有没有不可兴奋细胞?不可兴奋细胞的膜电位与那些可兴奋细胞的膜电位差不多的?不可兴奋细胞维持这种外正内负膜电位有何意义?

有没有不可兴奋细胞?不可兴奋细胞的膜电位与那些可兴奋细胞的膜电位差不多的?不可兴奋细胞维持这种外正内负膜电位有何意义?
有没有不可兴奋细胞?不可兴奋细胞的膜电位与那些可兴奋细胞的膜电位差不多的?
不可兴奋细胞维持这种外正内负膜电位有何意义?

有没有不可兴奋细胞?不可兴奋细胞的膜电位与那些可兴奋细胞的膜电位差不多的?不可兴奋细胞维持这种外正内负膜电位有何意义?
有不可兴奋细胞
Non-Excitable Cells
These are cells which cannot propagate action potential.
Fibroblasts
These are connective tissue cells.They are located in the interstitial space between myocytes,providing structure and support for the heart muscle.
Adipocites
These cells make up the fat layer that surrounds and cushions the heart.
Endothelial Cells
These are cells that line the inside of arteries,veins and form the walls of capillaries.Though initially thought that these cells served no particular purpose,it has been recently shown that these cells release special chemicals which can affect other cells within the vessel wall (smooth muscle cells) and cells in the blood stream.
膜还是不太一样的,它没有电压门控性的Na+ or Ca2+通道
Non-excitable cell types are characterized by an inability to generate all-or-none action potentials in response to depolarizing stimuli due to a lack of voltage-gated Na+ or Ca2+ channels (Rink & Jacob,1989; Fewtrell,1993; Clapham,1995; Berridge,1997).Consequently,membrane potential changes are proposed to influence [Ca2+]i responses mainly by altering the driving force for Ca2+ entry through ligand-gated or second messenger-operated channels.Indeed,several reports have shown that depolarization results in a decrease in [Ca2+]i and hyperpolarization causes an increase of [Ca2+]i during activation of mast cells,lymphocytes and related cell lines (Penner et al.1988; Lewis & Cahalan,1989; Demaurex et al.1992).
Previous electrophysiological recordings from rat bone marrow-derived megakaryocytes have failed to detect voltage-dependent inward currents,which implies that this is a non-excitable cell type (Uneyama et al.1993a; Somasundaram & Mahaut-Smith,1994; Hussain & Mahaut-Smith,1998).We now report that,during stimulation of metabotropic purinoceptors,membrane depolarization evokes an increase in [Ca2+]i,primarily due to release of Ca2+ from intracellular stores.Brief reports of this work have appeared elsewhere in abstract form (Mahaut-Smith et al.1998a,b).