Outward currents of single hippocampal cells obtained from the adult guinea‐pig.

Abstract

SUMMARY1. Neurones were isolated from the hippocampus of adult guinea-pigs by enzymatic and mechanical treatment. The electrophysiological properties of these cells were examined immediately after dissociation by intracellular recordings using lowresistance electrodes (2-5 MC). Co2" consisted of a shift to the positive direction of the voltage dependence of the current.7. The delayed currents can be divided into Ca2+-dependent and Ca2+-independent components. The component persistent in the Co2+ solution (K-current) decayed slowly with maintained depolarization (time constant > 3 s). The current elicited by a fixed depolarization increased gradually as the hyperpolarizing pre-pulse increased in amplitude and reached its half-maximum value as the hyperpolarizing pre-pulse was at -87 mV.8. Ca2"-dependent outward currents can be divided into two types based on their voltage-dependent properties. One type had a high threshold (-30 mV) and did not decline during sustained depolarization. A second component with a lower threshold (-60 mV) decayed completely at holding potentials depolarized to -55 mV. Halfmaximal current was elicited by depolarization when the preceding hyperpolarization was at -95 mV. These Ca2_-dependent currents are named K1(Ca)-and K2(Ca)-currents.9. Outward currents in the hippocampal pyramidal cells can be separated into four types by their kinetic and pharmacological properties. These include the Acurrent, K-current, Kl(ca)-current and K2(ca)-current. All outward currents, except Kl(ca)-current, exhibit inactivating properties with the A-current and K2(ca)-current showing complete inactivation near the resting potential (about -55 mV). These results suggest that the resting levels of the hippocampal cells can significantly affect the repolarization process and thereby determine the firing pattern of the cells.

Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

“…2 for comparison). The LFS-induced decrease in fEPSPs could have also been caused by a temporary decrease in excitability of the postsynaptic membrane by an increased GABA receptor-mediated inhibition, which would reduce the magnitude of EPSPs 11,36,52 and/or by increased outward potassium conductance 17,40,48 (for review see Ref. 44).…”

Three Kinetically Distinct Ca2+-Independent Depolarization-Activated K+ Currents in Callosal-Projecting Rat Visual Cortical Neurons

“…Rapidly activating and inactivating currents, similar to I A in CP neurons, have been characterized in neurons from rat hippocampus Segal and Barker 1984;Storm 1988), dentate gyrus (Beck et al 1992), neostriatum (Surmeier et al 1989), lateral geniculate nucleus (Budde et al 1992), thalamus , sensorimotor cortex (Foehring and Surmeier 1993;Hamill et al 1991), and visual cortex (Albert and Nerbonne 1995;Foehring and Surmeier 1993); the guinea pig (Numann et al 1987) and embryonic mouse (Wu and Barish 1992) hippocampus; and cat sensorimotor cortex (Spain et al 1991). The time-and voltage-dependent properties and the pharmacological sensitivities of the currents termed I A in these different preparations are similar.…”

“…The slowly activating, TEA-sensitive K + current, which we have termed I K , in CP neurons closely resembles delayed rectifier type-currents described in neurons from rat thalamus , sensorimotor cortex (Foehring and Surmeier 1993;Hamill et al 1991), dentate gyrus (Beck et al 1992), lateral geniculate nucleus (LGN) (Budde et al 1992), hippocampus (Segal and Barker 1984), globus pallidus (Stefani et al 1995), and visual cortex (Albert and Nerbonne 1995;Foehring and Surmeier 1993) and from guinea pig hippocampus (Numann et al 1987). As in CP neurons, the threshold of I K activation in these cells is between −45 and −35 mV, i.e., positive to that of I A described in the same cells.…”

“…Two types of K + currents that are likely to subserve these functions have been described in a number of mammalian CNS neurons: a rapidly activating and inactivating current that is blocked by 4-aminopyridine and usually is referred to as I A (Beck et al 1992;Budde et al 1992;Ficker and Heinemann 1992;Numann et al 1987;Segal and Barker 1984;Storm 1988;Surmeier et al 1989;Wu and Barish 1992); and a 4-aminopyridine-insensitive, delayed, outwardly rectifying K + current, usually referred to as I K (Beck et al 1992;Budde et al 1992;Numann et al 1987;Rudy 1988;Segal and Barker 1984;Storm 1990). These are broad classifications, however, and the detailed time-and voltagedependent properties of the various currents termed I A and I K do vary among cells (Rudy 1988;Storm 1990).…”

Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat

“…As one of the important second messengers, calcium regulates: 7,14 (i) the modulation of calciumdependent enzymes; (ii) several calcium-dependent calcium and potassium channels; 3,22,35 (iii) gene transcription like that initiated by immediate early genes; 2 (iv) calcium-dependent transmitter release; and (v) forms of synaptic plasticity induced by elevation of postsynaptic calcium levels. 34 The sustained component of the HVA current was the same in all experimental groups.…”