Effects of divalent cations on Schaffer collateral axon function

Owen, Benjamin; Woode, Franklin; Grover, Lawrence M.

doi:10.1007/s00221-020-06026-z

Cited by 3 publications

(1 citation statement)

References 24 publications

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“…Surface screening effects offer an unlikely explanation, because then basal excitability of Schaffer collaterals should be altered, too, which is not the case. 56 A novel and unorthodox way of thinking about this issue comes from a recent study showing that Ca 2+ -evoked release of the glio-transmitter ATP from astrocytes regulates axon excitability and conduction in an activity-dependent fashion. 57 Adopting this concept, which was developed for myelinated axons from cortical pyramidal cells, to distal Schaffer collaterals, which are unmyelinated, 58 the following sequence of events might occur: Sustained 1 Hz delivery of paired stimuli, but not of single stimuli, is sufficient to raise intracellular Ca 2+ in nearby astrocytes, leading to the release of ATP, which is then converted to adenosine, which eventually dampens axonal excitability through intermediate steps.…”

Section: Discussionmentioning

confidence: 99%

Tonic activin signaling shapes cellular and synaptic properties of CA1 neurons mainly in dorsal hippocampus

Dahlmanns,

Valero-Aracama,

Dahlmanns

et al. 2023

iScience

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Section: Discussionmentioning

confidence: 99%

Tonic activin signaling shapes cellular and synaptic properties of CA1 neurons mainly in dorsal hippocampus

Dahlmanns,

Valero-Aracama,

Dahlmanns

et al. 2023

iScience

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Effects of carbonic anhydrase activity on the excitability of hippocampal axons during high-frequency firing

Andreasen,

Nedergaard

2023

Brain Research

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Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat

Forsberg,

Zhou,

Jalali

et al. 2024

Journal of Neurochemistry

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It is well recognized that changes in the extracellular concentration of calcium ions influence the excitability of neurons, yet what mechanism(s) mediate these effects is still a matter of debate. Using patch‐clamp recordings from rat hippocampal CA1 pyramidal neurons, we examined the contribution of G‐proteins and intracellular calcium‐dependent signaling mechanisms to changes in intrinsic excitability evoked by altering the extracellular calcium concentration from physiological (1.2 mM) to a commonly used experimental (2 mM) level. We find that the inhibitory effect on intrinsic excitability of calcium ions is mainly expressed as an increased threshold for action potential firing (with no significant effect on resting membrane potential) that is not blocked by either the G‐protein inhibitor GDPβS or the calcium chelator BAPTA. Our results therefore argue that in the concentration range studied, G‐protein coupled calcium‐sensing receptors, non‐selective cation conductances, and intracellular calcium signaling pathways are not involved in mediating the effect of extracellular calcium ions on intrinsic excitability. Analysis of the derivative of the action potential, dV/dt versus membrane potential, indicates a current shift towards more depolarized membrane potentials at the higher calcium concentration. Our results are thus consistent with a mechanism in which extracellular calcium ions act directly on the voltage‐gated sodium channels by neutralizing negative charges on the extracellular surface of these channels to modulate the threshold for action potential activation.image

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Effects of divalent cations on Schaffer collateral axon function

Cited by 3 publications

References 24 publications

Tonic activin signaling shapes cellular and synaptic properties of CA1 neurons mainly in dorsal hippocampus

Tonic activin signaling shapes cellular and synaptic properties of CA1 neurons mainly in dorsal hippocampus

Effects of carbonic anhydrase activity on the excitability of hippocampal axons during high-frequency firing

Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat

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