Skip to main content
Help us understand how you use our websites. Take part in our 30 minute study now.

Control of bursting activity by modulation of ionic currents

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, I h , and persistent Na+ current, I P , 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,1/2increased from -30 mV to 4 mV. The interburst interval grows from 0.6 s to 125 s as the Vh,1/2decreases from 4 [mV] to -56 [mV] in accordance with a saddle-node bifurcation. In (2), we similarly show that the variation of Vh,1/2could 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 g h (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 g h 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 g h 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 I h and ICaF.


  1. 1.

    Angstadt JD, Friesen WO: Synchronized oscillatory activity in leech neurons induced by calcium channel blockers. J Neurophysiol. 1991, 66: 1858-1873.

    CAS  PubMed  Google Scholar 

  2. 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. 10.1007/BF00191850.

    CAS  Article  Google Scholar 

  3. 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.

    CAS  PubMed  Google Scholar 

Download references


This work is supported by NSF grant PHY-0750456.

Author information



Corresponding author

Correspondence to Gennady Cymbalyuk.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Malashchenko, T., Barnett, W., Burylko, O. et al. Control of bursting activity by modulation of ionic currents. BMC Neurosci 10, P27 (2009).

Download citation


  • Animal Model
  • Pharmacological Treatment
  • Large Range
  • Ionic Current
  • Maximal Conductance