English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Neuronal plasticity is initiated by transient elevations of neuronal networks activity leading to changes of synaptic properties and providing the basis for memory and learning [ 1 ]. An increase of electrical activity can be caused by electrical stimulation [ 2 ] or by pharmacological manipulations: elevation of extracellular K +  [ 3 ], blockage of inhibitory pathways [ 4 ] or by an increase of second messengers intracellular concentrations [ 5 ]. Neuronal plasticity is mediated by several biochemical pathways leading to the modulation of synaptic strength, density of ionic channels and morphological changes of neuronal arborisation [ 6 ]. On a time scale of a few minutes, neuronal plasticity is mediated by local protein trafficking [ 7 ] while, in order to sustain modifications beyond 2–3 h, changes of gene expression are required [ 8 ].    Findings  In the present manuscript we analysed the time course of changes of the evoked electrical activity during neuronal plasticity and we correlated it with a transcriptional analysis of the underlying changes of gene expression. Our investigation shows that treatment for 30 min. with the GABA A  receptor antagonist gabazine (GabT) causes a potentiation of the evoked electrical activity occurring 2–4 hours after GabT and the concomitant up-regulation of 342 genes. Inhibition of the ERK1/2 pathway reduced but did not abolish the potentiation of the evoked response caused by GabT. In fact not all the genes analysed were blocked by ERK1/2 inhibitors.    Conclusion  These results are in agreement with the notion that neuronal plasticity is mediated by several distinct pathways working in unison.

Characterization of the time course of changes of the evoked electrical activity in a model of a chemically-induced neuronal plasticity