Capsaicin inhibits activation of voltage-gated sodium currents in capsaicin-sensitive trigeminal ganglion neurons.

  title={Capsaicin inhibits activation of voltage-gated sodium currents in capsaicin-sensitive trigeminal ganglion neurons.},
  author={L A Liu and Marga Oortgiesen and L Li and Sidney A Simon},
  journal={Journal of neurophysiology},
  volume={85 2},
Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, repeated exposures of capsaicin will cause desensitization to nociceptive stimuli. In cultured trigeminal ganglion (TG) neurons, we investigated mechanisms underlying capsaicin-mediated inhibition of action potentials (APs) and modulation of voltage-gated sodium channels (VGSCs). Capsaicin (1 microM) inhibited APs and VGSCs only in capsaicin-sensitive neurons. Repeated applications… 

Capsaicin Blocks the Hyperpolarization-Activated Inward Currents via TRPV1 in the Rat Dorsal Root Ganglion Neurons

  • J. Kwak
  • Biology
    Experimental neurobiology
  • 2012
The inhibitory effects of capsaicin on Hyperpolarization-activated cation currents (Ih) are mediated by activation of TRPV1 and Ca2+-triggered cellular responses and are likely to be important in understanding the analgesic mechanism of Capsaicin.

Modulation of IA currents by capsaicin in rat trigeminal ganglion neurons.

In CS neurons, capsaicin decreases I(A) currents through the activation of vanilloid receptors, a reduction in which cGMP-PKG and calmodulin-dependent pathways should result in increased excitability of Capsaicin-sensitive nociceptors.

Capsaicin Indirectly Suppresses Voltage-Gated Na+ Currents Through TRPV1 in Rat Dorsal Root Ganglion Neurons

The findings suggest that capsaicin decreases both TTX-s andTTX-r INa+ as a result of an increase in [Na+]i through TRPV1.

Inhibition by capsaicin and its analogs of compound action potentials in frog sciatic nerves

It is concluded that Caps inhibits CAPs without TRPV1 activation and that a chemical structure bound to the vanillyl group of Caps analogs plays a role in determining the extent of CAP inhibition.

Effect of capsaicin on voltage-gated currents of trigeminal neurones in cell culture and slice preparations.

Depression of the voltage-gated currents may play an important role in the functional desensitization of the sensory receptors and in the analgesic effect induced by the agent and cell body of sensory neurones under native condition seems less sensitive to capsaicin then that of cells cultured in the presence of nerve growth factor.

Capsaicin causes robust reduction in glycinergic transmission to rat hypoglossal motor neurons via a TRPV1-independent mechanism.

Capsaicin reduces the amplitude of quantal and evoked glycinergic inhibitory neurotransmission to brainstem motor neurons without altering activity-dependent transmitter release and it is shown that capsaicin does not have any effect on either transient (It) or sustained (Is) potassium currents.

Capsaicin Enhances Glutamatergic Synaptic Transmission to Neonatal Rat Hypoglossal Motor Neurons via a TRPV1-Independent Mechanism

Capsaicin modulates glutamatergic excitatory, as well as glycinergic inhibitory, synaptic transmission in HMNs by differing pre- and post-synaptic mechanisms, which expands the understanding regarding the extent to which capsaicin can modulate synaptic transmission to central neurons.

Elevated temperatures alter TRPV1 agonist-evoked excitability of dorsal root ganglion neurons

Investigation of the effect of TRPV1 agonists and elevated temperatures on neuronal membrane excitability by electrophysiological techniques provides evidence that a synergistic interaction of TRpV1 ligands and elevated temperature activates TRPv1 receptors and results in profound effects on membranes excitability.



Capsazepine: a competitive antagonist of the sensory neurone excitant capsaicin

The present study shows the capsazepine acts as a competitive antagonist of capsaicin, with significant effects on the efflux of 86Rb+ from cultured DRG neurones evoked either by depolarization with high (50 mm) K+ solutions or by acidification of the external medium to pH 5.6.

Actions of capsaicin on peripheral nociceptors of the neonatal rat spinal cord‐tail in vitro: dependence of extracellular ions and independence of second messengers

The hypothesis that capsaicin‐induced activation, desensitization and impairment of peripheral nociceptor function is mediated by separate mechanisms is tested by use of an in vitro preparation of the neonatal rat spinal cord with the functionally attached tail.

Conduction-block induced by capsaicin in crayfish giant axon

Hyperalgesic agents increase a tetrodotoxin-resistant Na+ current in nociceptors.

Modulation of TTX-R INa is a mechanism for sensitization of mammalian nociceptors, as indicated by results indicating that three agents that produce tenderness or hyperalgesia in vivo, prostaglandin E2, adenosine, and serotonin, modulate TTx-R Ina.

Capsaicin Binds to the Intracellular Domain of the Capsaicin-Activated Ion Channel

Results indicate that CAP and its analog bind to the cytosolic domain of the CAP receptor and suggest that an endogenous CAP-like substance other than H+ may be present in the cell.