Until we know more of the relations of these processes to each other in the neuropile it would be unwise to say more. It is possible that the effective part of the discharge of such cells is not as it is in conduction in long pathways, the internal circuit that returns through the same fiber, but the external circuit that enters other processes, ...” (3). 4. Inhibition The inhibitory chemical transmitter substance postulated by Eccles has never been detected in spite of numerous efforts to do so. The mechanism(s) of inhibition is perhaps the key to the question of cellular interaction and, in one form or another, must be accounted for in any adequate theory. Other rather specific forms of excitation and inhibition interaction have been proposed at one time or another. Perhaps the best example is the polar neuron of Gesell (8) and, more recently, Retzlaff (18). In such a concept, excitatory and inhibitory couplings differ basically because of a macroscopic structural difference at the cellular level; that is, various arrangements or orientation of intimate cellular structures give rise to either excitation or inhibition. 5. Long-Term Memory Most modern theories of semipermanent structural change (or _engrams_, as they are sometimes called) look either to the molecular level or to the cellular level. Various specific locales for the engram have been suggested, including (1) modifications of RNA molecular structure, (2) changes of cell size, synapse area or dendrite extensions, (3) neuropile modification, and (4) local changes in the cell membrane. There is, in fact, rather direct evidence of the growth of neurons or their dendrites with use and the diminution or atrophy of dendrites with disuse. The apical dendrite of pyramidal neurones becomes thicker and more twisted with continuing activity, nerve fibers swell when active, sprout additional branches (at least in the spinal cord) and presumably increase the size and number of their terminal knobs. As pointed out by Konorski (11), the morphological conception of plasticity according to which plastic changes would be related to the formation and multiplication of new synaptic junctions goes back at least as far as Ramon y Cajal in 1904. Whatever the substrate of the memory trace, it is, at least in adults, remarkably immune to extensive brain damage and as Young (24) has said: “ ... this question of the nature of the memory trace is one of the most obscure and disputed in the whole of biology.” 6. Field Effects and Learning