lesions or incomplete vlPAG lesions. L5 SNL, Sham ACC stimulated animals with an incomplete lesion of the vlPAG avoided noxious hindpaw stimulation significantly more than L5 SNL, ACC stimulated animals with an incomplete vlPAG lesion. There was not a significant avoidance response following vlPAG lesions in ACC stimulated, L5 SNL animals. * p < 0.05 compared to sham ligated + sham ACC stimulation treated animals (Reprint from LaBuda and Fuchs, 2005).
Mentions: Data from neuroanatomical and behavioral pharmacological studies strongly suggest the existence of a supraspinal pain suppression system at the level of the periaqueductal gray (PAG). Research investigating this system indicates that activation of the ACC might recruit the pain suppression system at the level of the PAG. Indeed, focal brain stimulation of the ACC has been shown to inhibit the response of dorsal horn neurons to mechanical stimulation (Figure 3; Senapati et al., 2005; Ma et al., 2011), although evidence for facilitation of a nociceptive behavioral response has also been reported (Calejesan et al., 2000). We conducted an experiment to determine whether the effect of ACC activation was due to the activation of an endogenous pain suppression system at the level of the PAG (LaBuda and Fuchs, 2005). As seen in Figure 4, focal electrical stimulation of the ACC significantly reduced escape/avoidance behavior as revealed by animals spending less time in the light side of the chamber. Of additional interest is the finding that lesions of the vlPAG significantly attenuated the effect of ACC activation. Animals with lesions of the vlPAG and stimulation of the ACC spent more time in the light side of the chamber compared to animals that had no lesions (or incomplete lesions) of the vlPAG and received stimulation of the ACC. In no instance was there a change in the mechanical paw withdrawal threshold. The results of this study further support the notion that sensory and affective pain processing can be differentiated using the PEAP.

Bottom Line: Of primary interest is the contribution of the cingulate cortex in processing the affective component of pain.The purpose of this review is to summarize recent data obtained using novel behavioral paradigms in animals based on measuring escape and/or avoidance of a noxious stimulus.These paradigms have successfully been used to study the nature of the neuroanatomical and neurochemical contributions of the anterior cingulate cortex (ACC) to higher order pain processing in rodents.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, University of Texas at Arlington, Arlington TX, USA ; Department of Biology, University of Texas at Arlington, Arlington TX, USA.

ABSTRACT
The neural network that contributes to the suffering which accompanies persistent pain states involves a number of brain regions. Of primary interest is the contribution of the cingulate cortex in processing the affective component of pain. The purpose of this review is to summarize recent data obtained using novel behavioral paradigms in animals based on measuring escape and/or avoidance of a noxious stimulus. These paradigms have successfully been used to study the nature of the neuroanatomical and neurochemical contributions of the anterior cingulate cortex (ACC) to higher order pain processing in rodents.

No MeSH data available.


Related in: MedlinePlus