DIFFERENTIAL TIME-COURSE OF SLOW AFTERHYPERPOLARIZATIONS AND ASSOCIATED CA2- FURTHER DISSOCIATION BY CA2+ BUFFER( TRANSIENTS IN RAT CA1 PYRAMIDAL NEURONS )

Hippocampal neurons exhibit a slow after hyperpolarization following m embrane depolarization; this is thought to reflect an underlying Ca2+- dependent K+ current. This current is potentiated by intermediate conc entrations (0.1-1.0 mM) of exogenous Ca2+ buffer [Schwindt P. C. et al . (1992) Neuroscience 47, 571-578; Zhang L. et al. (1995) J. Neurophys iol. 74, 2225-2241]. The relationship between the slow afterhyperpolar ization and associated Ca2+ transients was investigated in the presenc e and absence of added exogenous Ca2+ buffer. Slow afterhyperpolarizat ions and underlying K+ currents were measured using whole-cell patch-c lamp recordings from hippocampal CA1 neurons in acute rat brain slices . Inclusion of fluorescent Ca2+ indicators in the patch pipette soluti on allowed simultaneous measurement of the evoked subcellular Ca2+ tra nsients using a confocal microscope. The peak Ca2+ signal exhibited an incremental increase with each action potential. This increase eventu ally reached a plateau with increasing numbers of action potentials. s uggesting dye saturation with peak Ca2+ concentrations. As the K-D for Ca2+ of the indicator dyes used was between 200 and 300 nM, it is pre dicted that saturation will occur when the peak Ca2+ signal exceeds 1 mu M. This occurred with fewer action potentials in dendritic vs somat ic compartments. Neither compartment exhibited averaged Ca2+ transient s matching the slow afterhyperpolarization time-course, dendritic Ca2 transients being most divergent. Intracellular accumulation of exogen ous Ca2+ buffer, tither by inclusion in the patch pipette or by incuba tion of the brain slice with its membrane-permeable form, caused a pro longation of the slow afterhyperpolarization but not of the somatic Ca 2+ transient. The initial rate of decline of the dendritic Ca transien t was diminished, but remained faster than that of the slow afterhyper polarization. We conclude that neither dendritic nor somatic Ca2+ sign als match the slow afterhyperpolarization time-course, with this disso ciation bring further magnified by addition of exogenous Ca2+ buffer. The implications of this result are discussed. (C) 1998 IBRO. Publishe d by Elsevier Science Ltd.