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MMP9 may regulate synaptic plasticity by enabling structural synaptic remodeling similar to that associated with activity-dependent plasticity [26], [27].
PIK has been shown to regulate synaptic plasticity by controlling exocytosis of AMPA-type glutamate receptors [15] and by coupling group I mGluRs to translation initiation [16].
Results from the data described suggest the presence of MR at LA synapses placing them in position to regulate synaptic plasticity underlying the acquisition of fear memories.
MMP-9 was specifically shown to regulate synaptic plasticity in the hippocampus by gain- and loss-of-function studies on LTP in vitro [23], [24].
Although the patho-physiological significance of this crosstalk remains to be elucidated, we tentatively propose that it could regulate synaptic plasticity and/or excitotoxicity as NMDA-Rs play a crucial role in these phenomena.
Mammalian MAGI/S-SCAM is a multi-PDZ domain synaptic scaffolding protein that interacts with a number of postsynaptic signaling proteins and is thereby thought to regulate synaptic plasticity [1], [2], [3].
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NO is produced by nNOS post synaptically in the central nervous system and regulates synaptic plasticity (Steinert et al., 2011).
BDNF/TrkB signaling regulates synaptic plasticity in various neuronal systems, including glutamatergic pathways.
In addition to its synaptogenesis function, EphB-ephrinB signaling also plays an important role in regulating synaptic plasticity.
Understanding the mechanisms by which Cdk5 regulates synaptic plasticity may therefore provide important insights in the design of novel therapeutic strategies for neurodegenerative diseases.
ERKs are highly expressed in post-mitotic neurons and in differentiated cells and involved in adaptive responses such as long-term potentiation in post mitotic neurons and in regulating synaptic plasticity of the hippocampus [38 40].
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