|I have been studying on molecular mechanism of synaptic transmission employing
electrophysiological measurements of responses recorded from a cholinergic
model synapse formed between sympathetic ganglion neurons in long-term
culture. Roles of proteins for neurotransmitter release have been extensively
examined by perturbing their functions with injection of neurotoxins, synthetic
peptides, recombinant proteins or with transfection of cDNA/siRNA (see
update article, Ma and Mochida, Neurosci Res., 2007). With this approach,
I have been demonstrated unique functions of N- and P/Q-type calcium channels
(Neuron 1996, PNAS 1998, 2003a,b, Neuron 2008, J. Physiol. 2011, PNAS 2012,
JBC 2013), SNARE-associated proteins (Syntaxin: Neuroscience 1995, J. Neurosci.
2002; Snapin: nature neurosci. 1999; Syntaphilin: Neuron 2000; SNAP-29:
PNAS 2001, Tomosyn: JCB 2005, 2008; JBC 2009, 2010; VAMP2: Neuron 2010),
synaptic vesicle associated proteins (Synaptotagmin: Neuroscience 1997;
Doc2: PNAS 1998; SV2s: Mol. Cell. Neurosci. 2005, Mol Pharmacol. 2012;
TRPM7: Neuron 2006; V-ATPase: Neuron 2010), G proteins (Goβγ J Physiol.
2005), active zone proteins (CAST: JCB 2004; SAD: Neuron 2006), motor proteins
(Myosin II and V: Neuron 1994; J Physiol. 2005) in regulation of transmitter
secretion, synaptic vesicle docking/priming and synaptic vesicle trafficking.
Endocytic proteins (dynamin/amphyphysin, JBC 2009; dynamin 1, 2, 3 JBC
2013) and axonal mitochondria transport (KIF5/syntabulin, J Neurosci. 2009)
are required to maintain synaptic transmission. The presynaptic (PNAS 2010)
and postsynaptic metabotropic glutamate receptors functions have also been
studied (J. Neurochem. 2003).