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Acta Physiologica 2007; Volume 190, Supplement 655
XXXIV Congress of The Spanish Society for Physiological Sciences
7/3/2007-7/7/2007
Valladolid, Spain
ACTIVATION AND MODULATION OF TRPC5 CHANNEL BY OSMOTIC STIMULI
Abstract number: S19
Gomis1 A
1CSIC-UMH, Instituto de Neurociencias de Alicante. 03550 Sant Joan D'Alacant. Alicante.Spain
Mammalian canonical transient receptor potential (TRPC) genes encode a family of nonselective cation channels that are activated following stimulation of G-protein-coupled membrane receptors linked to phospholipase C. TRPCs are molecular candidates for Ca2+ entry channels in brain since they are highly expressed in the nervous system, form Ca2+ -permeable channels in recombinant expression systems and are activated by agonist that induce intracellular Ca2+ release. However, their mechanisms of activation and endogenous regulators remain poorly understood. We have been focused our studies on the TRPC5 channel. We used a combination of cellular Ca2+ imaging and patch-clamp techniques.
We show that hyposmotic stimuli (210mOsm), that cause membrane stretch, produce an increase in the intracellular calcium concentration in HEK293 cells transfected with TRPC5. During whole-cell recordings, the application of hypotonic stimulus activates the characteristic doubly rectifying currents mediated by TRPC5. The activation of TRPC5 is promoted with the co-expression of the histamine receptor type I (H1). The presence of external calcium increases the percentage of responding cells. Activation of inositol polyphosphate 5-phosphatase IV (5ptase IV), leading to reduced membrane phosphatidylinositol 4,5-bisphosphate (PIP2) levels, produced an abolition of hipotonically-evoked calcium elevations and prevented activation of TRPC5.
These data show that TRPC5 is activated downstream of an osmotic stimulus whose activation is potentiated by the presence of membrane receptors and is modulated by PIP2 membrane levels. The activation of TRPC5 by osmotically induced stretch may play a role in sensory transduction.
Supported by: Ministerio de Educación y Ciencia. BFU2005-03986
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 190, Supplement 655 :S19