Depolarization Induced Hydrolysis of Cytoplasmic ACh in Mouse Brain
Acetylcholine (ACh) release occurs from cholinergic nerve endings in brain by different processes. Spontaneous ACh release, for example, appears to occur primarily from the cytosol by a Ca2+ independent process (5–7) and may be synthesized by a soluble, cytoplasmic form of choline-O-acetyltransferase (EC 22.214.171.124, ChAT) (3). In contrast, the evoked form of ACh release appears to occur from a vesicular fraction by a Ca2+ dependent process (6–9, 18) and it may be synthesized by a membrane-bound form of ChAT closely associated with the vesicular fraction (1–3, 17). Recent reports suggest that the Ca2+ dependent and Ca2+ independent forms of ACh release differ in yet another respect. Depolarization of brain tissue only stimulates the Ca2+ dependent, not the Ca2+ independent form of ACh release (9, 13–14). That depolarization of brain tissue is unable to stimulate the Ca2+ independent release of ACh is difficult to reconcile with the finding that high K+ induced depolarization of brain tissue not only lowers the ACh content of the vesicular fraction but also lowers the ACh content of the cytoplasmic fraction (16). One might expect that elevated K+ would exclusively lower the level of vesicular ACh since it only stimulates the Ca2+ dependent form of ACh release. One possible explanation for the K+ induced reduction of cytoplasmic ACh in the absence of a corresponding stimulation of Ca2+ independent ACh release is that high K+ may cause the hydrolysis of cytoplasmic ACh and thereby lower its level.
KeywordsAChE Inhibitor Subcellular Level Independent Form Cytoplasmic Pool Mouse Forebrain
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