Nazim Kourdougli
@n_kourdougli
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Postdoc in Neurosciences at UCLA. Dissecting neural circuits during early postnatal development. Passionate about art and gastronomy. He/him.
Joined November 2017
🚨Thrilled to see my main postdoc work now published @NeuroCellPress! 🪄 https://t.co/esEUYd5y4J 🧵1/6👇
cell.com
Kourdougli et al. use all-optical in vivo approaches to show that parvalbumin interneurons are hypoactive and decoupled from excitatory partners in the developing neocortex of fragile X syndrome...
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Now published in @NatureComms! Very cool story from a former PhD student from the Portera-Cailliau’s lab!
A tour de force by Trishala Chari, PhD in C. Portera-Cailliau lab dissecting social touch brain circuitry in autism using neuropixels recordings in S1-Striatum-BLA!
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Thrilled to be part of this story, describing Epac2 as a new therapeutic target in FXS mice using a combination of transcriptomics, in vivo calcium imaging and behaviors from the C. Portera-Cailliau lab!
https://t.co/QGvdq8T1Qv Excited to share my postdoctoral work! We mapped how loss of FMRP alters excitatory and inhibitory neurons in Fragile X Syndrome (FXS), the leading monogenic cause of autism. Huge molecular divergence — and a new therapeutic target! 🧵
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Excited to share our preprint led by @ainchung & Jason Alipio showing how few immature adult-born DGCs preferentially recruit inhibition of CA2 and CA3 to disproportionately affect hippocampal network properties and social memory. We began by asking 1/n https://t.co/JrxeQtkV8j
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We are excited to share our latest work showing that mice display rescue-like prosocial behavior toward unresponsive partners. @ScienceMagazine
https://t.co/Jzwna46rFy
science.org
Humans often take actions to assist others experiencing unresponsiveness, such as transient loss of consciousness. How other animals react to unresponsive conspecifics—and the neural mechanisms...
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New paper from providing insight into how a gene variant that causes cognitive impairment (Syngap1 haploinsufficiency) does so through impairing how sensory and motor signals converge in cortex to support perception and adaptive behavior. @cureSYNGAP1
https://t.co/hdKo7j68Nw
nature.com
Nature Communications - Whether and how highly penetrant NDD (neurodevelopmental disorder) genes such as Syngap1 regulate sensorimotor integration are not fully understood. This study shows that...
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Our latest study - psilocybin evokes structural neural plasticity, and we wanted to know how this maps onto pyramidal cell type-specific circuits to produce behavioral effects. 🍄🔬🧠 Link to @biorxivpreprint: https://t.co/xvQh1JmBPf Led by Ling-Xiao Shao and @ItsClaraLiao.
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Paper is out! @NatureComms Mapping dense neural projections at the single-cell level is challenging—but we tackled it with axonal BARseq, a new technique that maps long-range projections from >8000 neurons in a single brain. 🧠 @TonyZador
https://t.co/Mty01CnBsg
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We have a great lineup of speakers for our first Neurodevelopmental symposium at Northwestern. Virtual registration option available. Please signup. https://t.co/xUwfuKaCrJ
sites.google.com
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The first social behavior of a mammal infant is to form a social bond with the mother. In this work, we found that somatostatin-expressing neurons in the ZI of preweaning mice respond to social interactions with their mother. Here's a video highlighting our main findings.
So happy to share our new work that is now out @sciencemagazine: We show how neurons in the mouse zona incerta (ZI) modulate infant social behaviors and learning. This work was led by the AMAZING graduate student Yuexuan Li @yuexuan_li. 🎉 https://t.co/hNnNZmZVEw
#ScienceResearch
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🪄So happy to see another piece of work of my postdoc in C. Portera-Cailliau lab @UCLANeurology now out in Biological Psychiatry🪄 in collaboration with @ContractorAnis lab! 🧵n1/6 https://t.co/9VcDZafPu9
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A tour de force by Trishala Chari, PhD in C. Portera-Cailliau lab dissecting social touch brain circuitry in autism using neuropixels recordings in S1-Striatum-BLA!
A failure to discriminate social from non-social touch at the circuit level may underlie social avoidance in autism https://t.co/sYWSZAA7AB
#biorxiv_neursci
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6/ On a side note, as previously described we did not observe a major effect of bumetanide on network synchrony in S1BF at P6 in WT mice (see works of D. Isbrandt lab, K. Holthoff lab and others). End
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5/🚨Very importantly, we used another diuretic that does not cross the BBB (chlorothiazide) as a control for our bumetanide experiments. This allowed us to further ascertain that bumetanide effects are (mostly?) mediated though a central effect on neural networks.
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4/ Chronic bumetanide also restored feedforward inhibition (in vitro ephys) and PV-IN network engagement (in vivo imaging) in FXS mice. We and others had previously shown immaturity and hypofunction of PV-INs (D. Feldman lab, A. Contractor lab, Portera-Cailliau lab).
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3/ Chronic bumetanide treatment during S1BF critical period restores whisker-responsiveness to WT levels and alleviates behavioral manifestations of sensory hypersensitivity in FXS mice.
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2/ Using in vivo calcium imaging, we show that there is network hyperexcitability in S1BF of neonatal FXS mice (P6). This can be rescued by acute systemic bumetanide treatment -GABA polarity changes in FXS mice were previously reported: A. Contractor lab, Y. Ben-Ari lab etc.
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1/ Here, we assessed the effect of restored chloride homeostasis on developmental sensory circuits disparities in FXS mice using the loop diuretic bumetanide, in vivo calcium imaging and ephys .
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🪄So happy to see another piece of work of my postdoc in C. Portera-Cailliau lab @UCLANeurology now out in Biological Psychiatry🪄 in collaboration with @ContractorAnis lab! 🧵n1/6 https://t.co/9VcDZafPu9
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Network state transitions during cortical development — a Review by Michelle W. Wu, Nazim Kourdougli & Carlos Portera-Cailliau @UCLANeurology @UCLA_BRI @N_kourdougli
https://t.co/7vTZ44vSaX
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