Pain Medicine


Purple and white patternPersistent pain results in suffering and poor quality of life. In addition, the lack of proper control of persistent pain may lead to the development of physical and mental disabilities, which further devastate the patient’s quality of life. The main goal of our research activities is to identify pivotal mechanisms in neuronal processing of information induced by various persistent painful conditions, which could be used to develop new pain killers. Hence, our activities will ultimately improve patients’ quality of life.

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Citation

BibTex format

@article{Nagy:2017:10.1002/cne.24154,
author = {Nagy, I and Suosa-Valente, J and Varga, A and Torres, Perez J and Jenes, A and Wahba, J and Mackie, K and Cravatt, B and Ueda, N and Tsuboi, K and Santha, P and Jancso, G and Tailor, H and Avelino, A},
doi = {10.1002/cne.24154},
journal = {Journal of Comparative Neurology},
pages = {1778--1796},
title = {Inflammation of peripheral tissues and injury to peripheral nerves induce diferring effects in the expression of the calcium-sensitive anandamide synthesising enzyme and related molecules in ratprimary sensory neuron},
url = {http://dx.doi.org/10.1002/cne.24154},
volume = {525},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Elevation  of  intracellular  Ca2+  concentration  induces  the  synthesis  of  N0arachydonoylethanolamine  (anandamide)  in  a  sub0population  of  primary  sensory neurons. N0acylphosphatidylethanolamine phospholipase D (NAPE0PLD) is the only known enzyme, which synthesises anandamide in a Ca2+0dependent manner. NAPE0PLD mRNA, as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1) and the inhibitory cannabinoid type 1 (CB1)  receptor  and  the  main  anandamide0hydrolysing enzyme  fatty  acid  amide hydrolase  (FAAH)  are  all  expressed  by  sub0populations  of  nociceptive  primary sensory neurons. Thus, NAPE0PLD, TRPV1, the CB1 receptor and FAAH could form an  autocrine  signalling  system,  which  could  shape  the  activity  of  a  major  sub0population  of  nociceptive  primary  sensory  neurons, hence  contribute  to  the development of pain. While the expression patterns of TRPV1, the CB1 receptor and FAAH  have  been  comprehensively  elucidated,  little  is  known  about  NAPE0PLD expression  in  primary  sensory  neurons  under  physiological  and  pathological conditions.  We  report  that  NAPE0PLD  is  expressed  by  about  a  third  of  primary sensory  neurons,  the  overwhelming  majority  of  which  also  express  nociceptive markers as well as the CB1 receptor, TRPV1 and FAAH. Inflammation of peripheral tissues and injury to peripheral nerves induce differing but concerted changes in the expression pattern of NAPE0PLD, the CB1 receptor, TRPV1 and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signalling system,  in  a  major  proportion  of  nociceptive  primary  sensory  neurons,  and  that alterations in that autocrine signalling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain.
AU  - Nagy,I
AU  - Suosa-Valente,J
AU  - Varga,A
AU  - Torres,Perez J
AU  - Jenes,A
AU  - Wahba,J
AU  - Mackie,K
AU  - Cravatt,B
AU  - Ueda,N
AU  - Tsuboi,K
AU  - Santha,P
AU  - Jancso,G
AU  - Tailor,H
AU  - Avelino,A
DO  - 10.1002/cne.24154
EP  - 1796
PY  - 2017///
SN  - 1096-9861
SP  - 1778
TI  - Inflammation of peripheral tissues and injury to peripheral nerves induce diferring effects in the expression of the calcium-sensitive anandamide synthesising enzyme and related molecules in ratprimary sensory neuron
T2  - Journal of Comparative Neurology
UR  - http://dx.doi.org/10.1002/cne.24154
UR  - http://hdl.handle.net/10044/1/43081
VL  - 525
ER  -
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