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Spinal cord injuries induce changes in CB1 cannabinoid receptor and C-C chemokine expression in brain areas underlying circuitry of chronic pain conditions.
J Neurotrauma 2011; 28(4):619-34JN

Abstract

Due to their involvement in neuro-modulatory processes, the endogenous cannabinoid system and chemokine network, which were shown to interact which each other, are potential key elements in the cascades underlying central neuropathic pain development after spinal cord injury (SCI). Expression profiles of cannabinoid receptor type-1 (CB(1)), and of the chemokines chemokine ligand 2 (C-C motif) (CCL2), chemokine ligand 3 (C-C motif) (CCL3), plus their main receptors CCR2 and CCR1, were investigated in brain regions related to pain, emotion, learning, and memory in a rat SCI paradigm of post-traumatic neuropathic pain. Immunoreactivity (IR) was investigated 7 days and 42 days after sham operation, and moderate (100-kdyn), and severe (200-kdyn) thoracic spinal cord contusion lesions. Hippocampal (HC) subregions, amygdaloid complex, anterior cingulate cortex (ACC), periaqueductal gray (PAG), and thalamic nuclei were analyzed. Seven days after lesioning, CB(1) IR was induced in thalamic nuclei and HC subregions (CA3 and dentate gyrus), and downregulated in amygdaloid nuclei, ACC, and PAG. On day 42, CB(1) IR remained elevated in the HC and thalamic areas, and was induced in ACC after 100-kdyn, but downregulated after 200-kdyn lesions. It remained reduced in the PAG of severely lesioned animals, paralleling their prolonged neuropathic pain-related behavior. Double-labeling revealed partial co-expression of CB(1) with the pain-related vanilloid receptor transient receptor potential vanilloid receptor 1 (TRPV1), and chemokines (CCL2 and CCL3). These chemokines were induced in the PAG, thalamus, and HC, especially in the chronic time course after severe SCI. Thus interactions of CB(1), C-C chemokines, and TRPV1 likely play a role in SCI-induced plastic changes in the brain, underlying emotional-affective pain responses and central pain development after spinal cord lesions.

Authors+Show Affiliations

Department of Neurosurgery, University of Schleswig-Holstein Medical Center, Kiel, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21265596

Citation

Knerlich-Lukoschus, Friederike, et al. "Spinal Cord Injuries Induce Changes in CB1 Cannabinoid Receptor and C-C Chemokine Expression in Brain Areas Underlying Circuitry of Chronic Pain Conditions." Journal of Neurotrauma, vol. 28, no. 4, 2011, pp. 619-34.
Knerlich-Lukoschus F, Noack M, von der Ropp-Brenner B, et al. Spinal cord injuries induce changes in CB1 cannabinoid receptor and C-C chemokine expression in brain areas underlying circuitry of chronic pain conditions. J Neurotrauma. 2011;28(4):619-34.
Knerlich-Lukoschus, F., Noack, M., von der Ropp-Brenner, B., Lucius, R., Mehdorn, H. M., & Held-Feindt, J. (2011). Spinal cord injuries induce changes in CB1 cannabinoid receptor and C-C chemokine expression in brain areas underlying circuitry of chronic pain conditions. Journal of Neurotrauma, 28(4), pp. 619-34. doi:10.1089/neu.2010.1652.
Knerlich-Lukoschus F, et al. Spinal Cord Injuries Induce Changes in CB1 Cannabinoid Receptor and C-C Chemokine Expression in Brain Areas Underlying Circuitry of Chronic Pain Conditions. J Neurotrauma. 2011;28(4):619-34. PubMed PMID: 21265596.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Spinal cord injuries induce changes in CB1 cannabinoid receptor and C-C chemokine expression in brain areas underlying circuitry of chronic pain conditions. AU - Knerlich-Lukoschus,Friederike, AU - Noack,Malte, AU - von der Ropp-Brenner,Beata, AU - Lucius,Ralph, AU - Mehdorn,Hubertus Maximilian, AU - Held-Feindt,Janka, PY - 2011/1/27/entrez PY - 2011/1/27/pubmed PY - 2011/8/13/medline SP - 619 EP - 34 JF - Journal of neurotrauma JO - J. Neurotrauma VL - 28 IS - 4 N2 - Due to their involvement in neuro-modulatory processes, the endogenous cannabinoid system and chemokine network, which were shown to interact which each other, are potential key elements in the cascades underlying central neuropathic pain development after spinal cord injury (SCI). Expression profiles of cannabinoid receptor type-1 (CB(1)), and of the chemokines chemokine ligand 2 (C-C motif) (CCL2), chemokine ligand 3 (C-C motif) (CCL3), plus their main receptors CCR2 and CCR1, were investigated in brain regions related to pain, emotion, learning, and memory in a rat SCI paradigm of post-traumatic neuropathic pain. Immunoreactivity (IR) was investigated 7 days and 42 days after sham operation, and moderate (100-kdyn), and severe (200-kdyn) thoracic spinal cord contusion lesions. Hippocampal (HC) subregions, amygdaloid complex, anterior cingulate cortex (ACC), periaqueductal gray (PAG), and thalamic nuclei were analyzed. Seven days after lesioning, CB(1) IR was induced in thalamic nuclei and HC subregions (CA3 and dentate gyrus), and downregulated in amygdaloid nuclei, ACC, and PAG. On day 42, CB(1) IR remained elevated in the HC and thalamic areas, and was induced in ACC after 100-kdyn, but downregulated after 200-kdyn lesions. It remained reduced in the PAG of severely lesioned animals, paralleling their prolonged neuropathic pain-related behavior. Double-labeling revealed partial co-expression of CB(1) with the pain-related vanilloid receptor transient receptor potential vanilloid receptor 1 (TRPV1), and chemokines (CCL2 and CCL3). These chemokines were induced in the PAG, thalamus, and HC, especially in the chronic time course after severe SCI. Thus interactions of CB(1), C-C chemokines, and TRPV1 likely play a role in SCI-induced plastic changes in the brain, underlying emotional-affective pain responses and central pain development after spinal cord lesions. SN - 1557-9042 UR - https://www.unboundmedicine.com/medline/citation/21265596/abstract/Spinal_Cord_Injuries_Induce_Changes_of_CB1_Cannabinoid_Receptor_and_C_C_Chemokine_Expression_in_Brain_Areas_Underlying_Circuitry_of_Chronic_Pain_Conditions_ L2 - https://www.liebertpub.com/doi/full/10.1089/neu.2010.1652?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -