A possible physiological mechanism for short-term memory

Memory formation for a passive avoidance task in day-old chickens is shown to be inhibited by intracranial injections of very low concentrations (1 and 2 mM) of potassium chloride. The effects occur early after learning, in the first of a postulated three phase sequence of memory formation. Concentrations between 2.5 and 5.0 mM KCl inhibit the second of the three phase sequence. Potassium chloride concentrations lower than 1 mM or comparable to normal CSF levels (7 mM) produce no effects on memory. Concentrations of sodium chloride different from normal CSF concentrations in the young chick also produce small but consistent memory deficits, the effects being independent of those due to potassium chloride. An argument is made for a mechanism of short-term memory formation involving afferent post-tetanic hyperpolarization which is inhibited by potassium accumulation at synapses caused by glia inactivation.