Calcium-dependent current generating the afterhyperpolarization of hippocampal neurons

Abstract

A single-electrode voltage-clamp technique was employed on in vitro hippocampal slices to examine the membrane current responsible for the slow afterhyperpolarization (AHP) in CA1 pyramidal cells. This was achieved by using conventional procedures to evoke an AHP in current clamp, followed rapidly by a switch into voltage clamp (hybrid clamp). The AHP current showed a dependence on extracellular K+, which was close to that predicted for a K+ current by the Nernst equation. The AHP current could be blocked by Cd2+ or norepinephrine. Although the AHP current showed a requirement for voltage-dependent Ca2+ entry, the current did not show any clear intrinsic voltage dependence. Once activated, AHP current is not turned off by hyperpolarizing the membrane potential. The effects of norepinephrine, Cd2+, and tetraethylammonium (TEA) were used to identify an AHP current component to the outward current evoked by depolarizing voltage commands from holding potentials that approximate to the resting potential for these cells. The AHP current can contribute significantly to the outward current during the depolarizing command. Upon repolarization it is evident as a slow outward tail current. This slow tail current had the same time constant as AHP currents evoked by hybrid clamp. Fast components to the tail currents were also observed. These were sensitive to Cd2+ and TEA. They probably represent a voltage-sensitive gKCa, sometimes termed C-current. The strong sensitivity to voltage and TEA displayed by the conventionally described gKCa (IC) are properties inconsistent with the AHP. It seems likely that the AHP current (IAHP) represents a Ca2+-activated K+ current separate from IC and that these two currents coexist in the same cell.

β-Adrenergic Stimulation Selectively Inhibits Long-Lasting L-Type Calcium Channel Facilitation in Hippocampal Pyramidal Neurons

“…5). Both protocols featured a voltage excursion to ϩ40 mV, which is close to the peak of the action potential measured in hippocampal neurons (Lancaster and Adams, 1986). Delayed facilitation was also induced by a 50 Hz train of action potential waveforms ( Fig.…”

“…It indicates that a train of only 10 action potential waveforms, at a lower frequency than the likely maximum firing frequency (100 Hz; Lancaster and Adams, 1986), evokes robust delayed facilitation at Ϫ20 mV. In three of three patches that did not exhibit delayed facilitation with a 200 msec rectangular prepulse, we were able to produce it when the protocol was switched to a train of action potential waveforms.…”

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…Activation of the SK channels is voltage independent and highly sensitive to intracellular Ca 2+ (Hille 2001;Sah and Davies 2000); BK channel activation is both voltage-and Ca 2+ -dependent (Vergara et al 1998;Dopico et al 1999). While activation of BK channels contributes to the falling phase of individual action potentials and the generation of the fast after hyperpolarizing potential (AHP) or hyperpolarizing after potential in many types of neurons (Lancaster and Adams 1986;Lancaster and Nicoll 1987;MacDermott and Weight 1982;Womack and Khodakhah 2002), including MNCs (Dopico et al 1999), SK channel activation is responsible for the generation of the AHP following a train of action potentials (Armstrong et al 1994;Bourque and Brown 1987;Greffrath et al 1998;Kirkpatrick and Bourque 1996;Lancaster and Adams 1986;Lancaster and Nicoll 1987;Sah and Bekkers 1996). This apamin-sensitive AHP is intermediate between the fast AHP (~50 ms) and "slow" AHP (lasting >5 s) (GhamariLangroudi and Bourque 2004).…”

Electrophysiological characterization of neurons in the dorsolateral pontine rapid-eye-movement sleep induction zone of the rat: Intrinsic membrane properties and responses to carbachol and orexins

“…Thus, it seems that they lack the calcium-activated potassium channel responsible for this property in hippocampal and neocortical pyramidal neurons (Lancaster and Adams, 1986).…”