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Regulation of PV interneuron plasticity by neuropeptide-encoding genes

Increasing the activity of individual parvalbumin-expressing interneurons in the mouse brain modulates the number and strength of inhibitory parvalbumin synapses received by these cells through changes in the expression of the neuropeptide-encoding genes Vgf and Scg2.

Martijn Selten
Clémence Bernard
Oscar Marín
ResearchOpen Access30 Apr 2025
Nature

Volume: 643, P: 173-181
A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons

SFPQ is a splicing factor and its mutations are associated to amyotrophic lateral sclerosis (ALS) patients. Here, the authors show that SFPQ represses the use of pathogenic cryptic last exons in zebrafish, mouse and human cells.

Patricia M. Gordon
Fursham Hamid
Corinne Houart
ResearchOpen Access26 Mar 2021
Nature Communications

Volume: 12, P: 1-13
Cadherins orchestrate specific patterns of perisomatic inhibition onto distinct pyramidal cell populations

How cortical interneurons establish precise connections among intermingled populations of excitatory neurons remains unclear. Here, the authors reveal that Cadherins instruct cell type and input-specific synaptic targeting of interneurons onto different pyramidal cell populations.

Julie Jézéquel
Giuseppe Condomitti
Beatriz Rico
ResearchOpen Access14 May 2025
Nature Communications

Volume: 16, P: 1-15
Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS

Nuclear depletion and cytoplasmic accumulation of splicing factor SFPQ are hallmarks of ALS. Here the authors demonstrate a relationship between loss of SFPQ and the emergence in neurites of intron-retaining mRNAs enriched in ALS models and tissues.

Richard Taylor
Fursham Hamid
Corinne Houart
ResearchOpen Access22 Nov 2022
Nature Communications

Volume: 13, P: 1-14

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Regulation of PV interneuron plasticity by neuropeptide-encoding genes

A conserved role for the ALS-linked splicing factor SFPQ in repression of pathogenic cryptic last exons

Cadherins orchestrate specific patterns of perisomatic inhibition onto distinct pyramidal cell populations

Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS

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