Results 211 to 220 of about 176,830 (333)

Hcfc1 and Ogt Mediate Zebrafish CNS Regeneration Through Hippo/Yap Signalling

open access: yesCell Proliferation, EarlyView.
This work identifies Hcfc1 and Ogt as key regulators of zebrafish CNS regeneration through modulation of Hippo/Yap signalling. Loss of Hcfc1 or Ogt activity inhibition impairs regeneration, which is restored by Yap overexpression, revealing a new regulatory axis that enhances CNS regenerative capacity.
Priyanka P. Srivastava   +9 more
wiley   +1 more source

Distinct Activity Profiles of Somatostatin-Expressing Interneurons in the Neocortex

open access: yesFrontiers in Cellular Neuroscience, 2017
Srikanth Ramaswamy   +2 more
doaj   +1 more source

Intravenous immunoglobulin and febrile status epilepticus in children with Dravet syndrome: A retrospective multicentre study

open access: yesDevelopmental Medicine &Child Neurology, EarlyView.
This multicenter retrospective study evaluated the use of intravenous immunoglobulin (IVIG) in 14 children with Dravet syndrome as a preventive strategy against febrile status epilepticus. Over a 6‐month period, IVIG was associated with a significant reduction in hospitalizations for febrile status epilepticus.
Romane Marc   +9 more
wiley   +1 more source

Ion channels in migraine disorders [PDF]

open access: yes, 2018
Pietrobon, Daniela
core   +1 more source

Synaptic ultrastructural alterations in human focal cortical dysplasia: Insights from volume electron microscopy

open access: yesEpilepsia, EarlyView.
Abstract Objective Focal cortical dysplasia (FCD) is a developmental malformation of the cerebral cortex and a leading cause of drug‐resistant epilepsy in children and young adults. Disruption of the excitation–inhibition (E–I) balance is a hallmark of neuronal hyperexcitability in FCD, yet the underlying synaptic ultrastructural changes remain poorly ...
Gyu Hyun Kim   +6 more
wiley   +1 more source

3-Nitrotyrosine activates excitatory interneurons by inhibiting GABA receptors in the rat spinal dorsal horn. [PDF]

open access: yesPain Rep
Kaimochi Y   +9 more
europepmc   +1 more source

C1q neutralization during epileptogenesis attenuates complement‐mediated synaptic elimination and epileptiform activity

open access: yesEpilepsia, EarlyView.
Abstract Objective Accumulating evidence indicates that aberrant C1q‐C3 complement signaling in microglia and astrocytes drives synaptic dysfunction and neuronal loss. C1q‐mediated synaptic dysfunction disrupts neuronal circuitry balance and can lead to network hyperexcitability in epilepsy.
Yoonyi Jeong   +5 more
wiley   +1 more source

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