Frequency‐dependent requirement for calcium store‐operated mechanisms in induction of homosynaptic long‐term depression at hippocampus CA1 synapses

Nakano, Makoto; Yamada, Shusaku; Udagawa, Rie; Kato, Nobuo

doi:10.1111/j.0953-816x.2004.03390.x

Cited by 28 publications

(17 citation statements)

References 42 publications

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“…This is consistent with published LTD data suggesting a preferential response to 1.0 Hz stimulation when compared to other low frequencies [40]. These results also approximate frequency-dependent effects seen in low-frequency rTMS in humans, whereby 1.0 Hz stimulation has the most prominent effect on MEP size [35], [41].…”

Section: Discussionsupporting

confidence: 91%

Suppression of Motor Cortical Excitability in Anesthetized Rats by Low Frequency Repetitive Transcranial Magnetic Stimulation

et al. 2014

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Repetitive transcranial magnetic stimulation (rTMS) is a widely-used method for modulating cortical excitability in humans, by mechanisms thought to involve use-dependent synaptic plasticity. For example, when low frequency rTMS (LF rTMS) is applied over the motor cortex, in humans, it predictably leads to a suppression of the motor evoked potential (MEP), presumably reflecting long-term depression (LTD) – like mechanisms. Yet how closely such rTMS effects actually match LTD is unknown. We therefore sought to (1) reproduce cortico-spinal depression by LF rTMS in rats, (2) establish a reliable animal model for rTMS effects that may enable mechanistic studies, and (3) test whether LTD-like properties are evident in the rat LF rTMS setup. Lateralized MEPs were obtained from anesthetized Long-Evans rats. To test frequency-dependence of LF rTMS, rats underwent rTMS at one of three frequencies, 0.25, 0.5, or 1 Hz. We next tested the dependence of rTMS effects on N-methyl-D-aspartate glutamate receptor (NMDAR), by application of two NMDAR antagonists. We find that 1 Hz rTMS preferentially depresses unilateral MEP in rats, and that this LTD-like effect is blocked by NMDAR antagonists. These are the first electrophysiological data showing depression of cortical excitability following LF rTMS in rats, and the first to demonstrate dependence of this form of cortical plasticity on the NMDAR. We also note that our report is the first to show that the capacity for LTD-type cortical suppression by rTMS is present under barbiturate anesthesia, suggesting that future neuromodulatory rTMS applications under anesthesia may be considered.

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Section: Discussionsupporting

confidence: 91%

Suppression of Motor Cortical Excitability in Anesthetized Rats by Low Frequency Repetitive Transcranial Magnetic Stimulation

et al. 2014

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“…2B) and the EC 50 for stimulation was within the range of Ca 2+ that is observed within the synaptic cleft, making it highly sensitive to respond to changes in Ca 2+ O that is modulated by synaptic activity [22,25,27]. Synaptic activity regulates intracellular Ca 2+ stores through both IP 3 -and RyRsensitive stores that exert effects on both short-and long-term plasticity [28,30,32,[45][46][47][48]] (see Berridge [49] for review). However, what is not clear is the degree to which Ca 2+ O -modulation of intracellular signaling, e.g.…”

Section: Implications For Ca 2+ O -Regulated Camkii Phosphorylation Imentioning

confidence: 99%

CaMKII inactivation by extracellular Ca2+ depletion in dorsal root ganglion neurons

Cohen

Fields

2006

Cell Calcium

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A mechanism by which Ca 2+ /CaM-dependent protein kinase (CaMKII) O has profound effects on intracellular Ca 2+ signaling and CaMKII autophosphorylation, in the absence of measurable changes in intracellular Ca 2+ . These findings have wide-ranging significance, because [Ca 2+ ] O is manipulated in many experimental studies. Moreover, this explanation for the paradoxical changes in CaMKII phosphorylation in response to manipulating [Ca 2+ ] O provides a possible mechanism linking activitydependent depletion of Ca 2+ from the synaptic cleft to a protein kinase regulating many neuronal properties.

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“…Caffeine-dependent LTD in hippocampal CA neurons is postsynaptically induced in a stimulation frequency-dependent manner. LTD requires both NMDA receptor activities and calcium release from internal calcium store [65].…”

Section: Fig (1) Basic Actions Of Caffeine At Synapsesmentioning

confidence: 99%

The Potential of Caffeine for Functional Modification from Cortical Synapses to Neuron Networks in the Brain

Yoshimura

2005

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Structure and function of the brain are use-dependent variables based on "synapse plasticity". Since synapses are driven by chemical transmitters, synaptic functions are liable to be modified by extrinsic chemicals displaying affinities for synaptic receptors or modulators. Caffeine is a widely used chemical substance that can invade synapses, and has several biochemical and metabolic actions on synaptic activities. This review focuses on the actions of caffeine on changes in structure and function in the region of the hippocampal formation and neocortex, which exhibit high synapse plasticity. At the synapse level, various synaptic receptors and channel activities are modulated by caffeine via mobilization of intracellular calcium, inhibition of phosphodiesterase, antagonism of adenosine receptors and GABA receptors. These actions of caffeine enable neurons to induce plastic changes in the properties of synaptic activities, such as synaptic transmission efficiency and morphology. At the network level, caffeine has the ability to activate cortical neural oscillators that deliver repetitive N-methyl-D-aspartate receptor-dependent signals to surrounding areas, causing strengthening of long-range inter-cortical communications. Caffeine might thus allow reorganization of cortical network functions via synaptic mobilizations.

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Frequency‐dependent requirement for calcium store‐operated mechanisms in induction of homosynaptic long‐term depression at hippocampus CA1 synapses

Cited by 28 publications

References 42 publications

Suppression of Motor Cortical Excitability in Anesthetized Rats by Low Frequency Repetitive Transcranial Magnetic Stimulation

Suppression of Motor Cortical Excitability in Anesthetized Rats by Low Frequency Repetitive Transcranial Magnetic Stimulation

CaMKII inactivation by extracellular Ca2+ depletion in dorsal root ganglion neurons

The Potential of Caffeine for Functional Modification from Cortical Synapses to Neuron Networks in the Brain

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