Molecular Control of Synaptic Plasticity
Main content
Synaptic plasticity shapes behavior and mediates memory formation. Our overriding goal is to elucidate the molecular control of long-term synaptic plasticity, and dysregulation of these mechanisms in cognitive disorders.
Our main lines of research are:
Arc protein as a master regulator of long-term synaptic plasticity
How does the Arc protein work? We aim to connect the biochemical and structural properties of Arc to synaptic plasticity and harness this knowledge to address the broader question of how synaptic plasticity mediates information storage in neural networks.
Translational control of synaptic plasticity
How are specific forms of translation orchestrated to mediate structural and functional modification of synapses? Previous works has uncovered a role for BDNF as a trigger for transcription and translation-dependent synaptic plasticity in the adult brain. We are particularly interested in BDNF-TrkB coupling to translation.
Non-coding RNAs
This line of work explores the expression and function of microRNAs and other non-coding RNAs in the context of long-term potentiation. Recent work looks at regulation of Argonaute-associated microRNAs, lncRNAs, and retrotransposon elements.
Methods
The Bramham lab integrates: 1) Electrophysiological studies of synaptic transmission in live rodents combined with genetic, optical, and pharmacological manipulations, 2) Single-particle tracking of proteins and fluorescence resonance energy transfer (FRET) imaging in primary neuronal cultures and hippocampal tissue slices, with two-photon applications in live rodents under development, 3) Biochemical and functional analysis of protein-protein interactions and post-translational modifications, 4) Expression and purification of recombinant proteins for biophysical and structural analyses.
Funding
Top Research (Toppforsk) grant from the Research Council of Norway on the Arc protein. In collaboration with Prof. Jan Haavik, Prof. Petri Kursula, and Prof Aurora Martinez in the Department of Biomedicine, UiB.
EU H2020 Joint Programme in Neurodegenerative Disorders. “Synaptic circuit protection in Alzheimers’s disease (AD) and Huntingtion’s disease (HD): BDNF/TrkB and Arc signaling as rescue factors”. Homepage: CircProt
