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FIGURE 25 (A) Ionotropic receptors and mechanisms of fast EPSPs: (A1) Fast EPSPs are produced by the binding of transmitter to specialized receptors that are directly associated with an ion channel (i.e., a ligand-gated channel); when the receptors are unbound, the channel is closed. (A2) Binding of transmitter to the receptor produces a conformational change in the channel protein such that the channel opens. In this example, the channel opening is associated with a selective increase in the permeability to Na+ and K+. The increase in permeability results in the EPSP shown in A3. The duration of the EPSP is directly related to the time that the transmitter remains bound to the receptor. (B) Metabotropic receptors and mechanisms of slow EPSPs; unlike fast EPSPs that are due to the binding of a transmitter with a receptor-channel complex, slow EPSPs involve the activation of receptors (metabotropic) that are not directly coupled to the channel. Rather, the coupling takes place through the activation of one of several second-messenger cascades (in this example, the cAMP cascade). Binding (B) of the transmitter to the receptor leads to activation of a G protein (G) and adenylyl cyclase (AC). The synthesis of cAMP is increased, cAMP-dependent protein kinase (PKA) is activated, and a channel protein is phosphorylated. The phosphorylation leads to closure of the channel; the subsequent depolarization associated with the slow EPSP is shown in panel B3. The decay of the response is due to both the breakdown of cAMP by cAMP-dependent phosphodiesterase and the removal of phosphate from channel proteins by protein phosphatases (not shown).

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