The primary function of the presynaptic nerve terminal is to release transmitter quanta and thus activate the postsynaptic target cell. In almost every step leading to the release of transmitter quanta, there is a substantial involvement of ion channels. In this review, the multitude of ion channels in the presynaptic terminal are surveyed. There are at least 12 different major categories of ion channels representing several tens of different ion channel types; the number of different ion channel molecules at presynaptic nerve terminals is many hundreds. We describe the different ion channel molecules at the surface membrane and inside the nerve terminal in the context of their possible role in the process of transmitter release. Frequently, a number of different ion channel molecules, with the same basic function, are present at the same nerve terminal. This is especially evident in the cases of calcium channels and potassium channels. This abundance of ion channels allows for a physiological and pharmacological fine tuning of the process of transmitter release and thus of synaptic transmission.

A new theory about the origins of consciousness that finds learning to be the driving force in the evolutionary transition to basic consciousness. What marked the evolutionary transition from organisms that lacked consciousness to those with consciousness—to minimal subjective experiencing, or, as Aristotle described it, “the sensitive soul”? In this book, Simona Ginsburg and Eva Jablonka propose a new theory about the origin of consciousness that finds learning to be the driving force in the transition to basic consciousness. Using a methodology similar to that used by scientists when they identified the transition from non-life to life, Ginsburg and Jablonka suggest a set of criteria, identify a marker for the transition to minimal consciousness, and explore the far-reaching biological, psychological, and philosophical implications. After presenting the historical, neurobiological, and philosophical foundations of their analysis, Ginsburg and Jablonka propose that the evolutionary marker of basic or minimal consciousness is a complex form of associative learning, which they term unlimited associative learning (UAL). UAL enables an organism to ascribe motivational value to a novel, compound, non-reflex-inducing stimulus or action, and use it as the basis for future learning. Associative learning, Ginsburg and Jablonka argue, drove the Cambrian explosion and its massive diversification of organisms. Finally, Ginsburg and Jablonka propose symbolic language as a similar type of marker for the evolutionary transition to human rationality—to Aristotle's “rational soul.”

In view of the emerging role of the phosphoinositide system in cellular communication we examined its involvement in quantal-transmitter release, which is a key element in synaptic transmission. Transmitter release is normally activated by an increase in intracellular calcium, achieved either by entry of calcium ions through the presynaptic membrane or by intracellular calcium liberation. One of the targets of the phosphoinositide signalling system is the enzyme protein kinase C (PKC), which can be activated experimentally by tumour promoting phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA). Such activation of PKC may be implicated in transmitter release in two ways. First, phorbol esters were found to increase secretion and enhance calcium currents; it might therefore be expected that they would increase synaptic transmitter release. But phorbol esters also inhibit the calcium current in dorsal root ganglion neurones. We report that the phorbol ester TPA augments synaptic transmission at the neuromuscular junction by increasing transmitter liberation. Activation of PKC also depends synaptic depression.

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Learning involves a usually adaptive response to an input (an external stimulus or the organism's own behaviour) in which the input-response relation is memorized; some physical traces of the relation persist and can later be the basis of a more effective response. Using toy models we show that this characterization applies not only to the paradigmatic case of neural learning, but also to cellular responses that are based on epigenetic mechanisms of cell memory. The models suggest that the research agenda of epigenetics needs to be expanded.