a(MESH:"Potassium Channels")
Picomolar levels of Abeta can also rescue neuronal cell death induced by inhibition of Abeta generation (by exposure to inhibitors of beta- or gamma-scretases) [160], possibly through regulating the potassium ion channel expression, hence affecting neuronal excitability [161] PubMed:21214928
As a consequence, stimulation of ACh muscarinic receptors can promote the opening or closing of Ca2+, K+, or Cl- channels, which might facilitate either depolarization or hyperpolarization, depending on the cell type where these receptors are expressed PubMed:26813123
Activation of muscarinic receptors can block various types of K+ currents by inhibiting many resting and voltage-gated K+ channels PubMed:26813123
Stimulation of Gαq coupled muscarinic receptors leads to activation of phospholipase C and formation of inositol phosphates and other second messengers, which can promote closure of K+ channels, thus facilitating cell excitability PubMed:26813123
Stimulation of Gαq coupled muscarinic receptors leads to activation of phospholipase C and formation of inositol phosphates and other second messengers, which can promote closure of K+ channels, thus facilitating cell excitability PubMed:26813123
Stimulation of Gαq coupled muscarinic receptors leads to activation of phospholipase C and formation of inositol phosphates and other second messengers, which can promote closure of K+ channels, thus facilitating cell excitability PubMed:26813123
Picomolar levels of Abeta can also rescue neuronal cell death induced by inhibition of Abeta generation (by exposure to inhibitors of beta- or gamma-scretases) [160], possibly through regulating the potassium ion channel expression, hence affecting neuronal excitability [161] PubMed:21214928
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