Variation in the pattern of [Ca2+]i change induced by acetylcholine in cultured hippocampal neurons

Iijima, Toshio; Kudo, Yoshihisa; Ogura, Akihiko; Akita, K.; Matsumoto, Gen

doi:10.1016/0006-8993(90)91552-r

Cited by 8 publications

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“…Although cytosolic [Ca 2+ ] has not been measured in the present experiments, a number of previous reports provide this kind of estimate both at rest and under various experimental conditions. Thus, the mean resting [Ca 2+ ], measured by means of fluorescent Ca 2+ indicators at the resting potential and in the presence of normal extracellular [Ca 2+ ], was found to be rather low, 30 nM (Knöpfel, Charpak, Brown & Gähwiler, 1990) or 20‐80 nM (Iijima, Kudo, Ogura, Akita & Matsumoto, 1990). Membrane depolarization to ‐30 mV (Knöpfel et al 1990) or muscarinic stimulation (Iijima et al .…”

Section: Discussionmentioning

confidence: 94%

“…Thus, the mean resting [Ca 2+ ], measured by means of fluorescent Ca 2+ indicators at the resting potential and in the presence of normal extracellular [Ca 2+ ], was found to be rather low, 30 nM (Knöpfel, Charpak, Brown & Gähwiler, 1990) or 20‐80 nM (Iijima, Kudo, Ogura, Akita & Matsumoto, 1990). Membrane depolarization to ‐30 mV (Knöpfel et al 1990) or muscarinic stimulation (Iijima et al . 1990; Wakamori, Hidaka & Akaike, 1993) increased this mean level considerably, up to 500 nM.…”

Section: Discussionmentioning

confidence: 94%

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Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones

Selyanko

Sim

1998

The Journal of Physiology

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1. Whole-cell perforated-patch recording from cultured CA1-CA3 pyramidal neurones from neonatal rat hippocampus (20-22°C; [K¤]ï = 2·5 mÒ) revealed two previously recorded non-inactivating (sustained) K¤ outward currents: a voltage-independent 'leak' current (Ileak) operating at all negative potentials, and, at potentials ü −60 mV, a time-and voltagedependent 'M-current' (IK(M)). Both were inhibited by 1 mÒ Ba¥ or 10 ìÒ oxotremorine-M (Oxo-M). In ruptured-patch recording using Ca¥-free pipette solution, Ileak was strongly enhanced, and was inhibited by 1 mÒ Ba¥ but unaffected by 0·5 mÒ 4-aminopyridine (4_AP), 1 mÒ tetraethylammonium (TEA) or 1-10 nÒ margatoxin. 2. Single channels underlying these currents were sought in cell-attached patch recordings. A single class of channels of conductance •7 pS showing sustained activity at resting potential and above was identified. These normally had a very low open probability (Pï < 0·1), which, however, showed a dramatic and reversible increase (to about 0·9 at •0 mV) following the removal of Ca¥ from the bath. Under these (Ca¥-free) conditions, single-channel Pï showed both voltage-dependent and voltage-independent components on patch depolarization from resting potential. The mean activation curve was fitted by a modified Boltzmann equation. When tested, all channels were reversibly inhibited by addition of 10 ìÒ Oxo-M to the bath solution. 3. The channels maintained their high Pï in patches excised in inside-out mode into a Ca¥-free internal solution and were strongly inhibited by application of Ca¥ to the inner face of the membrane (IC50 = 122 nÒ); this inhibition was observed in the absence of MgATP, and therefore was direct and unrelated to channel phosphorylationÏdephosphorylation. 4. Channels in patches excised in outside-out mode were blocked by 1 mÒ Ba¥ but were unaffected by 4-AP or TEA. 5. Channels in cell-attached patches were inhibited after single spikes, yielding inward ensemble currents lasting several hundred milliseconds. This was prevented in Ca¥-free solution, implying that it was due to Ca¥ entry. 6. The properties of these channels (block by internal Ca¥ and external Oxo-M and Ba¥, and the presence of both voltage-dependent and voltage-independent components in their PïÏV relationship) show points of resemblance to those expected for channels associated with both Ileak and IK(M) components of the sustained macroscopic currents. For this reason we designate them Ksust ('sustained current') channels. Inhibition of these channels by Ca¥ entry during an action potential may account for some forms of Ca¥-dependent afterdepolarization. Their high sensitivity to internal Ca¥ may provide a new, positive feedback mechanism for cell excitation operating at low (near-resting) [Ca¥]i.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 94%

Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones

Selyanko

Sim

1998

The Journal of Physiology

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Imaging of caffeine‐inducible release of intracellular calcium in cultured embryonic mouse telencephalic neurons

Tsai

Barish

1995

J. Neurobiol.

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To gain a better understanding of Ca(2+)-induced Ca2+ release in central neurons, we have studied the increase in intracellular Ca2+ concentration ([Ca2+]i) induced by application of caffeine to cells cultured from embryonic mouse telencephalon (hippocampus or cortex). The magnitudes and distributions of changes in [Ca2+]i in neuron somata were measured by quantitative video microscopy. We observed that application of caffeine to pyramidally shaped neurons typically initiated an increase in [Ca2+]i in the cytoplasmic region between the nucleus and the base of a major dendrite. [Ca2+] in this region increased over a period of 3 to 6 s and was followed by, with a slight delay, a surge of Ca2+ that moved across the soma and into or over the nucleus. Similar Ca2+ responses to caffeine were observed in Ca(2+)-containing and nominally Ca(2+)-free external solutions, suggesting that caffeine was inducing Ca2+ release from intracellular stores. Ca2+ responses to caffeine were potentiated by inducing a tonic Ca2+ influx through N-methyl-D-aspartate (NMDA)-type glutamate receptors activated by 0.3 microM glutamate and multiple responses to caffeine could be elicited by using this Ca2+ influx to refill the intracellular stores. Ryanodine inhibition of caffeine-induced Ca2+ release was use- and concentration-dependent; the median effective concentration EC50 for ryanodine declined from 22 microM for the first application of caffeine to 20 nM for the fourth. We conclude, based on these responses to caffeine, that ryanodine-sensitive mechanisms of intracellular Ca2+ release are active in hippocampal and cortical neurons and may be involved in generation of directed Ca2+ waves that engulf the nucleus.

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Involvement of postsynaptic G proteins in hippocampal long-term potentiation

Katsuki¹,

Kaneko²,

Satoh³

1992

Brain Research

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Variation in the pattern of [Ca2+]i change induced by acetylcholine in cultured hippocampal neurons

Cited by 8 publications

References 50 publications

Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones

Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones

Imaging of caffeine‐inducible release of intracellular calcium in cultured embryonic mouse telencephalic neurons

Involvement of postsynaptic G proteins in hippocampal long-term potentiation

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Variation in the pattern of [Ca2+]i change induced by acetylcholine in cultured hippocampal neurons

Cited by 8 publications

References 50 publications

Ca2+‐inhibited non‐inactivating K+ channels in cultured rat hippocampal pyramidal neurones

Ca2+‐inhibited non‐inactivating K+ channels in cultured rat hippocampal pyramidal neurones

Imaging of caffeine‐inducible release of intracellular calcium in cultured embryonic mouse telencephalic neurons

Involvement of postsynaptic G proteins in hippocampal long-term potentiation

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Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones

Ca²⁺‐inhibited non‐inactivating K⁺ channels in cultured rat hippocampal pyramidal neurones