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Kaoutsar Nasrallah on Muck Rack

Kaoutsar Nasrallah

As seen in: BioRxiv, Cell Press, Biological Psychiatry
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Articles

Developmental Disruption of Mef2c in Medial Ganglionic Eminence-derived cortical inhibitory interneurons impairs cellular and circuit function

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By Claire Ward, Albert Einstein College, Kaoutsar Nasrallah
| Biological Psychiatry Verified
Abstract MEF2C is strongly linked to various neurodevelopmental disorders (NDDs) including autism, intellectual disability, schizophrenia, and attention-deficit/hyperactivity. Mice constitutively lacking one copy of Mef2c, or selectively lacking both copies of Mef2c in cortical excitatory neurons, display a variety of behavioral phenotypes associated with NDDs. The MEF2C protein is a transcription factor necessary for cellular development and synaptic modulation of excitatory neurons.
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Developmental disruption of Mef2c in Medial Ganglionic Eminence-derived cortical inhibitory interneurons impairs cellular and circuit function

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By Claire Ward, Kaoutsar Nasrallah, Duy Tran, Ehsan Sabri
| BioRxiv
Abstract Background: MEF2C is strongly linked to various neurodevelopmental disorders (NDDs) including autism, intellectual disability, schizophrenia, and attention-deficit/hyperactivity. Mice constitutively lacking one copy of Mef2c, or selectively lacking both copies of Mef2c in cortical excitatory neurons, display a variety of behavioral phenotypes associated with NDDs. The MEF2C protein is a transcription factor necessary for cellular development and synaptic modulation of excitatory neurons.
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Retrograde adenosine/A2A receptor signaling facilitates excitatory synaptic transmission and seizures

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By Kaoutsar Nasrallah, Coralie Berthoux, Yuki Hashimotodani, Andres Chavez Verified
| BioRxiv
Abstract Retrograde signaling at the synapse is a fundamental way by which neurons communicate and neuronal circuit function is fine-tuned upon activity. While long-term changes in neurotransmitter release commonly rely on retrograde signaling, the mechanisms remain poorly understood.
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