SWS therefore provides a window for neocortical and hippocampal circuits to reactivate pathways and modify synapses involved in specific memory functions [28], [29], [30], [31], [32], [33].
In particular, temporal correlation among motor and sensory events is believed to modify synapses through a Hebbian type learning process [43].
Each compartment therefore receives specific dopaminergic input capable of modifying the synapses between the KCs and specific MBONs.
Now, Genç et al. have genetically modified a mouse synapse in vivo and shown that protein kinase C brings about post-tetanic potentiation by phosphorylating Munc18-1.
The DANs are the most prevalent modulatory neurons in the MB and dopamine is thought to act locally to modify KC MBON synapses (Aso et al., 2010; Waddell, 2013).
Our finding that several proteins whose expression profiles are known to reflect the vulnerability status of axons and synapses have modified expression levels in the brains of two NCL mouse models provides further evidence in support of synaptic and axonal vulnerability in these disorders.
The role of these proteins in axonal and synaptic pathology remains unclear, although previous studies have suggested that Pttg1 may modify ubiquitination pathways in synapses and axons (29, 31) and VDAC1 is known to be a core regulator of mitochondrial form and function (30).
Therefore, we investigated whether sensory experience modified the structure of axonal varicosities, which form the presynaptic terminals, at putative synapses in spared cortex.
Here we used genetically modified mice lacking the GluA1 subunit (Gria1−/− mice) to investigate GluA1-independent mechanisms of LTP at CA3 CA1 synapses in transverse hippocampal slices.
These results have important implications for designing studies of NAc synapses in the context of behavioral analysis, and expand our understanding of how different forms of stress modify NAc synaptic function.
