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Diacylglycerol- and Ca2+-mediated activation of protein kinase C (PKC) is regarded as a key triggering step in numerous cellular processes, from the regulation of gene transcription to the modulation of stimulus secretion coupling in hormone and neurotransmitter release. However, because of the ubiquitous and often redundant expression of the known PKC isoforms, the large number of identified PKC regulators and substrates, and the presence of alternative diacylglycerol and Ca2+ receptors that are also activated by commonly used PKC activators, the precise role of PKC activity in these processes and the identity of the relevant PKC isoforms and substrates have often remained elusive. Particularly in stimulus secretion coupling and the related process of synaptic transmission, the identification of steps at which PKC is involved has been difficult. This is because in many studies the physiological readout is a signal which is several steps downstream of the one modulated by PKC, and, at least until recently, reagents used to stimulate or block PKC have often been quite unspecific. In the analysis of synaptic transmission, for instance, many preparations allow only to record postsynaptic responses to presynaptic nerve stimulation. If a PKC effect is observed in such a system, a first question to be answered is whether postsynaptic sensitivity has changed or else presynaptic transmitter release. Even if in a suitable experimental paradigm an observed effect is shown to be caused by presynaptic PKC action, a key question remains: does PKC act on the electrical excitability of the nerve terminal or on the transmitter release process? Furthermore, in case of an answer in favor of the latter possibility, one would have to ask whether it is actually the release machinery of a given secretory vesicle that is altered or rather the regulation of the availability of release-ready vesicles, i.e., the …

Specificity emerges in the dissection of diacylglycerol- and protein kinase C-mediated signalling pathways