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Acta Physiologica Congress

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Acta Physiologica 2010; Volume 200, Supplement 681
Abstracts of the 61st National Congress of the Italian Physiological Society
9/15/2010-9/17/2010
Varese, Italy


AXOTOMY AND DENERVATION OF RAT SUPERIOR CERVICAL GANGLION NEURONS DIFFERENTLY MODULATE THE EXPRESSION OF VOLTAGE-GATED K+ CHANNELS
Abstract number: P54

DE STEFANO1,2 ME, DI PENTIMA1 M, DEL SIGNORE1 A, PAGGI1,2 P

1Istituto Pasteur-Fondazione Cenci Bolognetti, Dip. di Biologia Cellulare e dello Sviluppo, Rome, Italy
2Center for Research in Neurobiology Daniel Bovet, Rome, Italy

Voltage-gated K+ channels (Kv) are made of four transmembrane alfa subunits and four cytoplasmic regulatory subunits. In particular, Kv4 and Kv1 families are responsible for the fast inactivating K+ inward current, a reduction of which has been demonstrated after axotomy of rat superior cervical ganglion (SCG) neurons. Here we report on a different modulation in Kv4.2, Kv1.4 and the accessory subunit beta 2 expression by axotomy and denervation. Rat SCG neurons were either axotomized or denervated by crushing post- and preganglionic nerves, respectively. Rats were killed at different postoperative days (d) and mRNA and protein levels compared to control. After axotomy, mRNA of all proteins decreased significantly by 1 d, returning to control level (except for beta 2) after 6 d, consistent with the known reduction in gene expression of proteins not necessary for axon regeneration, as Kv are. Beta 2 protein levels decrease accordingly, but those of Kv1.4 increase significantly. Since Kv1 family channels are mainly presynaptic and axonal, this increase suggests Kv1.4 accumulation in the perikaryon consequent to reduced export along functionally inactive axons. Reduction in beta 2 subunit protein levels, in fact, is consistent with its role in Kv1 insertion into membrane and activity. Denervation does not affect Kv1.4 mRNA levels, while those of Kv4.2 (mainly somatodendritic) are reduced, as expected after functional silencing ganglionic neurons by removal of presynaptic boutons.

To cite this abstract, please use the following information:
Acta Physiologica 2010; Volume 200, Supplement 681 :P54

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