Adenylate cyclase postsynaptic nerve

As described in Chapter 4, regulatory G proteins act as an intermediate link between receptor activation and the intracellular effector mechanism that ultimately causes a change in cellular activity. In the case of opioid receptors, these G proteins interact with three primary cellular effectors calcium channels, potassium channels, and the adenyl cyclase enzyme.27 At the presynaptic terminal, stimulation of opioid receptors activates G proteins that in turn inhibit the opening of calcium channels on the nerve membrane.65 Decreased calcium entry into the presynaptic terminal causes decreased neurotransmitter release because calcium influx mediates transmitter release at a chemical synapse. At the postsynaptic neuron, opioid receptors are linked via G proteins to potassium channels, and... 

The heart contains primarily postsynaptic /f i-receptors, which cause increased rate and force of contraction when stimulated. This effect appears to be mediated by activation of adenylate cyclase and subsequent generation and accumulation of cAMP. Stimulation of postsynaptic cardiac i -receptors causes a significant increase in contractility without an increase in rate, an effect apparently not mediated by cAMP. The increased contractility is more pronounced at lower heart rates and has a slower onset and longer duration in comparison with /Si-mediated inotropic response. Presynaptic 2-adrenoceptors also are found in the heart and appear to be activated by norepinephrine released by the sympathetic nerve itself. Their activation inhibits further norepinephrine release from the nerve terminal. 

Fig. 24.3. Schematic representation of a 5 enkephalinergic nerve terminal. (1) Pro-opioid proteins (proenkephalin A) are synthesized in the cell nucleus. (2) Pro-opioid proteins undergo microtubular transport to the nerve terminal. (3) Active endogenous opioids (E) are cleaved from the pro-opioid proteins by the action of processing proteases. (4) The active peptides (E) are taken up and stored in presynaptic vesicles. (5) The peptides are released when the presynaptic neuron fires. (6) The endogenous opioid peptides bind to postsynaptic receptors and activate second messenger systems. (7) For all opioid receptors, the second messenger effect is primarily mediated by a G-inhibitory (Gj/o) protein complex, which promotes the inactivation of adenylate cyclase (AC), a decrease in intracellular cyclic-adenosine-3, 5 -monophosphate (cAMP),...

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