Presynaptic large-conductance calcium-activated potassium channels control synaptic transmission in the superficial dorsal horn of the mouse

Furukawa, Naoki; Takasusuki, Toshifumi; Fukushima, Toshikazu; Hori, Yasushi

doi:10.1016/j.neulet.2008.08.022

Cited by 17 publications

(29 citation statements)

References 29 publications

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“…In organotypic hippocampal slice cultures, BK channel blockade by iberiotoxin or paxilline increases the probability of glutamate release at synapses between CA3 pyramidal neurons, as reflected by increased frequency of spontaneous excitatory postsynaptic currents (EPSCs), increased amplitude of evoked EPSCs, and reduced paired-pulse ratio (Raffaelli et al, 2004). Likewise, iberiotoxin increases the frequency of spontaneous EPSCs in acute spinal cord slices (Furukawa, Takasusuki, Fukushima, & Hori, 2008). …”

Section: Role Of Bk Channels In Cns Cellular Physiologymentioning

confidence: 99%

“…Consistent with this hypothesis, BK channels located in calcitonin gene-related peptide terminals were recently shown to mediate the analgesic effect of a peripherally acting μ opioid receptor agonist in a model of trigeminal nociception (Baillie, Schmidhammer, & Mulligan, 2015). BK channels are also present on presynaptic terminals in the superficial dorsal horn, where they inhibit transmitter release from primary afferents and inhibitory interneurons (Furukawa et al, 2008; Song & Marvizon, 2005). …”

Section: Role Of Bk Channels In Cns Function and Pathologiesmentioning

confidence: 99%

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BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

136

170

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Large conductance Ca2+- and voltage-activated K+ (BK) channels are widely distributed in the postnatal central nervous system (CNS). BK channels play a pleiotropic role in regulating the activity of brain and spinal cord neural circuits by providing a negative feedback mechanism for local increases in intracellular Ca2+ concentrations. In neurons, they regulate the timing and duration of K+ influx such that they can either increase or decrease firing depending on the cellular context, and they can suppress neurotransmitter release from presynaptic terminals. In addition, BK channels located in astrocytes and arterial myocytes modulate cerebral blood flow. Not surprisingly, both loss and gain of BK channel function have been associated with CNS disorders such as epilepsy, ataxia, mental retardation, and chronic pain. On the other hand, the neuroprotective role played by BK channels in a number of pathological situations could potentially be leveraged to correct neurological dysfunction.

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Section: Role Of Bk Channels In Cns Cellular Physiologymentioning

confidence: 99%

Section: Role Of Bk Channels In Cns Function and Pathologiesmentioning

confidence: 99%

BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

136

170

View full text Add to dashboard Cite

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“…BK Ca are expressed intrinsic membrane proteins and are involved in the regulation of neuronal excitability (13)(14)(15)(16)(17). Because of their high conductance, activation of BK Ca channels shortens the action potential duration, enhances the rate of repolarization, reduces the depolarization and contributes to the rapid after-hyperpolarization.…”

Section: Introductionmentioning

confidence: 99%

“…Because of their high conductance, activation of BK Ca channels shortens the action potential duration, enhances the rate of repolarization, reduces the depolarization and contributes to the rapid after-hyperpolarization. All these features make BK Ca channels ideal feedback regulators of cell excitability (13)(14)(15)(16)(17). It has been reported BK Ca channels are expressed abundantly in the trigeminal ganglion (TG) (18), dorsal root ganglia (DRG) (17) and superficial dorsal horn (16) and play a role in the antihyperalgesia effect in neuropathic pain (15,17).…”

Section: Introductionmentioning

confidence: 99%

“…In DRG neurons, opening BK Ca channels by NS1619 leads to the reduction of depolarization-evoked action potential firing and 4-aminopyridine-induced neuronal hyperexcitability (19). IbTX itself presynaptically increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) recorded in the superficial dorsal horn and thus modulated nociceptive transmission (16).…”

Section: Introductionmentioning

confidence: 99%

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The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain

Liu

et al. 2014

Cephalalgia

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BK Potassium Channels Suppress Cavα2δ Subunit Function to Reduce Inflammatory and Neuropathic Pain

et al. 2018

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Cavα2δ subunits contribute to the cell-surface expression of Cav2 calcium channels. Upregulation of Cavα2δ-1 in dorsal root ganglion neurons occurs after nerve injury and results in an increased synaptic abundance of Cav2.2 channels in the spinal dorsal horn, thus enhancing the transmission of pain signals. Here, we report that large conductance calcium-activated potassium (BK) channels interact with the Cavα2δ subunit. Coexpression of BK channels with the Cav2 calcium channels reduces their cell-surface expression and whole-cell current density by competing the Cavα2δ subunit away from the Cav2 complex. Biochemical analysis reveals that the extracellular N terminus region of the BK channel is the key molecular determinant of this effect. Intrathecally delivered virus constructs encoding a membrane-anchored BK channel N terminus peptide produces long-lasting analgesia in mouse models of inflammatory and neuropathic pain. Collectively, our data reveal an endogenous ligand of the Cavα2δ subunit with analgesic properties.

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Presynaptic large-conductance calcium-activated potassium channels control synaptic transmission in the superficial dorsal horn of the mouse

Cited by 17 publications

References 29 publications

BK Channels in the Central Nervous System

BK Channels in the Central Nervous System

The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain

BK Potassium Channels Suppress Cavα2δ Subunit Function to Reduce Inflammatory and Neuropathic Pain

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