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Acetylcholine also has other effects on neurons. One effect is to cause a slow depolarization[citation needed] by blocking a tonically active K+ current, which increases neuronal excitability. Alternatively, acetylcholine can activate non-specific cation conductances to directly excite neurons.[10] An effect upon postsynaptic M4-muscarinic ACh receptors is to open inward-rectifier potassium ion channel (Kir) and cause inhibition.[11] The influence of acetylcholine on specific neuron types can be dependent upon the duration of cholinergic stimulation. For instance, transient exposure to acetylcholine (up to several seconds) can inhibit cortical pyramidal neurons via M1 type muscarinic receptors that are linked to Gq-type G-protein alpha subunits. M1 receptor activation can induce calcium-release from intracellular stores, which then activate a calcium-activated potassium conductance which inhibits pyramidal neuron firing.[12] On the other hand, tonic M1 receptor activation is strongly
New Page Title Here Home Articles About Ray Peat Products Art Gallery Books/Newsletter Contact --> Links --> Loading --> RayPeat.com ©2006-2025 Ray Peat and Ray Peat Publishing All Rights Reserved --> A R T I C L E The dark side of stress (learned helplessness) ========================================== Acetylcholine is the "neurotransmitter" of cholinergic nerves, including the parasympathetic system. Cholinesterase (or acetylcholinesterase) is an enzyme that destroys acetylcholine, limiting the action of the cholinergic nerves. Attaching a phosphate group to the cholinesterase enzyme in
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