Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N‐arachidonoylphosphatidylethanolamine

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00489989" target="_blank" >RIV/67985823:_____/18:00489989 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/18:10362642

Výsledek na webu

<a href="http://dx.doi.org/10.1111/bph.13849" target="_blank" >http://dx.doi.org/10.1111/bph.13849</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/bph.13849" target="_blank" >10.1111/bph.13849</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N‐arachidonoylphosphatidylethanolamine

Popis výsledku v původním jazyce

Endocannabinoids play an important role in modulating spinal nociceptive signalling, crucial for the development of pain. The cannabinoid CB1 receptor and the TRPV1 cation channel are both activated by the endocannabinoid anandamide, a product of biosynthesis from the endogenous lipid precursor N‐arachidonoylphosphatidylethanolamine (20:4‐NAPE). Here, we report CB1 receptor‐ and TRPV1‐mediated effects of 20:4‐NAPE on spinal synaptic transmission in control and inflammatory conditions. Spontaneous (sEPSCs) and dorsal root stimulation‐evoked (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. While 20:4‐NAPE treatment inhibited the excitatory synaptic transmission in both naive and inflammatory conditions, peripheral inflammation altered the underlying mechanisms. Our data indicate that 20:4‐NAPE application induced mainly CB1 receptor‐mediated inhibitory effects in naive animals while TRPV1‐mediated mechanisms were also involved after inflammation. Increasing anandamide levels for analgesic purposes by applying substrate for its local synthesis may be more effective than systemic anandamide application or inhibition of its degradation.

Název v anglickém jazyce

Peripheral inflammation affects modulation of nociceptive synaptic transmission in the spinal cord induced by N‐arachidonoylphosphatidylethanolamine

Popis výsledku anglicky

Endocannabinoids play an important role in modulating spinal nociceptive signalling, crucial for the development of pain. The cannabinoid CB1 receptor and the TRPV1 cation channel are both activated by the endocannabinoid anandamide, a product of biosynthesis from the endogenous lipid precursor N‐arachidonoylphosphatidylethanolamine (20:4‐NAPE). Here, we report CB1 receptor‐ and TRPV1‐mediated effects of 20:4‐NAPE on spinal synaptic transmission in control and inflammatory conditions. Spontaneous (sEPSCs) and dorsal root stimulation‐evoked (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. While 20:4‐NAPE treatment inhibited the excitatory synaptic transmission in both naive and inflammatory conditions, peripheral inflammation altered the underlying mechanisms. Our data indicate that 20:4‐NAPE application induced mainly CB1 receptor‐mediated inhibitory effects in naive animals while TRPV1‐mediated mechanisms were also involved after inflammation. Increasing anandamide levels for analgesic purposes by applying substrate for its local synthesis may be more effective than systemic anandamide application or inhibition of its degradation.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

British Journal of Pharmacology

ISSN

0007-1188

e-ISSN

—

Svazek periodika

175

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

15

Strana od-do

2322-2356

Kód UT WoS článku

000434071600015

EID výsledku v databázi Scopus

2-s2.0-85020379780