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One frequently used mechanism by which neurons modulate synaptic strength is through the regulation of the number of neurotransmitter receptors at the surface of synapses [3].
Mutants show a reduction in excitatory neurosecretion, and mth appears to modulate synaptic strength in neurons by regulating vesicle trafficking [20]; this may be important in sensorimotor ability, as mth mutants also show enhanced visuomotor synchronization and phototaxis [21].
Induction of LTP and LTD in the CA1 region of the hippocampus involves numerous protein kinases and/or phosphatases [13], [18], which are believed to be critical for the translation of electrical activity into persistent subcellular alterations that may modulate synaptic strength.
Importantly, these pathways have a high degree of convergence, which has a common consequence; i.e., many modulate synaptic strength and change the coupling between neurons.
We have recently shown that synaptic dispersion and reclustering of Munc18-1 allows neurons to modulate synaptic strength upon network activity (Cijsouw et al., 2014).
Spines are, thus, primary sites of signal integration, in which a variety of receptors and receptor-channels modulate synaptic strength and plasticity, with intracellular Ca2+ as a major player.
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While this timing contradicts the idea that phasic dopamine release in this case is directly modulating the prepress phasic excitation of DLS neurons, it is still consistent with a role for dopamine in plasticity, perhaps modulating the synaptic strength of circuitry underlying stimulus-response associations.
Conversely, anodal modulation of synaptic strength prior to motor learning has been shown to compromise performance (Kuo et al., 2008), an effect that was further modulated by the presence of a partial NMDA-receptor agonist (d-cycloserine).
All of which can ultimately modulate the neurons' intrinsic properties or synaptic strength.
We find that synaptic strength is strongly modulated on short- and long-lasting time scales during the presentation of the natural stimulus trains.
This study highlights the ability of prion protein to modulate vesicles and release properties leading to enhanced synaptic strength and transmission thereby corroborating and extending information gained from mouse models.
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