Adenylate cyclase postsynaptic

Postsynaptic, excitatory, activates adenylate cyclase Postsynaptic, depressive, activates adenylate cyclase... 

Postsynaptic, variable effects, stimulates adenylate cyclase Postsynaptic and presynaptic, variable effects, inhibits adenylate cyclase... 

Initially, it was proposed that the 5-HTjb receptor is located exclusively in the brain of the rat and some other rodents, whereas the 5-HTid receptor, a close species homolog, is specific to the guinea pig and higher mammalian species, including humans (Waeber et al., 1989). However, recent studies have characterized the 5-HTiB receptor also in the human brain (Bidmon et al., 2001 Varnas et al., 2005). The 5-HT, B receptor is linked to the inhibition of adenylate cyclase, and is located at presynaptic (5-HT axon terminals) and postsynaptic... 

The second-messenger linkage of postsynaptic 5-HTj receptors has been connected in various neurons with either inhibition of adenylate cyclase, stimulation of adenylate cyclase, or inhibition of phosphoinositide turnover (Harrington et al. 1992]. 

Yocca ED, Iben L, Meller E Lack of apparent receptor reserve at postsynaptic 5-hydroxytryptamine lA receptors negatively coupled to adenyl cyclase activity in rat hippocampal membranes. Mol Pharmacol 41 1066-1072, 1992 Yoney TH, Pigott TA, L Heureux F, et al. Seasonal variation in obsessive-compulsive disorder preliminary experience with light treatment. Am J Psychiatry 148 1727-1729, 1991... 

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... 

Many monoamine neurotransmitters are now thought to work by this receptor-linked second messenger system. In some cases, however, stimulation of the postsynaptic receptors can cause the inhibition of adenylate cyclase activity. For example, D2 dopamine receptors inhibit, while D receptors stimulate, the activity of the cyclase. 

The DA, and DA classification differs from other classifications basedion anatomical locations (presynaptic/postsynaptic) or response (increase in adenylate cyclase/no change in adenylate cyclase excitation/contraction). The subdivision of receptors described in this paper also differs from subdivisions based on the use of binding assays (2). 

Figure 8 Simplified diagram of a signaling cascade that involves NE, BDNF, and CREB after NE acts on the postsynaptic fi-noradrenergic receptor. NE couples to a G protein (Gas), which stimulates the production of cAMP from adenosine triphosphate (ATP). This reaction is catalyzed by adenylate cyclase (AC). cAMP activates protein kinase A (PKA). Inside the cell, PKA phosphorylates (P) the CREB protein, which binds upstream from specific regions of genes and regulates their expression. BDNF is one target of cAMP signaling pathways in the brain. CRE, cyclic AMP regulatory element ER, endoplasmic reticulum, [reprinted from Reference 76 with permission of the author and the publisher, Canadian Medical Association].

Postsynaptically norepinephrine may interact with a- or 3-receptors, which couple with an adenylate (or guanylate) cyclase to initiate postsynaptic events (16,17). Presynaptic a- and 3-receptors have also been implicated in the modulation of transmitter release. While an adenylate cyclase has been associated with the presynaptic 3-receptor, the presynaptic a-receptor appears to be involved only with modulation of Ca++ fluxes (18,19). 

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. 

Strader CD, Pickel VM, Joh TH, Strohsacker MW, Shorr RGL, Lefkowitz RJ, Caron MG (1983) Antibodies to the /8-adrenergic receptor attenuation of catecholamine-sensitive adenylate cyclase and demonstration of postsynaptic receptor localization in brain. Proc. Natl Acad. Scl USA, 80, 1840-1844. 

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