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Prostaglandin E(2) inhibits calcium current in two sub-populations of acutely isolated mouse trigeminal sensory neurons.
- Source :
-
The Journal of physiology [J Physiol] 2002 Mar 01; Vol. 539 (Pt 2), pp. 433-44. - Publication Year :
- 2002
-
Abstract
- Prostaglandins are important mediators of pain and inflammation. We have examined the effects of prostanoids on voltage-activated calcium currents (I(Ca)) in acutely isolated mouse trigeminal sensory neurons, using standard whole cell voltage clamp techniques. Trigeminal neurons were divided into two populations based on the presence (Type 2) or absence (Type 1) of low voltage-activated T-type I(Ca). The absence of T-type I(Ca) is highly correlated with sensitivity to mu-opioid agonists and the VR1 agonist capsaicin. In both populations of cells, high voltage-activated I(Ca) was inhibited by PGE(2) with an EC(50) of about 35 nM, to a maximum of 30 %. T-type I(Ca) was not inhibited by PGE(2). Pertussis toxin pre-treatment abolished the effects of PGE(2) in Type 2 cells, but not in Type 1 cells, whereas treatment with cholera toxin prevented the effects of PGE(2) in Type 1 cells, but not in Type 2 cells. Inhibition of I(Ca) by PGE(2) was associated with slowing of current activation and could be relieved with a large positive pre-pulse, consistent with inhibition of I(Ca) by G protein betagamma subunits. Reverse transcription-polymerase chain reaction of mRNA from trigeminal ganglia indicated that all four EP prostanoid receptors were present. However, in both Type 1 and Type 2 cells the effects of PGE(2) were only mimicked by the selective EP(3) receptor agonist ONO-AE-248, and not by selective agonists for EP(1) (ONO-DI-004), EP(2) (ONO-AE1-259) and EP(4) (ONO-AE1-329) receptors. These data indicate that two populations of neurons in trigeminal ganglia differing in their calcium channel expression, sensitivity to mu-opioids and capsaicin also have divergent mechanisms of PGE(2)-mediated inhibition of calcium channels, with Gi/Go type G proteins involved in one population, and Gs type G proteins in the other.
- Subjects :
- Animals
Calcium Channels metabolism
Calcium Channels, N-Type drug effects
Calcium Channels, N-Type metabolism
Calcium Channels, Q-Type drug effects
Calcium Channels, Q-Type metabolism
Cholera Toxin pharmacology
Electrophysiology
Female
GTP-Binding Protein alpha Subunits, Gi-Go drug effects
GTP-Binding Protein alpha Subunits, Gi-Go metabolism
GTP-Binding Protein alpha Subunits, Gs drug effects
GTP-Binding Protein alpha Subunits, Gs metabolism
GTP-Binding Proteins drug effects
GTP-Binding Proteins metabolism
In Vitro Techniques
Ion Channel Gating
Male
Mice
Mice, Inbred C57BL
Patch-Clamp Techniques
Pertussis Toxin
RNA genetics
RNA isolation & purification
Reverse Transcriptase Polymerase Chain Reaction
Trigeminal Nerve drug effects
Virulence Factors, Bordetella pharmacology
Calcium Channel Blockers pharmacology
Calcium Channels drug effects
Dinoprostone pharmacology
Neurons, Afferent drug effects
Trigeminal Nerve metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0022-3751
- Volume :
- 539
- Issue :
- Pt 2
- Database :
- MEDLINE
- Journal :
- The Journal of physiology
- Publication Type :
- Academic Journal
- Accession number :
- 11882676
- Full Text :
- https://doi.org/10.1113/jphysiol.2001.013322