Abstract

Sympathetic neurons are important determinants of cardiovascular function. Kv1 channels modulate many aspects of neuronal function. We tested the hypothesis that two Kv1 channels, Kv1.1 and Kv1.3, modulate membrane excitability of and neurotransmitter release from postganglionic sympathetic neurons (PSNs). Western analyses indicated that Kv1.1 and Kv1.3 channels were expressed in PSNs in vitro and in vivo. Immunohistochemical analyses indicated that Kv1.1 channels were localized to cell bodies, axons and terminals; Kv1.3 channels were localized only to cells bodies. Specific inhibitors were used to assess the functional role of Kv1.1 (dendrotoxin (DTX); 100 nM) and Kv1.3 (margatoxin (MgTX); 1 nM) channels. Whole cell patch clamp electrophysiology indicated that DTX and MgTX had no effect on currents measured in cell bodies of PSNs. DTX enhanced and MgTX inhibited the effect of agonist (10 and 3 μM DMPP, respectively) on tritiated norepinephrine release (p < 0.05 ; unpaired t-test). Release (% total) in the presence of DTX (13.28 ± 2.36 (mean + s.e; n = 5.)) was greater than that in the absence (6.9 ± 0.96; n = 15). Release in the presence of MgTx (2.58 ± 0.74; n = 5) was less than that in the absence (6.66 ± 0.98; n = 16). These data indicate that Kv1.1 and Kv1.3 channels are expressed by and affect the function of PSNs, and suggest that these channels would influence sympathetic control of cardiovascular function. HL076774

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.