Acetylcholine mediated signal transduction

D2-like receptors couple mainly to Gi/o proteins, as mentioned above. However, there is no direct evidence to support this coupling for the release-modulating autoreceptors. Moreover, the subsequent intracellular signal transduction has never been studied directly in axon terminals. Mouse AtT-20 pituitary cells, which release acetylcholine and adrenocorticotropic hormone, have been used as a model for axon terminals. When expressed in these cells, D3 receptors mediated inhibition of P/Q-type calcium channels and activation of G protein-coupled inward rectifier potassium channels (Kuzhikandathil et al. 1998 Kuzhikandathil and Oxford 1999). Both would explain the autoreceptor-mediated inhibition of dopamine exocytosis. 

Endogenous opioid receptors have been identified, cloned, and sequenced. They are members of the trimeric G-protein-binding superfamily, which are coupled to signal transduction via adenyl cyclase, and to Ca and ion-channel transport. Three major receptor subtypes are known (mu, kappa, and delta). Mu (p) receptor activation results in sedation, euphoria (via dopamine release), analgesia, respiratory depression, and GI dysmoflity. Kappa (k) receptors mediate spinal analgesia, miosis (via acetylcholine... 

The acetylcholine receptors control ion channels and thus facilitate the propagation of an arriving action potential and the depolarisation of a postsynaptic target cell. Whereas the muscarinic receptor-type (mAChR) is coupled to a G-protein (guanosine nudeotide-binding membrane protein), which mediates the intracellular signal transduction to open an ion channel, the nicotinic acetylcholine receptor (nAChR) itself is an ion channel, operated by the ligand interaction directly. [126]... 

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