Yoel Yaari

Jerusalem, JM 91120, Israel

Last Updated: 09/26/2026

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Found 16 publications

Persistent Na+ and M-type K+ currents opposingly control spike gain in CA3 pyramidal cells.

Persistent Na+ and M-type K+ currents opposingly control spike gain in CA3 pyramidal cells.

Journal: Neurobiology of disease

Published: January 08, 2025

Corticotropin Releasing Factor Mediates KCa3.1 Inhibition, Hyperexcitability, and Seizures in Acquired Epilepsy.

Corticotropin Releasing Factor Mediates KCa3.1 Inhibition, Hyperexcitability, and Seizures in Acquired Epilepsy.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: December 15, 2021

Muscarinic regulation of the neuronal Na+ /K+ -ATPase in rat hippocampus.

Muscarinic regulation of the neuronal Na+ /K+ -ATPase in rat hippocampus.

Journal: The Journal of physiology

Published: February 02, 2021

Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy.

Protein Kinase A-Mediated Suppression of the Slow Afterhyperpolarizing KCa3.1 Current in Temporal Lobe Epilepsy.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: July 06, 2019

Age-Dependent Remarkable Regenerative Potential of the Dentate Gyrus Provided by Intrinsic Stem Cells.

Age-Dependent Remarkable Regenerative Potential of the Dentate Gyrus Provided by Intrinsic Stem Cells.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: May 05, 2019

Regulation of Neuronal Na+/K+-ATPase by Specific Protein Kinases and Protein Phosphatases.

Regulation of Neuronal Na+/K+-ATPase by Specific Protein Kinases and Protein Phosphatases.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: January 31, 2019

Differential contributions of Ca2+ -activated K+ channels and Na+ /K+ -ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells.

Differential contributions of Ca2+ -activated K+ channels and Na+ /K+ -ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells.

Journal: Hippocampus

Published: September 06, 2017

Plasticity of intrinsic firing response gain in principal hippocampal neurons following pilocarpine-induced status epilepticus.

Plasticity of intrinsic firing response gain in principal hippocampal neurons following pilocarpine-induced status epilepticus.

Journal: Neuroscience

Published: November 04, 2016

KV 7/M channels as targets for lipopolysaccharide-induced inflammatory neuronal hyperexcitability.

KV 7/M channels as targets for lipopolysaccharide-induced inflammatory neuronal hyperexcitability.

Journal: The Journal of physiology

Published: March 31, 2016

Downregulation of Spermine Augments Dendritic Persistent Sodium Currents and Synaptic Integration after Status Epilepticus.

Downregulation of Spermine Augments Dendritic Persistent Sodium Currents and Synaptic Integration after Status Epilepticus.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: November 21, 2015

Zinc regulates a key transcriptional pathway for epileptogenesis via metal-regulatory transcription factor 1.

Zinc regulates a key transcriptional pathway for epileptogenesis via metal-regulatory transcription factor 1.

Journal: Nature communications

Published: March 16, 2015

Role of small conductance Ca²⁺-activated K⁺ channels in controlling CA1 pyramidal cell excitability.

Role of small conductance Ca²⁺-activated K⁺ channels in controlling CA1 pyramidal cell excitability.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

Published: June 13, 2014

Showing 1-12 of 16

Last Updated: 09/26/2026