Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Eighteenth Annual Computational Neuroscience Meeting: CNS*2009

Open Access Poster presentation

Control of bursting activity by modulation of ionic currents

Tatiana Malashchenko1, William Barnett1, Oleksandr Burylko2 and Gennady Cymbalyuk1*

Author Affiliations

1 Department of Physics and Astronomy, Georgia State University, Atlanta, GA 30303, USA

2 Institute of Mathematics, NAS of Ukraine, 3 Tereshchenkivska str., Kiev, Ukraine 01601

For all author emails, please log on.

BMC Neuroscience 2009, 10(Suppl 1):P27  doi:10.1186/1471-2202-10-S1-P27

The electronic version of this article is the complete one and can be found online at:

Published:13 July 2009

© 2009 Malashchenko et al; licensee BioMed Central Ltd.

Poster presentation

Our study is focused on modulation of dynamics of single leech heart interneurons (HNs). We consider two models of HNs representing these neurons under two different pharmacological treatments: (1) blocking of Ca2+ currents and inhibitory coupling with the Ca2+-containing saline and partial blocking of K+ currents; (2) decoupling HNs with bicuculline. In (1), an HN demonstrates slow plateau-like oscillations [1,2]. In (2), an HN demonstrates endogenously bursting activity [3]. We analyze how the interburst interval and burst duration could be controlled by manipulating hyperpolarization-activated current, Ih, and persistent Na+ current, IP, namely by variation of their conductances and the half-activation voltages, V1/2. For example, burst duration increases greatly from 1.7 s to 8.9 s as Vh,1/2 increased from -30 mV to 4 mV. The interburst interval grows from 0.6 s to 125 s as the Vh,1/2 decreases from 4 [mV] to -56 [mV] in accordance with a saddle-node bifurcation. In (2), we similarly show that the variation of Vh,1/2 could be a target for modulation of the bursting. In both cases, we show co-existence of bursting and silence. Interestingly, the co-existence is sensitive to gh (and to maximal conductance of fast Ca2+ current, gCaF too in (2)) and is not sensitive to the maximal conductances of other currents. In (1), if gh is increased from 4 nS to 8 nS, the bistability is then observed in an almost five-fold larger range of the leak conductance values, gleak. In (2), if either gh is changed from 4 nS to 8 nS or gCaF is changed from 5 nS to 0 nS, the bistability is observed in an almost two-fold larger range of gleak. If the bistability is an indication of a dysfunctional dynamics, this observation describes a new, potentially pathological role of over-expression of Ih and ICaF.


This work is supported by NSF grant PHY-0750456.


  1. Angstadt JD, Friesen WO: Synchronized oscillatory activity in leech neurons induced by calcium channel blockers.

    J Neurophysiol 1991, 66:1858-1873. PubMed Abstract | Publisher Full Text OpenURL

  2. Opdyke CA, Calabrese RL: A persistent sodium current contributes to oscillatory activity in heart interneurons of the medicinal leech.

    J Comp Physiol 1994, 175:781-789. Publisher Full Text OpenURL

  3. Cymbalyuk GS, Gaudry Q, Masino MA, Calabrese RL: Bursting in leech heart interneurons: cell-autonomous and network-based mechanisms.

    J Neurosci 2002, 22:10580-10592. PubMed Abstract | Publisher Full Text OpenURL