Imperial College London
Alternate

DrIstvanNagy

Faculty of Medicine, Department of Surgery & Cancer

Reader in Nociceptive Mechanisms
 
 
 
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Contact

 

+44 (0)20 3315 8897i.nagy Website

 
 
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Assistant

 

Miss Steffi Klier +44 (0)20 3315 8816

 
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Location

 

G345Chelsea and Westminster HospitalChelsea and Westminster Campus

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Summary

 

Publications

Citation

BibTex format

@article{Nerandzic:2018:10.1111/bph.13849,
author = {Nerandzic, V and Mrozkova, P and Adamek, P and Spicarova, D and Nagy, I and Palecek, J},
doi = {10.1111/bph.13849},
journal = {British Journal of Pharmacology},
pages = {2322--2336},
title = {Peripheral inflammation alters N-arachidonoylphosphatidylethanolamine (20:4-NAPE) induced modulation of nociceptive spinal cord synaptic transmiss},
url = {http://dx.doi.org/10.1111/bph.13849},
volume = {175},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Background and Purpose Endocannabinoids play an important role in modulating spinal nociceptive signalling, crucial for the development of pain. The cannabinoid receptor 1 (CB1) and the transient receptor potential  cation  channel  subfamily  V  member  1  (TRPV1)  are  both  activated  by  the endocannabinoid anandamide that  is a  product of biosynthesis  from the endogenous lipid precursor N1arachidonoylphosphatidylethanolamine (20:41NAPE). Here we are first to report CB1 receptor1  and TRPV11mediated effects  of 20:41NAPE application on spinal synaptic transmission in control and inflammatory conditions. Experimental Approach Spontaneous (sEPSCs) and dorsal root stimulation1evoked (eEPSCs) excitatory postsynaptic currents  from  superficial  dorsal  horn  neurons  in  rat  spinal  cord  slices  were  assessed. Peripheral  inflammation  was  induced  by  carrageenan.  Anandamide  concentration  was assessed by mass spectrometry. Key Results Application of 20:41NAPE increased anandamide concentration in vitro. 20:41NAPE (20 μM) decreased sEPSCs frequency and eEPSCs amplitude in control and inflammatory conditions. The inhibitory effect of 20:41NAPE was sensitive to CB1 antagonist PF514273 (0.2 μM) in both conditions, but to the TRPV1 antagonist SB366791 (10 μM) only after inflammation. After inflammation 20:41NAPE increased sEPSCs frequency in the presence of PF514273 and this increase was blocked by SB366791.  Conclusions and Implications While 20:41NAPE treatment produced an inhibitory effect on excitatory synaptic transmission in both naive and inflammatory conditions, peripheral inflammation altered the underlying mechanisms. Our data indicate that 20:41NAPE application induced mainly CB1 receptor1mediated inhibitory effects in naive animals while TRPV11mediated mechanisms were also involved after inflammation. Increasing anandamide levels for analgesic purposes by applying substrate  for  its  local  synthesis  may  be  superior  to  systemic  anand
AU  - Nerandzic,V
AU  - Mrozkova,P
AU  - Adamek,P
AU  - Spicarova,D
AU  - Nagy,I
AU  - Palecek,J
DO  - 10.1111/bph.13849
EP  - 2336
PY  - 2018///
SN  - 1476-5381
SP  - 2322
TI  - Peripheral inflammation alters N-arachidonoylphosphatidylethanolamine (20:4-NAPE) induced modulation of nociceptive spinal cord synaptic transmiss
T2  - British Journal of Pharmacology
UR  - http://dx.doi.org/10.1111/bph.13849
UR  - http://hdl.handle.net/10044/1/48351
VL  - 175
ER  -
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