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The ratio of the responses to pulses with higher frequency to the baseline was calculated as the weight modification of synaptic plasticity.
As memories are thought to be encoded by modification of synaptic strength, LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.
Especially the modification of synaptic connections as a crucial element of structural plasticity and long-term memory has been in the focus of intense research [1].
However, we cannot exclude the possibility that a change in retinoid signaling influences neurogenesis and memory through a modification of synaptic plasticity.
Modification of synaptic weights happens very fast during the activated state of the hippocampus [2], with entorhinal-hippocampal network oscillations at theta frequency playing a crucial role in this process [3].
The long-term mechanisms involving NMDAR and probably LTP pathways shown in the present study, suggest a modification of synaptic functioning by the cholinergic system, which would give a neurobiological basis to this attention-gated reinforcement learning.
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It is widely accepted that changes in gene expression contribute to enduring modifications of synaptic strength and are required for long-term memory.
Subtle changes in dendritic integrity might imply functional modifications of synaptic circuits in respective regions.
This apparent discrepancy probably results from the fact that in order to get an adequate amount of material, the prior PSD analysis had been performed on whole cortex extracts, and this may have occluded subtle modifications of synaptic AMPARs restricted to the more specific regions under investigation in our current study.
Nevertheless, given that synapses labelled on both sides represented ∼9% of total number of contacts, our data raise the interesting possibility that ERK could play a role in matching pre- and postsynaptic changes during long-term modifications of synaptic efficacy [42].
Early phase LTP involves posttranslational modifications of synaptic proteins, such as phosphorylation of synaptic AMPA receptors [ 35].
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