PMID- 16192372
OWN - NLM
STAT- MEDLINE
DCOM- 20060221
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 25
IP  - 39
DP  - 2005 Sep 28
TI  - Bradykinin-induced functional competence and trafficking of the delta-opioid 
      receptor in trigeminal nociceptors.
PG  - 8825-32
AB  - Peripheral opioid analgesia is increased substantially after inflammation. We 
      evaluated the hypothesis that an inflammatory mediator, bradykinin (BK), evokes 
      functional competence of the delta-opioid receptor (DOR) for inhibiting 
      trigeminal ganglia (TG) sensory neurons. We also evaluated whether BK evokes 
      trafficking of the DOR to the plasma membrane. Rat TG cultures were pretreated 
      with BK (10 microm) or vehicle, and the effects of DOR agonists 
      ([D-Pen2,5]-enkephalin or [D-Ala2, D-Leu5]-enkephalin) on BK (10 
      microm)/prostagladin E2 (PGE2; 1 microm)-stimulated immunoreactive calcitonin 
      gene-related peptide (iCGRP) release or PGE2 (1 microm)-stimulated cAMP 
      accumulation were measured. The effect of BK treatment on opioid receptor 
      trafficking was evaluated by DOR immunohistochemistry, cell-surface DOR 
      biotinylation, and live imaging of neurons transfected with mDOR-green 
      fluorescent protein. BK pretreatment rapidly and significantly increased DOR 
      agonist inhibition of evoked iCGRP release and cAMP accumulation. These effects 
      of BK pretreatment were blocked by a B2 receptor antagonist (HOE-140; 10 microm) 
      or a protein kinase C (PKC) inhibitor [bisindolymaleimide (BIS); 1 microm]. 
      Moreover, BK treatment rapidly and significantly increased the accumulation of 
      DOR in the plasma membrane. However, BK-induced trafficking of DOR was not 
      reversed by pretreatment with BIS, nor was trafficking evoked by application of a 
      PKC activator PMA (200 nm). These data suggest that BK, in a PKC-dependent 
      manner, induces rapid functional competence of DOR for inhibiting TG nociceptors 
      and in a PKC-independent manner rapidly induces trafficking of DOR to the plasma 
      membrane. These findings indicate that exposure to certain inflammatory mediators 
      rapidly alters the signaling properties and neuronal localization of DOR, 
      possibly contributing to peripheral opioid analgesia.
FAU - Patwardhan, Amol M
AU  - Patwardhan AM
AD  - Department of Pharmacology, University of Texas Health Science Center, San 
      Antonio, Texas 78229, USA.
FAU - Berg, Kelly A
AU  - Berg KA
FAU - Akopain, Armen N
AU  - Akopain AN
FAU - Jeske, Nathaniel A
AU  - Jeske NA
FAU - Gamper, Nikita
AU  - Gamper N
FAU - Clarke, William P
AU  - Clarke WP
FAU - Hargreaves, Kenneth M
AU  - Hargreaves KM
LA  - eng
GR  - F31 DA016179/DA/NIDA NIH HHS/United States
GR  - F32 DE016500/DE/NIDCR NIH HHS/United States
GR  - DE016500/DE/NIDCR NIH HHS/United States
GR  - P01 DA 016179/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Inflammation Mediators)
RN  - 0 (Receptor, Bradykinin B2)
RN  - 0 (Receptors, Opioid, delta)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 147336-22-9 (Green Fluorescent Proteins)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Animals
MH  - Bradykinin/pharmacology/*physiology
MH  - Cell Membrane/metabolism
MH  - Enzyme Activation/physiology
MH  - Green Fluorescent Proteins/genetics
MH  - In Vitro Techniques
MH  - Inflammation Mediators/pharmacology/*physiology
MH  - Male
MH  - Neural Inhibition/physiology
MH  - Neurons, Afferent/metabolism
MH  - Nociceptors/metabolism/*physiology
MH  - Protein Kinase C/metabolism
MH  - Protein Transport/drug effects/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Bradykinin B2/metabolism/physiology
MH  - Receptors, Opioid, delta/agonists/drug effects/*metabolism/physiology
MH  - Recombinant Fusion Proteins/metabolism
MH  - Trigeminal Ganglion/*metabolism/physiology
PMC - PMC6725594
EDAT- 2005/09/30 09:00
MHDA- 2006/02/24 09:00
PMCR- 2006/03/28
CRDT- 2005/09/30 09:00
PHST- 2005/09/30 09:00 [pubmed]
PHST- 2006/02/24 09:00 [medline]
PHST- 2005/09/30 09:00 [entrez]
PHST- 2006/03/28 00:00 [pmc-release]
AID - 25/39/8825 [pii]
AID - 10.1523/JNEUROSCI.0160-05.2005 [doi]
PST - ppublish
SO  - J Neurosci. 2005 Sep 28;25(39):8825-32. doi: 10.1523/JNEUROSCI.0160-05.2005.