KAINATE INDUCES AN INTRACELLULAR NA-ACTIVATED K+ CURRENT IN CULTURED EMBRYONIC RAT HIPPOCAMPAL-NEURONS()

1. In embryonic rat hippocampal neurones cultured for <3 days, kainate induced an inward current at negative potentials that recovered to ba seline levels immediately upon termination of agonist application. How ever, in neurones cultured for longer, the kainate-induced current was often followed by a long-lasting inward current that slowly recovered to baseline levels. The amplitude of the delayed current (I-delay) tr iggered by kainate was positively related both to the duration of appl ication at constant agonist concentration and to concentration at cons tant application duration. 2. I-delay could last for several minutes a nd was accompanied by a conductance increase, which closely paralleled current amplitude. Depression of the kainate-induced current response at receptor level with CNQX or at ionic level with Na+-free solution had any effect on I-delay. Li+ effected the same response as Na+ in me diating kainate-induced I-delay. 3. GABA-activated Cl- current, which was associated with the same amount of inwardly directed charge flow a t the same potential as that induced by kainate, did not trigger a lon glasting delayed current. 4. I-delay depended on the existence of extr acellular K+ and its amplitude increased with the increase in K+ conce ntration. Neither applying Cl-- or Ca2+-free solutions nor increasing intracellular Ca2+ buffering speed and capacity altered I-delay. Expos ure to the specific K-Ca channel blockers apamin and charybdotoxin als o failed to alter I-delay. However, I-delay could be blocked by Cs+, B a2+ and high concentrations of 4-aminopyridine (4-AP) and TEA. 5. Insi de-out excised patch-clamp recordings revealed that low density or hig hly clustered Na+- activated K+ channels were expressed in the cell bo dies of cultured embryonic rat hippocampal neurones. These could be th e elementary channels underlying I-delay.