Envisioning the role of inwardly rectifying potassium (Kir) channel in epilepsy

Abstract

Epilepsy is a neurological disease characterized by two spontaneous seizures occurring within 24 hr, or two spontaneous seizures within 10 years after an unprovoked seizure (Fisher et al., 2014). The disease occurs by an increased tendency to generate seizures attributed to abnormal brain activity, caused by the disruption of the dynamic excitatory and inhibitory neuronal balance in the central nervous system (CNS) (Navidhamidi et al., 2017). Aberrant connectivity between neuronal networks may result in pathologically synchronized discharges and subsequently recurrent seizures (Aronica & Muhlebner, 2017). Epilepsy not only poses a significant burden on the patients and their families, but is also associated with significant social, behavioral, and economic effects (Tatum et al., 2009).Epilepsy affects people of all ages and has emerged as a global health concern affecting more than 70 million patients worldwide.Despite the recent advances in pre-clinical and clinical research, the

Metabotropic glutamate receptor 5‐mediated inhibition of inward‐rectifying K+ channel 4.1 contributes to orofacial ectopic mechanical allodynia following inferior alveolar nerve transection in male mice

“…to the relationships between Kir4.1 dysfunction and various diseases, including depression, epilepsy, and multiple sclerosis (Akyuz et al, 2022;Brickshawana et al, 2014;Cui et al, 2018;Kinboshi et al, 2020;Xiong et al, 2019). The present findings regarding the role of Kir4.1 in orofacial allodynia suggest that Kir4.1 may be also considered as a therapeutic target for neuropathic pain.…”

“…Similarly, a previous study reported that silencing Kir4.1 in the TG via direct injection of long double‐stranded RNA induced orofacial pain‐like behaviors in rats (Vit et al, 2008). In recent years, increasing attention has been paid to the relationships between Kir4.1 dysfunction and various diseases, including depression, epilepsy, and multiple sclerosis (Akyuz et al, 2022; Brickshawana et al, 2014; Cui et al, 2018; Kinboshi et al, 2020; Xiong et al, 2019). The present findings regarding the role of Kir4.1 in orofacial allodynia suggest that Kir4.1 may be also considered as a therapeutic target for neuropathic pain.…”

“…The underlying mechanisms by which Kir4.1 regulates the function of the nervous system is still being explored (Cui et al, 2018;Ohno et al, 2018Ohno et al, , 2021. Studies have confirmed the involvement of Kir4.1 in regulating the electrophysiological properties of neurons and glia by affecting K + homeostasis (Akyuz et al, 2022;Tang et al, 2010). Recent emerging evidence has also supported the regulatory effects of Kir4.1 on brain-derived neurotrophic factor and extracellular glutamate levels in astrocytes (Leo et al, 2021;Ohno et al, 2018Ohno et al, , 2021.…”

Calcium buffering tunes intrinsic excitability of spinal dorsal horn parvalbumin-expressing interneurons: A computational model

“…The effect of hyperpolarization-activated cation current I h were evident in both naïve- and CCI-PVIN recordings ( Table 4 ). The voltage-gated subthreshold currents, including M-type potassium current I M (Shah et al, 2008), the persistent sodium current I NaP (Vervaeke et al, 2006), and the inward rectifier potassium current I Kir (Akyuz et al, 2022), has been associated with generating mAHP and spike frequency adaptation. Despite the fact that these currents also modulate the passive membrane properties, which remain unaffected following nerve injury, their contribution to the PVINs excitability remains to be determined.…”

Levetiracetam ameliorates epileptogenesis by modulating the adenosinergic pathway in a kindling model of epilepsy in mice

“…Epilepsy is a chronic, severe, and devastating neurological condition characterized by repeated intermittent seizures that affect over 65 million people worldwide [ 1 , 2 ]. Focal seizures occur more frequently in both adults and children compared to generalized seizures.…”