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Hypocalcemia-induced seizure: demystifying the calcium paradox.

Han P, Trinidad BJ, Shi J - ASN Neuro (2015)

Bottom Line: The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum.Nevertheless, several studies primarily addressing other biophysical issues have provided some clues.In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox.

View Article: PubMed Central - PubMed

Affiliation: Barrow Neurological Institute, Dignity Health St Joseph's Hospital and Medical Center and Medical Center, Phoenix, AZ, USA PengCheng.Han@dignityhealth.org.

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Modulation of firing frequency. (a) Afterhyperpolarization determines the interspike interval. (b) Injected depolarizing current enhances firing frequency. Figures modified from Han et al. (2007). AHP = afterhyperpolarization.
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fig1-1759091415578050: Modulation of firing frequency. (a) Afterhyperpolarization determines the interspike interval. (b) Injected depolarizing current enhances firing frequency. Figures modified from Han et al. (2007). AHP = afterhyperpolarization.

Mentions: The interval between adjacent action potential spikes (interspike interval) is a key factor that determines firing frequency (Han et al., 2007). After the membrane potential repolarizes back to resting level, a further transient hyperpolarization may be present after the end of the action potential. This hyperpolarization valley is named the afterhyperpolarization (AHP, Figure 1a). It is the valley’s depth (AHP amplitude) that determines the time interval before reaching back to the next firing threshold. A basic rule of thumb is that a small AHP translates into a higher firing frequency while a larger AHP will reduce firing frequency. While multiple types of potassium channels contribute to AHP, it is the KCa channels that may fine tune the actual depth of the AHP (Sah, 1996). KCa channels have an intracellular domain that binds to intracellular calcium. High internal Ca2+ enhances K+ outflow thus increasing the AHP and slowing the firing rate. This suggests a reasonable model that action potentials open VGCC leading to a transient increase in cytoplasmic Ca, which in turn modulates these KCa. Conversely, low external calcium would provide less calcium influx and diminish KCa activation.Figure 1.


Hypocalcemia-induced seizure: demystifying the calcium paradox.

Han P, Trinidad BJ, Shi J - ASN Neuro (2015)

Modulation of firing frequency. (a) Afterhyperpolarization determines the interspike interval. (b) Injected depolarizing current enhances firing frequency. Figures modified from Han et al. (2007). AHP = afterhyperpolarization.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License 1 - License 2 - License 3
Show All Figures
getmorefigures.php?uid=PMC4374060&req=5

fig1-1759091415578050: Modulation of firing frequency. (a) Afterhyperpolarization determines the interspike interval. (b) Injected depolarizing current enhances firing frequency. Figures modified from Han et al. (2007). AHP = afterhyperpolarization.
Mentions: The interval between adjacent action potential spikes (interspike interval) is a key factor that determines firing frequency (Han et al., 2007). After the membrane potential repolarizes back to resting level, a further transient hyperpolarization may be present after the end of the action potential. This hyperpolarization valley is named the afterhyperpolarization (AHP, Figure 1a). It is the valley’s depth (AHP amplitude) that determines the time interval before reaching back to the next firing threshold. A basic rule of thumb is that a small AHP translates into a higher firing frequency while a larger AHP will reduce firing frequency. While multiple types of potassium channels contribute to AHP, it is the KCa channels that may fine tune the actual depth of the AHP (Sah, 1996). KCa channels have an intracellular domain that binds to intracellular calcium. High internal Ca2+ enhances K+ outflow thus increasing the AHP and slowing the firing rate. This suggests a reasonable model that action potentials open VGCC leading to a transient increase in cytoplasmic Ca, which in turn modulates these KCa. Conversely, low external calcium would provide less calcium influx and diminish KCa activation.Figure 1.

Bottom Line: The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum.Nevertheless, several studies primarily addressing other biophysical issues have provided some clues.In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox.

View Article: PubMed Central - PubMed

Affiliation: Barrow Neurological Institute, Dignity Health St Joseph's Hospital and Medical Center and Medical Center, Phoenix, AZ, USA PengCheng.Han@dignityhealth.org.

Show MeSH
Related in: MedlinePlus