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Published on: August 30, 2017
Src kinase controls signaling pathways in sensory neuron triggered by low-power infrared radiation
Vera B Plakhova1,1, Valentina A Penniyaynen1,1, Igor L Yachnev1,1
1Laboratory of Physiology of Excitable Membranes, Pavlov Institute of Physiology of the Russian Academy of Sciences, 6 Nab. Makarova, 199034, Saint Petersburg, Russia.
Abstract:
Low-power (non-thermal) infrared (IR) radiation with the wavelength of 10.6 μm activates the Na,K-ATPase transducer function in sensory neurons, which is manifested in decrease of NaV1.8 channel voltage sensitivity at the cellular membrane level and in inhibition of growth of chick embryo dorsal root ganglia neurites at the tissue level. It is shown that the effect of low-power IR radiation is totally blocked by a specific Src kinase inhibitor, PP2. Upon irradiation on the background of PP2, the effective charge of NaV1.8 channel activation gating system does not differ from its control value in patch-clamp experiments, and the area index of sensory ganglia neurites growth remains unchanged as compared with the control in organotypic tissue culture. The data obtained demonstrate that Src kinase is involved in intracellular signaling pathways triggered by CO2 laser low-power IR radiation by the transducer-activated mechanism. This is the first indication that in primary sensory neuron the signals of low-power IR radiation are sensed, amplified, and transduced by the Na,K-ATPase/Src complex and not by G proteins.
Insights
Low-power infrared radiation activates sensory neuron signaling via the Na,K-ATPase/Src complex. This pathway, distinct from G proteins, influences neuronal function and neurite growth.
Area of Science:
- Neuroscience
- Biophysics
- Cellular Signaling
Background:
- Low-power infrared (IR) radiation can modulate cellular functions.
- Sensory neurons play a critical role in pain and touch perception.
- The Na,K-ATPase and Src kinase are known cellular signaling components.
Purpose of the Study:
- To investigate the molecular mechanisms by which low-power IR radiation affects sensory neurons.
- To identify the specific signaling pathways involved in IR radiation transduction in primary sensory neurons.
- To determine if G proteins are involved in the sensory neuron response to IR radiation.
Main Methods:
- Utilized patch-clamp electrophysiology to measure NaV1.8 channel voltage sensitivity.
- Employed organotypic tissue culture of chick embryo dorsal root ganglia to assess neurite growth.
- Administered a specific Src kinase inhibitor (PP2) to block kinase activity.
- Irradiated cells and tissues with 10.6 μm CO2 laser low-power IR radiation.
Main Results:
- Low-power IR radiation (10.6 μm) decreased NaV1.8 channel voltage sensitivity and inhibited neurite growth.
- The effects of IR radiation were completely blocked by the Src kinase inhibitor PP2.
- In the presence of PP2, IR irradiation did not alter NaV1.8 channel gating or neurite growth compared to controls.
- Src kinase is implicated in the intracellular signaling triggered by low-power IR radiation.
Conclusions:
- Low-power IR radiation is sensed, amplified, and transduced by the Na,K-ATPase/Src complex in primary sensory neurons.
- This signaling mechanism is independent of G proteins.
- Src kinase plays a crucial role in the cellular response to low-power IR radiation in sensory neurons.
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