Abstract
In primary cultures of hippocampal neurons from the embryonic rat, spontaneous depolarizations lasting up to 6 sec adn resembling paroxysmal depolarization shifts (PDAs) appeared after 11 day7s in vitro. These depolarizations are presumably generated by sy6naptic events, because: (1) both their appearance and duration are independent of membrane potential, (2) the amplitudes of the underlying currents depend monotonically on membrane potential, and (1) they are reversed at the reversal potential of the excitatory postsynaptic potentials (EPSPs). In addition, PDAs disappeared reversiblyy when sodium‐dependent action potentials were blocked by tetrodotoxin (10μM) and when synaptic transmission was reduced by elevated Mg^2+^ (5mM). Further, the fact that these depolarizations can apppear simultaneously in two neurons in paired recordings also points to a synaptic origin. Inhibition of glutaminergic synaptic transmission by kynurenic acid (50μM) and the NMDA‐antagonist D‐2‐amino‐5‐phosphonovaleric acid (APV; 50μM) led to a marked shortening of the depolarizations. This blocking effect of kynurenic acid and APV and comparison with the currents elicited by locally applied glutamate or NMDA provide evidence for an activation of both types of glutamate receptors to induce PDSs. The role of alteration of glutaminergic synaptic transmission in the induction and maintenance of these depolarizations is discussed in the context of results from the literature on the appearrance of PDSs in cultures grown under chronic blockade of glutamate receptors. © 1993 Wiley‐Liss, Inc.