Functions of synapsins in corticothalamic facilitation: important roles of synapsin I

Abstract

Key pointsr The synaptic vesicle associated proteins synapsin I and synapsin II have important functions in synaptic short-term plasticity.r We investigated their functions in cortical facilitatory feedback to neurons in dorsal lateral geniculate nucleus (dLGN), feedback that has important functions in state-dependent regulation of thalamic transmission of visual input to cortex.r We compared results from normal wild-type (WT) mice and synapsin knockout (KO) mice in several types of synaptic plasticity, and found clear differences between the responses of neurons in the synapsin I KO and the WT, but no significant differences between the synapsin II KO and the WT. AbstractThe synaptic vesicle associated proteins synapsin I (SynI) and synapsin II (SynII) have important functions in several types of synaptic short-term plasticity in the brain, but their separate functions in different types of synapses are not well known. We investigated possible distinct functions of the two synapsins in synaptic short-term plasticity at corticothalamic synapses on relay neurons in the dorsal lateral geniculate nucleus. These synapses provide excitatory feedback from visual cortex to the relay cells, feedback that can facilitate transmission of signals from retina to cortex. We compared results from normal wild-type (WT), SynI knockout (KO) and SynII KO mice, in three types of synaptic plasticity mainly linked to presynaptic mechanism. In SynI KO mice, paired-pulse stimulation elicited increased facilitation at short interpulse intervals compared to the WT. Pulse-train stimulation elicited weaker facilitation than in the WT, and also post-tetanic potentiation was weaker in SynI KO than in the WT. Between SynII KO and the WT we found no significant differences. Thus, SynI has important functions in these types of synaptic plasticity at corticothalamic synapses. Interestingly, our data are in contrast to the important role of SynII previously shown for sustained synaptic transmission during intense stimulation in excitatory synapses in other parts of the brain, and our results suggest that SynI and SynII may have different roles in similar types of STP in different parts of the brain.

Redox/methylation mediated abnormal DNA methylation as regulators of ambient fine particulate matter-induced neurodevelopment related impairment in human neuronal cells

“…Here, we demonstrated that the hypermethylation of NRXN1 and NLGN3 were correlated with the decreases in their mRNA and protein expression. In addition, synapsin 1 and PSD-95 are synapse-associated proteins that are important to synaptic formation, synaptic transmission and axon outgrowth 28 29 . Furthermore, our results of decreased protein expression of synapsin 1 and PSD-95 strongly support abnormal synaptic homeostasis caused by PM 2.5 .…”

Layer 6A pyramidal cells subtypes form synaptic microcircuits with distinct functional and structural properties

“…5). Moreover, synaptotagmin-7 and synapsin I have been shown to have important functions in short-term synaptic facilitation at CT synapses (Nikolaev and Heggelund 2015;Jackman et al 2016). If these molecules are also present at presynaptic terminals of intracortical connections established by CT PCs this may explain -at least in part -EPSP facilitation at these synapses.…”

Environmental pollution and mental health: a narrative review of literature

“…PM 2.5 exposition seems also associated with the reduction of expression of adhesion proteins such as Synapsin-1 and PSD-95, which are fundamental for the establishment of synapses, neurotransmission, and axonal growth. 43,44 These findings suggest the hypothesis that PM 2.5 is associated with synaptic homeostasis and activities involved in neurodevelopmental disorders. 41 Wei et al 40 have founded that PM 2.5 and its extracts promote cell cycle arrest, cell apoptosis and inhibition of cell proliferation in neuronal tissues.…”