Otherwise, it appears to be mediated through alterations in synaptic glutamate receptors such as AMPAR (Henley & Wilkinson, 2013).
Our findings suggest that the effects of acutely applied METH on synaptic transmission appear to be mediated through the activation of both serotonergic and dopaminergic receptor systems.
Although the primary mechanism of action of MPH is believed to involve increased synaptic dopamine and norepinephrine levels, it has been suggested that behavioral response to MPH may also be mediated through serotonergic mechanisms acting downstream of the dopamine system.
However, this finding is reminiscent of α-synuclein's neuroprotective effect in CSP-α-deficient mice [ 2], which is mediated through interaction with synaptic vesicles.
Overall, our results suggested here that the mechanosensitivity of the Cav1.3 channels is mediated through an intact synaptic F-actin network.
We hypothesize that the observed synaptic strengthening induced by ApLRRTK is mediated through the enhanced outgrowth of filopodial structures, which are known to allow the formation of synaptic contacts (Mattila and Lappalainen 2008) that are important for learning-related long-term synaptic strengthening (Cingolani and Goda 2008; Toni et al. 1999).
These results suggest that the anti-depressant-like effect of vitexin is mediated through an increase in catecholamine levels in the synaptic cleft as well as through interactions with the serotonergic 5-HT1A, noradrenergic α2, and dopaminergic D1, D2, and D3 receptors.
We show here that synaptic plasticity and memory deficits are mediated through production of sAPPβ and/or β-CTF, but not Aβ, during LTP and memory acquisition.
Transmission of photopic stimuli is mediated through light-evoked [Ca2+]i decreases in cone inner segments (IS) and synaptic terminals [3], which cause a decrease in exocytosis and activation of postsynaptic ON and OFF channels [4], [5].
