Spinal Actions of the NSAID Diclofenac on Nociceptive Transmission in Comparison to the Kv7 Channel Opener Flupirtine

Vicente-Baz, Jorge; Rivera-Arconada, Iván

doi:10.1016/j.neuroscience.2020.05.052

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…Diclofenac can directly depress spinal nociceptive transmission and spinal reflexes. The literature by Baz et al has emphasized that both diclofenac and flupirtine spinal effects are mediated through KCNQ channels [ 111 , 112 , 113 , 114 , 115 ]. Another study investigated the anti-nociceptive effects on chronic and inflammatory pain of the novel opener QO58-lysine on KCNQ channels, finding that there is a pharmacological effect of QO58-lysine effect on pain [ 85 , 86 ].…”

Section: Modulation Of Synaptic Plasticity By Kcnq Channelsmentioning

confidence: 99%

“…Additionally, future research into the ability of KCNQ modulators to treat other disorders related to dopaminergic pathways is another avenue that should be explored as well. Past studies have speculated that KCNQ openers, such as retigabine and ICA 27243, may be able to reduce the excitability of dopaminergic neurons in other tracts, such as the mesolimbic pathway, where overactivity results in schizophrenic symptoms [ 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 ]. This could be a potentially innovative tactic in clinical medicine as well, especially in the case of dementia-related psychosis, which is common onset among those with neurodegenerative disease.…”

Section: Kcnq Channels In Dopaminergic Motor Disordersmentioning

confidence: 99%

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Behavior of KCNQ Channels in Neural Plasticity and Motor Disorders

et al. 2022

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The broad distribution of voltage-gated potassium channels (VGKCs) in the human body makes them a critical component for the study of physiological and pathological function. Within the KCNQ family of VGKCs, these aqueous conduits serve an array of critical roles in homeostasis, especially in neural tissue. Moreover, the greater emphasis on genomic identification in the past century has led to a growth in literature on the role of the ion channels in pathological disease as well. Despite this, there is a need to consolidate the updated findings regarding both the pharmacotherapeutic and pathological roles of KCNQ channels, especially regarding neural plasticity and motor disorders which have the largest body of literature on this channel. Specifically, KCNQ channels serve a remarkable role in modulating the synaptic efficiency required to create appropriate plasticity in the brain. This role can serve as a foundation for clinical approaches to chronic pain. Additionally, KCNQ channels in motor disorders have been utilized as a direction for contemporary pharmacotherapeutic developments due to the muscarinic properties of this channel. The aim of this study is to provide a contemporary review of the behavior of these channels in neural plasticity and motor disorders. Upon review, the behavior of these channels is largely dependent on the physiological role that KCNQ modulatory factors (i.e., pharmacotherapeutic options) serve in pathological diseases.

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