Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Region- and age-specific deficits in gamma-aminobutyric acidergic neuron development in the telencephalon of the uPAR(-/-) mouse.

The Journal of comparative neurology - 5 Sept 2005

Eagleson Kathie L, Bonnin Alexandre, Levitt Pat

Abstract excerpt

We have previously shown that in adult mice with a null mutation in the urokinase-type plasminogen activator receptor (uPAR) gene, maintained on a C57BL/6J/129Sv background, there is a selective loss of GABAergic interneurons in anterior cingulate and parietal cortex, with the parvalbumin-expressing subpopulation preferentially affected. Here, we performed a more detailed anatomical analysis of uPAR(-/-) mutation...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Count
Share to gamma-Aminobutyric Acid

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Glutamate Decarboxylase

Share to Interneurons

Share to Parvalbumins

Share to Receptors, Urokinase Plasminogen Activator

Share to Somatostatin

Share to Telencephalon

Source

Identifiers

PMID: 16025458
DOI: 10.1002/cne.20647

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Region- and age-specific deficits in gamma-aminobutyric acidergic neuron development in the telencephalon of the uPAR(-/-) mouse.PMID 16025458Read ↗

Genetic disruption of cortical interneuron development causes region- and GABA cell type-specific deficits, epilepsy, and behavioral dysfunction.Semantic proximity Read ↗

Hyperactive MEK1 signaling in cortical GABAergic neurons causes embryonic parvalbumin-neuron death and defects in behavioral inhibitionSemantic proximity Read ↗

Prefrontal cognitive deficits in mice with altered cerebral cortical GABAergic interneurons.Semantic proximity Read ↗

Urokinase Receptor uPAR Overexpression in Mouse Brain Stimulates the Migration of Neurons into the Cortex during EmbryogenesisSemantic proximity Read ↗

Disruption of interneuron development.Semantic proximity Read ↗

Bacterial artificial chromosome transgenic analysis of dynamic expression patterns of regulator of G-protein signaling 4 during development. I. Cerebral cortex.Semantic proximity Read ↗

Hyperactivity and cortical disinhibition in mice with restricted expression of mutant huntingtin to parvalbumin-positive cells.Semantic proximity Read ↗

Prenatal Valproate Exposure Differentially Affects Parvalbumin-Expressing Neurons and Related Circuits in the Cortex and Striatum of MiceSemantic proximity Read ↗

Fgfr1 inactivation in the mouse telencephalon results in impaired maturation of interneurons expressing parvalbumin.Semantic proximity Read ↗

Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density.Semantic proximity Read ↗

NPAS1 represses the generation of specific subtypes of cortical interneurons.Semantic proximity Read ↗

Maturation of Purkinje cell firing properties relies on granule cell neurogenesisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.