PMID- 24312267
OWN - NLM
STAT- MEDLINE
DCOM- 20141217
LR  - 20220129
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 11
DP  - 2013
TI  - B-type natriuretic peptide-induced delayed modulation of TRPV1 and P2X3 receptors 
      of mouse trigeminal sensory neurons.
PG  - e81138
LID - 10.1371/journal.pone.0081138 [doi]
LID - e81138
AB  - Important pain transducers of noxious stimuli are small- and medium-diameter 
      sensory neurons that express transient receptor vanilloid-1 (TRPV1) channels 
      and/or adenosine triphosphate (ATP)-gated P2X3 receptors whose activity is 
      upregulated by endogenous neuropeptides in acute and chronic pain models. Little 
      is known about the role of endogenous modulators in restraining the expression 
      and function of TRPV1 and P2X3 receptors. In dorsal root ganglia, evidence 
      supports the involvement of the natriuretic peptide system in the modulation of 
      nociceptive transmission especially via the B-type natriuretic peptide (BNP) that 
      activates the natriuretic peptide receptor-A (NPR-A) to downregulate sensory 
      neuron excitability. Since the role of BNP in trigeminal ganglia (TG) is unclear, 
      we investigated the expression of BNP in mouse TG in situ or in primary cultures 
      and its effect on P2X3 and TRPV1 receptors of patch-clamped cultured neurons. 
      Against scant expression of BNP, almost all neurons expressed NPR-A at membrane 
      level. While BNP rapidly increased cGMP production and Akt kinase 
      phosphorylation, there was no early change in passive neuronal properties or 
      responses to capsaicin, alpha,beta-meATP or GABA. Nonetheless, 24 h application of BNP 
      depressed TRPV1 mediated currents (an effect blocked by the NPR-A antagonist 
      anantin) without changing responses to alpha,beta-meATP or GABA. Anantin alone decreased 
      basal cGMP production and enhanced control alpha,beta-meATP-evoked responses, implying 
      constitutive regulation of P2X3 receptors by ambient BNP. These data suggest a 
      slow modulatory action by BNP on TRPV1 and P2X3 receptors outlining the role of 
      this peptide as a negative regulator of trigeminal sensory neuron excitability to 
      nociceptive stimuli.
FAU - Vilotti, Sandra
AU  - Vilotti S
AD  - Neuroscience Department, International School for Advanced Studies (SISSA), 
      Trieste, Italy.
FAU - Marchenkova, Anna
AU  - Marchenkova A
FAU - Ntamati, Niels
AU  - Ntamati N
FAU - Nistri, Andrea
AU  - Nistri A
LA  - eng
GR  - GGP10082/TI_/Telethon/Italy
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131127
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Receptors, Purinergic P2X3)
RN  - 0 (TRPV Cation Channels)
RN  - 0 (TRPV1 protein, mouse)
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor)
RN  - EC 4.6.1.2 (atrial natriuretic factor receptor A)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation
MH  - Mice
MH  - Natriuretic Peptide, Brain/genetics/*metabolism
MH  - Nociception
MH  - Receptors, Atrial Natriuretic Factor/genetics/metabolism
MH  - Receptors, Purinergic P2X3/*metabolism
MH  - Sensory Receptor Cells/*metabolism
MH  - TRPV Cation Channels/*metabolism
MH  - Trigeminal Ganglion/*cytology/physiology
PMC - PMC3842315
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/12/07 06:00
MHDA- 2014/12/18 06:00
PMCR- 2013/11/27
CRDT- 2013/12/07 06:00
PHST- 2013/07/01 00:00 [received]
PHST- 2013/10/18 00:00 [accepted]
PHST- 2013/12/07 06:00 [entrez]
PHST- 2013/12/07 06:00 [pubmed]
PHST- 2014/12/18 06:00 [medline]
PHST- 2013/11/27 00:00 [pmc-release]
AID - PONE-D-13-27747 [pii]
AID - 10.1371/journal.pone.0081138 [doi]
PST - epublish
SO  - PLoS One. 2013 Nov 27;8(11):e81138. doi: 10.1371/journal.pone.0081138. 
      eCollection 2013.