Gene structure and chromosome mapping of the human small-conductance calcium-activated potassium channel SK1 gene (KCNN1)

1999 ◽  
Vol 86 (1) ◽  
pp. 70-73 ◽  
Author(s):  
M. Litt ◽  
D. LaMorticella ◽  
C.T. Bond ◽  
J.P. Adelman
Keyword(s):  
Potassium Channel ◽  
Gene Structure ◽  
Chromosome Mapping ◽  
Calcium Activated Potassium Channel ◽  
Small Conductance

scholarly journals Modeling of the Small-Conductance Calcium-Activated Potassium Channel and Cardiac Alternans

2016 ◽  
Vol 110 (3) ◽  
pp. 106a
Author(s):  
Matthew Kennedy ◽  
Donald M. Bers ◽  
Nipavan Chiamvimonvat ◽  
Daisuke Sato
Keyword(s):  
Potassium Channel ◽  
Cardiac Alternans ◽  
Calcium Activated Potassium Channel ◽  
Small Conductance

scholarly journals Ginkgo biloba L. Prevents Hypobaric Hypoxia–Induced Spatial Memory Deficit Through Small Conductance Calcium-Activated Potassium Channel Inhibition: The Role of ERK/CaMKII/CREB Signaling

2021 ◽  
Vol 12 ◽  
Author(s):  
Neetu Kushwah ◽  
Vishal Jain ◽  
Manisha Kadam ◽  
Rahul Kumar ◽  
Aastha Dheer ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Signaling Pathway ◽  
Ginkgo Biloba ◽  
Cognitive Functions ◽  
Memory Impairment ◽  
Hypobaric Hypoxia ◽  
Glutamate Excitotoxicity ◽  
Channel Inhibition ◽  
Calcium Activated Potassium Channel ◽  
Small Conductance

Hypobaric hypoxia (HH) is a stressful condition, which is more common at high altitudes and can impair cognitive functions. Ginkgo biloba L. leaf extract (GBE) is widely used as herbal medicine against different disorders. Its ability to improve cognitive functions, reduce oxidative stress, and promote cell survival makes it a putative therapeutic candidate against HH. The present study has been designed to explore the effect of GBE on HH-induced neurodegeneration and memory impairment as well as possible signaling mechanisms involved. 220–250 gm (approximately 6- to 8-week-old) Sprague Dawley rats were randomly divided into different groups. GBE was orally administered to respective groups at a dose of 100 mg/kg/day throughout the HH exposure, i.e., 14 days. Memory testing was performed followed by hippocampus isolation for further processing of different molecular and morphological parameters related to cognition. The results indicated that GBE ameliorates HH-induced memory impairment and oxidative damage and reduces apoptosis. Moreover, GBE modulates the activity of the small conductance calcium-activated potassium channels, which further reduces glutamate excitotoxicity and apoptosis. The exploration of the downstream signaling pathway demonstrated that GBE administration prevents HH-induced small conductance calcium-activated potassium channel activation, and that initiates pro-survival machinery by activating extracellular signal–regulated kinase (ERK)/calmodulin-dependent protein kinase II (CaMKII) and the cAMP response element–binding protein (CREB) signaling pathway. In summary, the current study demonstrates the beneficial effect of GBE on conditions like HH and provides various therapeutic targets involved in the mechanism of action of GBE-mediated neuroprotection.

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