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  • Open Access

Extracellular potassium concentration defines neuronal bursting properties

  • 1Email author,
  • 2,
  • 3 and
  • 2
BMC Neuroscience201516 (Suppl 1) :P215

https://doi.org/10.1186/1471-2202-16-S1-P215

  • Published:

Keywords

  • Leak Current
  • Reversal Potential
  • Rhythmic Activity
  • Burst Activity
  • Extracellular Potassium

Many neurons, or populations of neurons, in the brain are capable of producing rhythmic bursting activity. This ability is putatively responsible for rhythmogenic functions like breathing and locomotion. In vivo, rhythms are generated by synaptically interconnected neuronal networks, whereas rhythmic bursting behavior is often induced in vitro by elevating the extracellular potassium concentration (K out ) [1]. It is known that increasing K out raises the reversal potentials of potassium and leak currents [2]. However, the complete nature of how these effects underlie bursting activity has yet to be uncovered.

A mathematical modeling study was performed to elucidate the interplay between these factors and their roles in a neuron's transition from quiescence to rhythmic bursting. A conductance-based model of a neuron from the pre-Bötzinger Complex (pre-BötC) was used as a basis [3]. A potassium ion component was incorporated into the leak current, and model behaviors were investigated at varying concentrations of K out , taking into account its effect on delayed rectifier potassium current responsible for after-spike hyperpolarization. The primary aim of this modeling study was to evaluate the contribution of extracellular potassium ions in the leak and delayed rectifier potassium current, and the subsequent effect of these altered currents on the bursting properties of neurons. Furthermore, the initial model was modified to replicate experimental results and test for conditions of low K out as seen in vivo.

The analysis of our model shows that: (i) in vitro bursting behavior with elevated K out may occur due to attenuation of the delayed rectifier potassium current and (ii) no oscillations are generated at physiological levels of extracellular potassium. These results indicate that, according to the commonly-accepted models used in our study, neurons that naturally burst in in vitro preparations may not be able to burst in vivo under any circumstances. Accordingly, rhythmic activity in vivo should rely on other mechanisms. For example, Jasinski et al. [4] have shown that the recurrent synaptic excitation in combination with the sodium-potassium exchanger (pump) can result in the robust rhythmic network activity even with all intrinsic bursting mechanisms blocked.

Declarations

Acknowledgements

This work was supported by National Institutes of Health, grant R01 AT008632 to Y. I. M.; grants R33 HL087377; R01 NS057815; and R01 NS069220 to I. A. R.

Authors’ Affiliations

(1)
Department of Mathematical Sciences, Indiana University-Purdue University, IN, USA
(2)
Department of Neurobiology and Anatomy, Drexel University College of Medicine, PA 19123, USA
(3)
Carmel High School, Carmel, IN 46032, USA

References

  1. Smith JC, Ellenberger HH, Ballanyi K, Richter DW, Feldman JL: Pre-Botzinger Complex - a Brain-Stem Region That May Generate Respiratory Rhythm in Mammals. Science. 1991, 254 (5032): 726-729.PubMedPubMed CentralView ArticleGoogle Scholar
  2. Rybak IA, Shevtsova NA, St-John WM, Paton JFR, Pierrefiche O: Endogenous rhythm generation in the pre-Botzinger complex and ionic currents: modelling and in vitro studies. Eur J Neurosci. 2003, 18 (2): 239-257.PubMedView ArticleGoogle Scholar
  3. Butera RJ, Rinzel J, Smith JC: Models of respiratory rhythm generation in the pre-Botzinger complex. I. Bursting pacemaker neurons. J Neurophysiol. 1999, 82 (1): 382-397.PubMedGoogle Scholar
  4. Jasinski PE, Molkov YI, Shevtsova NA, Smith JC, Rybak IA: Sodium and calcium mechanisms of rhythmic bursting in excitatory neural networks of the pre-Botzinger complex: a computational modelling study. Eur J Neurosci. 2013, 37 (2): 212-230.PubMedPubMed CentralView ArticleGoogle Scholar

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