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Differential distribution of activated spinal neurons containing glycine and/or GABA and expressing c-fos in acute and chronic pain models.
Pain 2010; 151(2):356-65PAIN

Abstract

The inhibitory transmitters GABA and glycine play an important role in modulating pain transmission, both in normal and in pathological situations. In the present study we have combined in situ hybridization for identifying spinal neurons that use the transmitter(s) glycine and/or GABA (Gly/GABA neurons) with immunohistochemistry for c-fos, a marker for neuronal activation. This procedure was used with acute pain models induced by the injection of capsaicin or formalin; and chronic pain models using Complete Freund's Adjuvant (CFA, chronic inflammation), and the spared nerve injury (SNI) model (neuropathic pain). In all models Gly/GABA neurons were activated as indicated by their expression of c-fos. The pattern of Gly/GABA neuronal activation was different for every model, both anatomically and quantitatively. However, the averaged percentage of activated neurons that were Gly/GABA in the chronic phase (≥20h survival, 46%) was significantly higher than in the acute phase (≤2h survival, 34%). In addition, the total numbers of activated Gly/GABA neurons were similar in both phases, showing that the activation of non-Gly/GABA (presumed excitatory) neurons in the chronic phase decreased. Finally, morphine application equally decreased the total number of activated neurons and activated Gly/GABA neurons. This showed that morphine did not specifically activate Gly/GABA neurons to achieve nociceptive inhibition. The present study shows an increased activity of Gly/GABA neurons in acute and chronic models. This mechanism, together with mechanisms that antagonize the effects of GABA and glycine at the receptor level, may determine the sensitivity of our pain system during health and disease.

Authors+Show Affiliations

Department of Neuroscience, Erasmus University Medical Center, Rotterdam, The Netherlands.No 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

20727678

Citation

Hossaini, Mehdi, et al. "Differential Distribution of Activated Spinal Neurons Containing Glycine And/or GABA and Expressing C-fos in Acute and Chronic Pain Models." Pain, vol. 151, no. 2, 2010, pp. 356-65.
Hossaini M, Duraku LS, Saraç C, et al. Differential distribution of activated spinal neurons containing glycine and/or GABA and expressing c-fos in acute and chronic pain models. Pain. 2010;151(2):356-65.
Hossaini, M., Duraku, L. S., Saraç, C., Jongen, J. L., & Holstege, J. C. (2010). Differential distribution of activated spinal neurons containing glycine and/or GABA and expressing c-fos in acute and chronic pain models. Pain, 151(2), pp. 356-65. doi:10.1016/j.pain.2010.07.023.
Hossaini M, et al. Differential Distribution of Activated Spinal Neurons Containing Glycine And/or GABA and Expressing C-fos in Acute and Chronic Pain Models. Pain. 2010;151(2):356-65. PubMed PMID: 20727678.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential distribution of activated spinal neurons containing glycine and/or GABA and expressing c-fos in acute and chronic pain models. AU - Hossaini,Mehdi, AU - Duraku,Liron S, AU - Saraç,Ciğdem, AU - Jongen,Joost L M, AU - Holstege,Jan C, Y1 - 2010/08/19/ PY - 2010/04/12/received PY - 2010/07/09/revised PY - 2010/07/16/accepted PY - 2010/8/24/entrez PY - 2010/8/24/pubmed PY - 2011/2/15/medline SP - 356 EP - 65 JF - Pain JO - Pain VL - 151 IS - 2 N2 - The inhibitory transmitters GABA and glycine play an important role in modulating pain transmission, both in normal and in pathological situations. In the present study we have combined in situ hybridization for identifying spinal neurons that use the transmitter(s) glycine and/or GABA (Gly/GABA neurons) with immunohistochemistry for c-fos, a marker for neuronal activation. This procedure was used with acute pain models induced by the injection of capsaicin or formalin; and chronic pain models using Complete Freund's Adjuvant (CFA, chronic inflammation), and the spared nerve injury (SNI) model (neuropathic pain). In all models Gly/GABA neurons were activated as indicated by their expression of c-fos. The pattern of Gly/GABA neuronal activation was different for every model, both anatomically and quantitatively. However, the averaged percentage of activated neurons that were Gly/GABA in the chronic phase (≥20h survival, 46%) was significantly higher than in the acute phase (≤2h survival, 34%). In addition, the total numbers of activated Gly/GABA neurons were similar in both phases, showing that the activation of non-Gly/GABA (presumed excitatory) neurons in the chronic phase decreased. Finally, morphine application equally decreased the total number of activated neurons and activated Gly/GABA neurons. This showed that morphine did not specifically activate Gly/GABA neurons to achieve nociceptive inhibition. The present study shows an increased activity of Gly/GABA neurons in acute and chronic models. This mechanism, together with mechanisms that antagonize the effects of GABA and glycine at the receptor level, may determine the sensitivity of our pain system during health and disease. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/20727678/Differential_distribution_of_activated_spinal_neurons_containing_glycine_and/or_GABA_and_expressing_c_fos_in_acute_and_chronic_pain_models_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(10)00445-8 DB - PRIME DP - Unbound Medicine ER -