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1 November 2019

Harm Krugers

Neuroscience Symposium
Kalsbeek Group

The Neuroscience Symposia are organized weekly by the Netherlands Institute for Neuroscience. The presentations are given by researchers from the institute or by guest speakers. The title and content of the symposium is usually made known in the week prior to the presentation.

Colloquium room – Netherlands Institute for Neuroscience

4:00 pm – Stress, glutamatergic synapses and memory
5:00 pm – Discussion and drinks

Abstract
Emotionally arousing and stressful experiences are retained well. While this may be a highly adaptive behavioural response, such events also trigger inappropriate and vividly expressed memories in vulnerable individuals. The memory enhancing effects of stress are – at least in part – mediated by glucocorticoid hormones (GCs), which are released during and after stressful encounters. Our lab investigates a.o. how GCs modulate memory formation and why some individuals retain memories better than others.
First, we investigate how GCs modulate memory formation and modulate synapses, which are essential for memory formation. We find that GCs enhance neuronal communication by enhancing AMPA receptor (AMPAR) mediated synaptic transmission as well as NMDA receptor function. The effects on AMPAR function are mediated by protein synthesis, activation of glucocorticoid receptors, and involve increase in mobility and retention of AMPA receptors. GCs also rapidly, in a non-genomic fashion, increase retention of NMDARs, via activation of mineralocorticoid receptors. The effects of GCs on AMPAR function and retention are mediated by the mTOR pathway and targeting the mTOR pathway prevents GC effects on consolidation of fear memories. Second, we study whether GCs also determine memory accuracy and fear generalisation. Preliminary findings suggest that elevated GC levels enhance fear generalisation, which is accompanied by an increase in the sparse activation of neurons in the dentate gyrus that have been implicated in fear memories. Finally, we investigate how early life adversity affects glutamatergic synapses. Such experiences alter synaptic transmission, synaptic plasticity and the sensitivity to GCs later in life.

 

 

 

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