The excitability of CA1 pyramidal cell dendrites is modulated by a local Ca(2+)-dependent K(+)-conductance.

Intracellular recordings are made from distal apical dendrites of CA1 pyramidal neurones in the rat hippocampal slice preparation. Injection of a threshold current evoked two predominant firing patterns: fast spiking and compound spiking. Suprathreshold current injection evoked high frequency dendritic spiking followed by a pronounced slow afterhyperpolarization (sAHP(dend)) lasting for several hundred milliseconds, during which spiking was inhibited for a variable period. In fast spiking dendrites, the size of the sAHP(dend) depended on the number and frequency of preceding spikes, whereas, in compound spiking dendrites, it was more closely related to the size and duration of preceding Ca(2+)-spikes. During the peak of the sAHP(dend), the membrane conductance was increased by 56%. The sAHP(dend) was blocked by perfusion with Ca2+ and by intradendritic injection of ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 0.01 or 0.2 M), indicating that the activation of the sAHP(dend) depends on a rise in intradendritic Ca2+. The sAHP(dend) was also blocked by low concentrations (0.5-1 microM) of carbachol. The data presented here therefore, provide strong evidence that the sAHP(dend) is due to the activation of a local Ca(2+)-dependent K(+)-conductance. Possible implications of a dendritic Ca(2+)-dependent K(+)-conductance for the integration of synaptic potentials are discussed.