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<p>Synaptic plasticity within cortico-striatal circuits critically influences learning and behavior, with the nucleus accumbens (NAc) serving as a key mediating structure. Within the NAc, medium spiny neurons (MSNs) are known to mediate input integration, whose dendritic calcium levels are thought to influence cortico-striatal plasticity. Calcium responses have been observed to correlate with firing frequency and earlier firing onset. Inward rectifying potassium (K<sub>IR</sub>) currents inactivate significantly in ~40% of NAc MSNs. Studies have shown that this inactivation enhances firing frequency and advances firing onset. On the basis of these findings, we hypothesized that K<sub>IR</sub> inactivation may enhance intracellular calcium levels in MSNs, with implications for synaptic plasticity. Using an 189-compartment computational model of the MSN, the influence of K<sub>IR</sub> inactivation on calcium dynamics was investigated. We found that the amplitude of calcium influx was more than twice as large in the tertiary dendrite and at least 9% higher for higher input currents in response to K<sub>IR</sub> inactivation. Additionally, the average calcium concentration increased by up to 26.1% in the soma, with enhancements of 4.3–21.4% in the dendrites. Our findings suggest that K<sub>IR</sub> inactivation may significantly modulate synaptic plasticity, thereby impacting the learning mediated by the NAc core.</p>

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Enhancement of calcium responses by KIR current inactivation in medium spiny neurons

  • 期刊论文

  • 发表日期：

    2026年2月27日

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  • John Eric Steephen,
  • Mithun Padmakumar,
  • Rohit Manchanda

摘要

Synaptic plasticity within cortico-striatal circuits critically influences learning and behavior, with the nucleus accumbens (NAc) serving as a key mediating structure. Within the NAc, medium spiny neurons (MSNs) are known to mediate input integration, whose dendritic calcium levels are thought to influence cortico-striatal plasticity. Calcium responses have been observed to correlate with firing frequency and earlier firing onset. Inward rectifying potassium (KIR) currents inactivate significantly in ~40% of NAc MSNs. Studies have shown that this inactivation enhances firing frequency and advances firing onset. On the basis of these findings, we hypothesized that KIR inactivation may enhance intracellular calcium levels in MSNs, with implications for synaptic plasticity. Using an 189-compartment computational model of the MSN, the influence of KIR inactivation on calcium dynamics was investigated. We found that the amplitude of calcium influx was more than twice as large in the tertiary dendrite and at least 9% higher for higher input currents in response to KIR inactivation. Additionally, the average calcium concentration increased by up to 26.1% in the soma, with enhancements of 4.3–21.4% in the dendrites. Our findings suggest that KIR inactivation may significantly modulate synaptic plasticity, thereby impacting the learning mediated by the NAc core.