Messengers cascades

The train of events from sender to receiver is seen as following the sequence C + L = L (transmission) => L + C => L-VNOR. At the last step, the G-protein linkage induces the second messenger cascade whose amplification triggers the appropriate ion-channel (Chaps. 5 and 7). The role of the carrier(s) at either end of the transmission sequence is gradually emerging, but without any consensus on their exact contribution, or even on whether they are a crucial component for information transfer (Tegoni et al., 2000). 

Odorant recognition initiates a second-messenger cascade leading to the depolarization of the neuron and the generation of action potentials 821 Negative-feedback processes mediate adaptation of the olfactory transduction apparatus to prolonged or repetitive stimulation 823 Alternative second-messenger pathways maybe at work in olfactory transduction 823... 

The receptors start a second messenger cascade that is initiated by activation of G-proteins in the cell. These, in turn, interact with membrane-bound adenylyl cyclase, which catalyzes the formation of cyclic adenine monophosphate (cAMP) and opening of cAMP-gated cation channels. Depolarization then brings about an action potential, which travels along the axon of the olfactory sensory neuron. Many of the molecular components of this cascade are olfactoiy specific. 

Second messenger cascades in insect sensory cells... 

Second messenger cascades in vomeronasal sensory cells Although the functional implications of the PLC/IP3 cascade in olfactory neurons of nasal epithelium remains mysterious, there is mounting evidence that phospholipase C is a key enzyme for signal transduction in chemosensory neurons... 

G proteins are another family of membrane proteins believed to modulate mechanochemical transduction pathways. Mechanical stimulation changes the conformation of G protein that leads to growth-factorlike changes that initiate secondary messenger cascades leading to cell growth. It has been reported that cyclic strain of smooth muscle cells significantly decreased steady-state levels of G protein and adenylate cyclase activity. Muscular stimulation also appears to be coupled with G protein activation in small arteries. 

Acetylcholine receptors (AChRs) are of two types muscarinic (mAChR) and nicotinic (nAChR) based on the agonist activities of the natural alkaloids, muscarine and nicotine, respectively. These receptors are functionally different. The muscarinic type being G-protein coupled receptors mediate a slow metabolic response via second messenger cascades, while the nicotinic type are ligand-gated ion channels, which mediate a fast synaptic transmission of the neurotransmitter. Skeletal muscles are enriched with nAChRs and are devoid of mAChRs. 

More recent research has focused on examining underlying commonalities in the biochemical actions of the mood stabilizers used to treat bipolar disorder (Zhou et al., 2005), in studies of postmortem brain tissue (Post et al., 2003), and in signal transduction pathways and regulation of gene expression (Bezchlibnyk and Young, 2002). For example, altered levels or function of G-protein alpha subunits and protein kinase A and C have been found in bipolar patients, as well as disruption in second messenger cascades such as the ERK/MAPK pathways. 

Smooth muscle exhibits very diverse behaviors depending on which control mechanisms are present. Vascular smooth muscle, for example, lacks fast voltage-dependent Na+ or Ca + channels and so does not have action potentials or Ca + spikes. It has slow voltage-dependent Ca + channels that admit calcium in a graded fashion in response to fluctuations in membrane potential induced by humoral or transmitter effects on membrane ion conductances, and it has several membrane receptor-initiated second-messenger cascades that control Ca " " entry and Ca + release from its limited SR, and which moderate the effectiveness of Ca +. Vascular smooth muscle contraction is thus tonic rather than phasic, and is very dependent on extracellular Ca + therefore Ca + channel blockers effectively inhibit contraction. In contrast, gut smooth muscle does have fast voltage-dependent channels sufficient to produce action potentials and more SR than vascular smooth muscle, and also has gap junctions through which ion fluxes can occur. It also has receptor-mediated Ca +... 

Functional evidence also suggests that the adenylyl cyclase second messenger cascade in the cerebellum may be involved in cannabinoid withdrawal. An intrac-erebellar infusion of the cAMP blocker Rp-8Br-cAMPs reduced several behavioral... 

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