Bryndis Birnir

Professor of Physiology (Chair)

Uppsala University

Sweden

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Professor Bryndis Birnir is the Chair of Physiology at Uppsala University in Sweden. Her research focuses on GABAergic signaling and its implications in neurological disorders, including Alzheimer's disease and neurodevelopmental delays. Recent publications explore the effects of insulin and glucose on GABA-mediated inhibition, as well as the development of DNA gyrase inhibitors targeting antibiotic-resistant bacteria. Her work also addresses the transcriptional regulation of GABAergic systems in various models of disease.

Articles (11)

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2025

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2024

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2023

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2022

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2022

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2021

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2021

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2021

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2021

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2020

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2020

Collaborators (7)

Erik T. Jansson

Assistant professor

Uppsala University

SWEDEN

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Andrej Emanuel Cotman

SLOVENIA

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Jonas Bergquist

Uppsala University

SWEDEN

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Jens Schuster

Assistant Professor

Uppsala University

SWEDEN

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Joakim Klar

Uppsala University

SWEDEN

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Amol K. Bhandage

Researcher/Docent/Associate Professor

Uppsala University

SWEDEN

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Daniel Espes

Uppsala University

SWEDEN

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Bryndis Birnir

Research Interests

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Articles (11)

GABA-activated slow spontaneous inhibitory postsynaptic currents are decreased in dorsal hippocampal dentate gyrus granule cells in an aged mouse model of Alzheimer's disease

GABA-mediated inhibition of human CD4+ T cell functions is enhanced by insulin but impaired by high glucose levels

Discovery and Hit-to-Lead Optimization of Benzothiazole Scaffold-Based DNA Gyrase Inhibitors with Potent Activity against <i>Acinetobacter baumannii</i> and <i>Pseudomonas aeruginosa</i>.

ZEB2 haploinsufficient Mowat-Wilson syndrome induced pluripotent stem cells show disrupted GABAergic transcriptional regulation and function.

Monoallelic and bi-allelic variants in NCDN cause neurodevelopmental delay, intellectual disability, and epilepsy.

Endogenous Levels of Gamma Amino-Butyric Acid Are Correlated to Glutamic-Acid Decarboxylase Antibody Levels in Type 1 Diabetes

GABA induces a hormonal counter-regulatory response in subjects with long-standing type 1 diabetes.

Insulin differentially modulates GABA signalling in hippocampal neurons and, in an age‐dependent manner, normalizes GABA‐activated currents in the tg‐APPSwe mouse model of Alzheimer’s disease

Monoallelic and bi-allelic variants in NCDN cause neurodevelopmental delay, intellectual disability, and epilepsy.

Tonic GABA‐activated synaptic and extrasynaptic currents in dentate gyrus granule cells and CA3 pyramidal neurons along the mouse hippocampal dorsoventral axis

GABAA Receptor-Mediated Currents and Hormone mRNAs in Cells Expressing More Than One Hormone Transcript in Intact Human Pancreatic Islets

Collaborators (7)

Erik T. Jansson

Andrej Emanuel Cotman

Jonas Bergquist

Jens Schuster

Joakim Klar

Amol K. Bhandage

Daniel Espes

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