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Modulation of synaptically induced burst strength and spike onset timing by inactivating KIRcurrents in medium spiny neurons

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Background

The membrane potential of striatal medium spiny neurons (MSNs) fluctuates between down- and up-states. In ventral striatum, inward rectifying potassium (KIR) currents in 40% of MSNs inactivate [1]. The significance of this property is not clearly known. We describe a computational study investigating how synaptic integration is influenced by KIR current inactivation.

Methods

Two MSNs were modeled using NEURON, one equipped with non-inactivating KIR currents (henceforth, "Cell A") and the other with inactivating KIR currents (henceforth "Cell B") and their behaviors were compared in response to trains of inputs activating NMDA, AMPA and GABA synapses. Injected current inputs were then used to investigate the mechanisms underlying the observed differences.

Results

It was observed that the behavior of these two types of cells were different in several ways. For instance, Cell B when compared with Cell A (i) had a more depolarized mean down-state potential (+2.8 mV); (ii) had a mean burst strength (number of action potentials fired from an up-state) higher by 35% for same strength synaptic input (Figure 1A); (iii) showed noticeable differences in strength-duration curve; (iv) had a mean spike onset earlier by 14% for a given number of spikes fired from the up-state (Figure 1B). It was also found that while the higher input resistance offered by Cell B is responsible for the earlier spiking onset, the lower permeability to potassium ions underlies the enhanced burst strength.

Figure 1
figure1

Membrane response of Cell B to synaptic input compared with that of Cell A (action potentials chopped at -20 mV). A, Burst strength is higher for Cell B for a synaptic input of given strength. B, Spike onset latency is lower for Cell B for a given number of spikes fired from the up-state.

Discussion

Our model demonstrates the facilitatory effect of KIR current inactivation on MSN excitability in response to synaptic inputs. In view of the reports that dendritic intracellular calcium levels depend closely on burst strength as well as the spike onset time in MSNs [2], our findings suggest that KIR current inactivation may significantly modulate synaptic plasticity as well.

References

  1. 1.

    Mermelstein PG, Song W, Tkatch T, Yan Z, Surmeier DJ: Inwardly rectifying potassium (IRK) currents are correlated with IRK subunit expression in rat nucleus accumbens medium spiny neurons. J Neurosci. 1998, 18: 6650-6661.

  2. 2.

    Kerr JND, Plenz D: Action potential timing determines dendritic calcium during striatal up-states. J Neurosci. 2004, 24: 877-8852. 10.1523/JNEUROSCI.4475-03.2004.

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Author information

Correspondence to John Eric Steephen.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Steephen, J.E., Manchanda, R. Modulation of synaptically induced burst strength and spike onset timing by inactivating KIRcurrents in medium spiny neurons. BMC Neurosci 9, P57 (2008) doi:10.1186/1471-2202-9-S1-P57

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Keywords

  • Synaptic Plasticity
  • Lower Permeability
  • Onset Time
  • Facilitatory Effect
  • Synaptic Input