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Basolateral amygdala lesion inhibits the development of pain chronicity in neuropathic pain rats.

Li Z, Wang J, Chen L, Zhang M, Wan Y - PLoS ONE (2013)

Bottom Line: Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain.The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information.These results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Institute, Peking University, Beijing, PR China.

ABSTRACT

Background: Chronicity of pain is one of the most interesting questions in chronic pain study. Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain. The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information.

Objective: This study aimed to investigate whether amygdala or its subregions, the basolateral amygdala (BLA) and the central medial amygdala (CeA), contributes to the pain chronicity in the spared nerve injury (SNI)-induced neuropathic pain model of rats.

Methodology/principal findings: (1) Before the establishment of the SNI-induced neuropathic pain model of rats, lesion of the amygdaloid complex with stereotaxic injection of ibotenic acid (IBO) alleviated mechanical allodynia significantly at days 7 and 14, even no mechanical allodynia at day 28 after SNI; Lesion of the BLA, but not the CeA had similar effects; (2) however, 7 days after SNI when the neuropathic pain model was established, lesion of the amygdala complex or the BLA or the CeA, mechanical allodynia was not affected.

Conclusion: These results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity.

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Related in: MedlinePlus

Schematic representation of the maximum (grey zone) and the minimum (black zone) extent of lesion to the bilateral amygdala.Re-construction are presented on a series of coronal sections according to the stereotaxic atlas of Paxinos and Watson [30]. (A) Amygdaloid complex; (B) BLA; (C) CeA; (D) Photograph of coronal sections of the amygdala in sham lesion (left) and IBO lesion (right) rats. Note that loss of cell population and cell shrinkage in the regions of CeA and BLA in the IBO-lesioned rats.
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pone-0070921-g002: Schematic representation of the maximum (grey zone) and the minimum (black zone) extent of lesion to the bilateral amygdala.Re-construction are presented on a series of coronal sections according to the stereotaxic atlas of Paxinos and Watson [30]. (A) Amygdaloid complex; (B) BLA; (C) CeA; (D) Photograph of coronal sections of the amygdala in sham lesion (left) and IBO lesion (right) rats. Note that loss of cell population and cell shrinkage in the regions of CeA and BLA in the IBO-lesioned rats.

Mentions: After behavioral test, rats were anesthetized with pentobarbital sodium (50 mg/kg, i.p.) and perfused via aorta with 300 ml normal saline and 300 ml 4% paraformaldehyde solution in 0.1 M phosphate buffer (PB, pH 7.4). Brain samples were stored in 4% paraformaldehyde overnight and then sequentially in 20% and 30% sucrose solution in PBS (pH 7.2) for 24 h. Coronal brain sections were cut at 30 µm and stained with Nissl to confirm the lesion locations in the amygdala by microscopic inspection. Fig. 2 shows the schematic illustration of damages in the amygdaloid complex, the CeA and the BLA in all rats.


Basolateral amygdala lesion inhibits the development of pain chronicity in neuropathic pain rats.

Li Z, Wang J, Chen L, Zhang M, Wan Y - PLoS ONE (2013)

Schematic representation of the maximum (grey zone) and the minimum (black zone) extent of lesion to the bilateral amygdala.Re-construction are presented on a series of coronal sections according to the stereotaxic atlas of Paxinos and Watson [30]. (A) Amygdaloid complex; (B) BLA; (C) CeA; (D) Photograph of coronal sections of the amygdala in sham lesion (left) and IBO lesion (right) rats. Note that loss of cell population and cell shrinkage in the regions of CeA and BLA in the IBO-lesioned rats.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3733720&req=5

pone-0070921-g002: Schematic representation of the maximum (grey zone) and the minimum (black zone) extent of lesion to the bilateral amygdala.Re-construction are presented on a series of coronal sections according to the stereotaxic atlas of Paxinos and Watson [30]. (A) Amygdaloid complex; (B) BLA; (C) CeA; (D) Photograph of coronal sections of the amygdala in sham lesion (left) and IBO lesion (right) rats. Note that loss of cell population and cell shrinkage in the regions of CeA and BLA in the IBO-lesioned rats.
Mentions: After behavioral test, rats were anesthetized with pentobarbital sodium (50 mg/kg, i.p.) and perfused via aorta with 300 ml normal saline and 300 ml 4% paraformaldehyde solution in 0.1 M phosphate buffer (PB, pH 7.4). Brain samples were stored in 4% paraformaldehyde overnight and then sequentially in 20% and 30% sucrose solution in PBS (pH 7.2) for 24 h. Coronal brain sections were cut at 30 µm and stained with Nissl to confirm the lesion locations in the amygdala by microscopic inspection. Fig. 2 shows the schematic illustration of damages in the amygdaloid complex, the CeA and the BLA in all rats.

Bottom Line: Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain.The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information.These results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Institute, Peking University, Beijing, PR China.

ABSTRACT

Background: Chronicity of pain is one of the most interesting questions in chronic pain study. Clinical and experimental data suggest that supraspinal areas responsible for negative emotions such as depression and anxiety contribute to the chronicity of pain. The amygdala is suspected to be a potential structure for the pain chronicity due to its critical role in processing negative emotions and pain information.

Objective: This study aimed to investigate whether amygdala or its subregions, the basolateral amygdala (BLA) and the central medial amygdala (CeA), contributes to the pain chronicity in the spared nerve injury (SNI)-induced neuropathic pain model of rats.

Methodology/principal findings: (1) Before the establishment of the SNI-induced neuropathic pain model of rats, lesion of the amygdaloid complex with stereotaxic injection of ibotenic acid (IBO) alleviated mechanical allodynia significantly at days 7 and 14, even no mechanical allodynia at day 28 after SNI; Lesion of the BLA, but not the CeA had similar effects; (2) however, 7 days after SNI when the neuropathic pain model was established, lesion of the amygdala complex or the BLA or the CeA, mechanical allodynia was not affected.

Conclusion: These results suggest that BLA activities in the early stage after nerve injury might be crucial to the development of pain chronicity, and amygdala-related negative emotions and pain-related memories could promote pain chronicity.

Show MeSH
Related in: MedlinePlus