ArticlePloS one2011
Modulation of calcium-dependent inactivation of L-type Ca2+ channels via β-adrenergic signaling in thalamocortical relay neurons.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Differential effects of propranolol on head and upper limb tremor in patients with essential tremor and dystonia.Journal of neurology · 2018Trial
- Effect of Propranolol on Motor Cortex Excitability in Essential Tremor: An Exploratory Study.Tremor and other hyperkinetic movements (New York, N.Y.) · 2024Article
- Lactate ions induce synaptic plasticity to enhance output from the central respiratory network.The Journal of physiology · 2021Article
- The Role of L-type Calcium Channels in Olfactory Learning and Its Modulation by Norepinephrine.Frontiers in cellular neuroscience · 2017Article
- Noradrenaline Modulates the Membrane Potential and Holding Current of Medial Prefrontal Cortex Pyramidal Neurons via βFrontiers in cellular neuroscience · 2017Article
- Calcium-dependent inactivation of calcium channels in the medial striatum increases at eye opening.Journal of neurophysiology · 2015Article
- Ca2+/calcineurin-dependent inactivation of neuronal L-type Ca2+ channels requires priming by AKAP-anchored protein kinase A.Cell reports · 2014Article
- Approaches and tools for modeling signaling pathways and calcium dynamics in neurons.Journal of neuroscience methods · 2013Review
- Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates.Journal of neurophysiology · 2013Article
- Ca(2+)-dependent large conductance K(+) currents in thalamocortical relay neurons of different rat strains.Pflugers Archiv : European journal of physiology · 2013Article
- Localized calcineurin confers Ca2+-dependent inactivation on neuronal L-type Ca2+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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8 authors.
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Abstract
Neuronal high-voltage-activated (HVA) Ca(2+) channels are rapidly inactivated by a mechanism that is termed Ca(2+)-dependent inactivation (CDI). In this study we have shown that β-adrenergic receptor (βAR) stimulation inhibits CDI in rat thalamocortical (TC) relay neurons. This effect can be blocked by inhibition of cAMP-dependent protein kinase (PKA) with a cell-permeable inhibitor (myristoylated protein kinase inhibitor-(14-22)-amide) or A-kinase anchor protein (AKAP) St-Ht31 inhibitory peptide, suggesting a critical role of these molecules downstream of the receptor. Moreover, inhibition of protein phosphatases (PP) with okadaic acid revealed the involvement of phosphorylation events in modulation of CDI after βAR stimulation. Double fluorescence immunocytochemistry and pull down experiments further support the idea that modulation of CDI in TC neurons via βAR stimulation requires a protein complex consisting of Ca(V)1.2, PKA and proteins from the AKAP family. All together our data suggest that AKAPs mediate targeting of PKA to L-type Ca(2+) channels allowing their phosphorylation and thereby modulation of CDI.
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