Main research contributions
For many years,
one of my main areas of interest has been in the properties of neuronal calcium
channels and their modulation by G proteins, and the relationship of this to
presynaptic inhibition of transmitter release.
My group was the first to show that presynaptic inhibition by agents
such as adenosine involves a pertussis toxin
sensitive GTP binding protein (Prestwich and Dolphin,
1985), and was among the first to show that activation of such G proteins
results in inhibition of calcium currents, and this can be mimicked by the G
protein activator GTPgS (Scott and Dolphin, 1996, 1987).
More recently we have been investigating the mechanism of G protein
inhibition of calcium currents, and were the first to show that the
intracellular calcium channel b subunit interacts with modulation by G proteins (Campbell et al
1995). Most recently we have shown that
voltage-dependent G protein modulation by Gbg is lost in the absence of a calcium channel b subunit (Meir et al 2000). We have identified a
11 amino acid motif on the intracellular N terminus of the a1B calcium channel that is essential for its G
protein modulation (Page et al., 1998, Canti et al.,
1999), and are currently examining how this domain exerts its function.