Neurotransmitters stimulants

G proteins regulate intracellular concentrations of second messengers. G proteins control intracellular cAMP concentrations by mediating the ability of neurotransmitters to activate or inhibit adenylyl cyclase. The mechanism by which neurotransmitters stimulate adenylyl cyclase is well known. Activation of those neurotransmitter receptors that couple to Gs results in the generation of free G(IS subunits, which bind to and thus directly activate adenylyl cyclase. In addition, free Py-subunit complexes activate certain subtypes of adenylyl cyclase (see Ch. 21). A similar mechanism appears to be the case for G(IO f, a type of G protein structurally related to G that is enriched in olfactory epithelium and striatum (Ch. 50). 

Hint The cholinergic system is another name for the parasympathetic branch because an acetylcholine neurotransmitter stimulates receptor cells to produce a response. The enzyme acetylcholinesterase inactivates the acetylcholine before it reaches the receptor cell. 

Holmes I think the problem is that if the neurones are firing all the time it is not known which transmitter is making them fire and there may be a variety of neurotransmitters stimulating the neurones on which you are testing your drugs later on, i.e., you do not exactly know where you are to begin with. 

PAF biosynthesis via the de novo pathway is thought to be the primary source of the endogenous PAF in unstimulated cells and blood (Fig. 11). Physiological factors such as fatty acids and neurotransmitters stimulate PAF synthesis by this pathway, but, unlike the... 

The remaining step in the process is also a critical one. Somehow the action of the neurotransmitters must cease. If they continue to cross the synapse, or are not removed from the receptors of the postsynaptic cell, they will continue to activate that cell. An overexcited or inhibited nerve cell is not capable of proper function. For example, schizophrenia is a mental disease that is caused by the brain s inability to eliminate excitatory neurotransmitters. The nerve cells continue firing, even when they need not, and the incorrect brain chemistry results in debilitating symptoms such as auditory hallucinations—hearing voices that are not actually there, see also Enzymes Neurotoxins Neurotransmitters Stimulants. 

These results indicated the involvement of the presynaptic cholinergic and/or substance P neurons, where release of the corresponding neurotransmitter stimulated in turn postsynaptic and/or substance P receptors localized on smooth muscles [13, 15, 39, 65, 66]. Activation of these receptors results in muscle contraction. Morphine is also able to inhibit S-HT mediated contraction suggesting that opiate receptors inhibit the 5-HT4-stimulated acetylcholine release [15]. Much less is known about the localization of S-HT -Rs in myenteric nervous of human and other species. In vivo, h-HT -R agonists are clearly prokinetic in both human and dog [44, 67]. In rat, 5-HT4-RS have also been described on vagus nerves in which they trigger depolarization [68]. 

Kow, L. M., Pfaff, D. W. Estrogen effects on neuronal responsiveness to electrical and neurotransmitter stimulation an in vitro study on the ventromedial nucleus of the hypothalamus. Brain Research (1985), 347,1. 

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