ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Visinin-like neuronal calcium sensor proteins regulate the slow calcium-activated afterhyperpolarizing current in the rat cerebral cortex.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 27 citations in OpenAlex.
- Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Olfactory rule learning-induced enhancement in intrinsic neuronal excitability is maintained by shutdown of the cholinergic M-current.Frontiers in cellular neuroscience · 2022Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Specificity in the interaction of high-voltage-activated CaJournal of neurophysiology · 2018Article
- Biophysical and functional characterization of hippocalcin mutants responsible for human dystonia.Human molecular genetics · 2017Article
- The Voltage Activation of Cortical KCNQ Channels Depends on Global PIP2 Levels.Biophysical journal · 2016Article
- Chronic cocaine disrupts mesocortical learning mechanisms.Brain research · 2015Review
- Mutations in HPCA cause autosomal-recessive primary isolated dystonia.American journal of human genetics · 2015Article
- ¹H, ¹³C, and ¹⁵N chemical shift assignments of neuronal calcium sensor protein, hippocalcin.Biomolecular NMR assignments · 2014Article
- A sodium-pump-mediated afterhyperpolarization in pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells.Journal of neurophysiology · 2013Article
- What determines the kinetics of the slow afterhyperpolarization (sAHP) in neurons?Biophysical journal · 2013Article
- Hippocalcin and KCNQ channels contribute to the kinetics of the slow afterhyperpolarization.Biophysical journal · 2012Article
- Understanding the physiological roles of the neuronal calcium sensor proteins.Molecular brain · 2012Review
- The visinin-like proteins VILIP-1 and VILIP-3 in Alzheimer's disease-old wine in new bottles.Frontiers in molecular neuroscience · 2012Article
- The calcium-activated slow AHP: cutting through the Gordian knot.Frontiers in cellular neuroscience · 2012Article
- Essential role for phosphatidylinositol 4,5-bisphosphate in the expression, regulation, and gating of the slow afterhyperpolarization current in the cerebral cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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2 authors at 1 institution in 1 country.
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Abstract
Many neurons in the nervous systems express afterhyperpolarizations that are mediated by a slow calcium-activated potassium current. This current shapes neuronal firing and is inhibited by neuromodulators, suggesting an important role in the regulation of neuronal function. Surprisingly, very little is currently known about the molecular basis for this current or how it is gated by calcium. Recently, the neuronal calcium sensor protein hippocalcin was identified as a calcium sensor for the slow afterhyperpolarizing current in the hippocampus. However, while hippocalcin is very strongly expressed in the hippocampus, this protein shows a relatively restricted distribution in the brain. Furthermore, the genetic deletion of this protein only partly reduces the slow hyperpolarizing current in hippocampus. These considerations question whether hippocalcin can be the sole calcium sensor for the slow afterhyperpolarizing current. Here we use loss of function and overexpression strategies to show that hippocalcin functions as a calcium sensor for the slow afterhyperpolarizing current in the cerebral cortex, an area where hippocalcin is expressed at much lower levels than in hippocampus. In addition we show that neurocalcin δ, but not VILIP-2, can also act as a calcium sensor for the slow afterhyperpolarizing current. Finally we show that hippocalcin and neurocalcin δ both increase the calcium sensitivity of the afterhyperpolarizing current but do not alter its sensitivity to inhibition by carbachol acting through the Gαq-11-PLCβ signaling cascade. These results point to a general role for a subgroup of visinin-like neuronal calcium sensor proteins in the activation of the slow calcium-activated afterhyperpolarizing current.
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