Extracellular-signal-regulated kinases (ERKs) are emerging as important reg
ulators of neuronal function. Recent advances have increased our understand
ing of ERK signalling at the molecular level. In particular, it has became
evident that multiple second messengers, such as cyclic adenosine monophosp
hate, protein kinase A, calcium, and diacylglycerol, can control ERK signal
ling via the small G proteins Ras and Rap1. These findings may explain the
role of ERKs in the regulation of activity-dependent neuronal events, such
as synaptic plasticity, long-term potentiation and cell survival. Moreover,
they allow us to begin to develop a model to understand both the control o
f ERKs at the subcellular level and the generation of ERK signal specificit
y.