ArticleThe Journal of physiology2005
Intracellular calcium store filling by an L-type calcium current in the basolateral amygdala at subthreshold membrane potentials.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Latrophilin-1-Mediated GCells · 2026Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- Presynaptic store-operated CaNeuron · 2021Article
- α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IPScientific reports · 2019Article
- Preferential cholinergic excitation of corticopontine neurons.The Journal of physiology · 2018Article
- A unifying hypothesis for M1 muscarinic receptor signalling in pyramidal neurons.The Journal of physiology · 2017Article
- Visualization of Ca2+ Filling Mechanisms upon Synaptic Inputs in the Endoplasmic Reticulum of Cerebellar Purkinje Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Early stress prevents the potentiation of muscarinic excitation by calcium release in adult prefrontal cortex.Biological psychiatry · 2014Article
- Nuclear calcium signalling in the regulation of brain function.Nature reviews. Neuroscience · 2013Review
- Thalamocortical long-term potentiation becomes gated after the early critical period in the auditory cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Memory reconsolidation and its maintenance depend on L-voltage-dependent calcium channels and CaMKII functions regulating protein turnover in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Inositol 1,4,5-triphosphate drives glutamatergic and cholinergic inhibition selectively in spiny projection neurons in the striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Understanding calcium waves and sparks in central neurons.Nature reviews. Neuroscience · 2012Review
- Calcium signaling in synapse-to-nucleus communication.Cold Spring Harbor perspectives in biology · 2011Review
- Location and function of the slow afterhyperpolarization channels in the basolateral amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Hierarchical order of coexisting pre- and postsynaptic forms of long-term potentiation at synapses in amygdala.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Inositol trisphosphate 3-kinases: focus on immune and neuronal signaling.Cellular and molecular life sciences : CMLS · 2010Review
- Two slow calcium-activated afterhyperpolarization currents control burst firing dynamics in gonadotropin-releasing hormone neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Regulation of Kv channel expression and neuronal excitability in rat medial nucleus of the trapezoid body maintained in organotypic culture.The Journal of physiology · 2010Article
- Functional interplay between NMDA receptors, SK channels and voltage-gated Ca2+ channels regulates synaptic excitability in the medial prefrontal cortex.The Journal of physiology · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The long-term changes that underlie learning and memory are activated by rises in intracellular Ca2+ that activate a number of signalling pathways and trigger changes in gene transcription. Ca2+ rises due to influx via L-type voltage-dependent Ca2+ channels (L-VDCCs) and release from intracellular Ca2+ stores have been consistently implicated in the biochemical cascades that underlie the final changes in memory formation. Here, we show that pyramidal neurones in the basolateral amygdala express an L-VDCC that is active at resting membrane potentials. Subthreshold depolarization of neurones either by current injection or summating synaptic potentials led to a sustained rise in cytosolic Ca2+ that was blocked by the dihydropyridine nicardipine. Activation of metabotropic receptors released Ca2+ from intracellular Ca2+ stores. At hyperpolarized potentials, metabotropic-evoked store release ran down with repeated stimulation. Depolarization of cells to -50 mV, or maintaining them at the resting membrane potential, restored release from intracellular Ca2+ stores, an effect that was blocked by nicardipine. These results show that Ca2+ influx via a low-voltage-activated L-type Ca2+ current refills inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular Ca2+ stores, and maintains Ca2+ release and wave generation by metabotropic receptor activation.
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