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This Article Full Text Full Text (PDF) All Versions of this Article: 582/1/177    most recent jphysiol.2007.133330v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Snitsarev, V. Articles by Abboud, F. M. Search for Related Content PubMed PubMed Citation Articles by Snitsarev, V. Articles by Abboud, F. M. Related Collections Neuroscience

¹ Cardiovascular Research Center and Department of Internal Medicine
² Department of Molecular Physiology & Biophysics, University of Iowa, Iowa City, IA 52242, USA
³ Veterans Affairs Medical Center, Iowa City, IA 52246, USA

Nodose ganglion sensory neurones exert a significant reflex autonomic influence. We contrasted their mechanosensitivity, excitability and chemosensitivity in response to the stable prostacyclin (PGI₂) analogue carbacyclin (cPGI) in culture. Under current clamp conditions we measured changes in membrane potential (mV) and action potential (AP) responses to mechanically induced depolarizations and depolarizing current injections before and after superfusion of cPGI (1 µM and 10 µM). Chemosensitivity was indicated by augmentation of AP firing frequency and increased maximum gain of AP frequency (max. dAP/dmV), during superfusion with cPGI. Results indicate that two groups of neurones, A and B, are mechanosensitive (MS) and one group, C, is mechanoinsensitive (MI). Group A shows modest depolarization without AP generation during mechanical stimulation, and no increase in max. dAP/dmV, despite a marked increase in electrical depolarization with cPGI. Group B shows pronounced mechanical depolarization accompanied by enhanced AP discharge with cPGI, and an increase in max. dAP/dmV. Group C remains MI after cPGI but is more excitable and markedly chemosensitive (CS) with a pronounced enhancement of max. dAP/dmV with cPGI. The effect of cPGI on ionic conductances indicates that it does not sensitize the mechanically gated depolarizing degenerin/epithelial Na⁺ channels (DEG/ENaC), but it inhibits two voltage-gated K⁺ currents, Maxi-K and M-current, causing enhanced AP firing frequency and depolarization, respectively. We conclude that MS nodose neurones may be unimodal MS or bimodal MS/CS, and that MI neurones are unimodal CS, and much more CS to cPGI than MS/CS neurones. We suggest that the known excitatory effect of PGI₂ on baroreceptor and vagal afferent fibres is mediated by inhibition of voltage-gated K⁺ channels (Maxi-K and M-current) and not by an effect on mechanically gated DEG/ENaC channels.

(Received 26 March 2007; accepted after revision 18 April 2007; first published online 3 May 2007)
Corresponding author F. M. Abboud: Department of Internal Medicine, University of Iowa, 200 Hawkins Drive, Iowa City, IA, 52242, USA. Email: francois-abboud{at}uiowa.edu