Introduction Ikain function is centered at the synapse and, consequently, substantial scientific efforts have been directed towards exploring synaptic function. In neurochemical research, it has been customary to divide neuronal parts of the synapse into two. Since the early 1960s. ‘pinched-off presynaptic nerve terminals or ‘synaptosomes’ have been extensively used as a model of the presynaptic neuron [ 11. Our present understanding of nerve-terminal metabolism and bioenergetics [2], neurotransmitter release and uptake [ 3 ] , and electrophysiology is largely based on studies carried on synaptosomes. One of the interesting issues within neuroscience is the role(s) of 1.-glutamic acid. As the most abundant cerebral transmitter, glutamate mediates a majority of fast excitatory impulses in the cerebral cortex. and is therefore strongly involved in integrated brain function [4]. On the other hand, activation of postsynaptic glutamate receptors [ 51 evidently causes neuronal degeneration during brain energy failure, for example, following ischaemia [6,7]. In this paper, mechanisms of glutamate release from synaptosomes are discussed with major emphasis on their energy and CaL’ dependency and the contribution of various intraterminal glutamate pools to this release [XI. This discussion will be extended towards compartmentation of the transmitter glutamate in the intact cerebral cortex in the light of previous studies using ‘ € I and ‘€I{’.’C}n.m.r. spectroscopy [g-ll]. The aim in the latter part will be to weight the relevance of synaptosome studies to the conditions in an intact brain prepara-