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Acetylcholine receptor-inducing activity

Corfas G, Fischbach GD. 1993. The number of Na+ channels in cultured chick muscle is increased by ARIA, an acetylcholine receptor-inducing activity. J Neurosci 13 2118-2125. [Pg.260]

Abbreviations used in this chapter AChR, acetylcholine receptor ANP, atrial natriuretic peptide ARIA, acetylcholine receptor-inducing activity AzC, L-azetidine CGRP, calcitonin gene related peptide 3,4 DHP, 3,4-dehydro-1-proline EDHB, ethyl-3,4-dihydroxybenzoate PCB, polychlorinated biphenyl. [Pg.42]

Numerous studies have shown that the level of surface AChR increases in muscle cells in response to neural tissue and brain extracts (Neugebauer et al., 1985 Buc-Caron et al., 1983 Jessel et al., 1979). One such factor, ascorbic acid, increases the surface AChR level in rat-derived cloned L5 muscle cells (Knaack et al., 1986 Knaack and Podleski, 1985). Other factors, acetylcholine receptor-inducing activity (ARIA) and calcitonin gene related peptide (CGRP) also increase the sur-... [Pg.46]

Cronan T, Conrad J, et al (1985) Effects of chronically administered nicotine and sahne on motor activity in rats. Pharmacol Biochem Behav 22(5) 897-899 Curtis L, Buisson B, et al (2002) Potentiation of human alpha4beta2 neuronal nicotinic acetylcholine receptor by estradiol. Mol Pharmacol 61(1) 127-135 Dalton JC, Vickers GJ, et al (1986) Increased self-administration of cocaine following haloperidol sex-dependent effects of the antiestrogen tamoxifen. Pharmacol Biochem Behav 25(3) 497-501 Damsma G, Day J, et al (1989) Lack of tolerance to nicotine-induced dopamine release in the nucleus accumbens. Eur J Pharmacol 168(3) 363-368 Di Chiara G, Imperato A (1988) Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA 85(14) 5274-5278... [Pg.285]

Beside this there are some major differences with the neurotransmission in the autonomous nervous system The contractile activity of the skeletal muscle is almost completely dependent on the innervation. There is no basal tone and a loss of the innervation is identical to a total loss in function of the particular skeletal muscle. In contrast to the target organs of the parasympathetic nervous system the skeletal muscle cells only have acetylcholine receptors at the site of the so-called end-plate, the connection between neuron and muscle cell with the rest of the cell surface being insensitive to the transmitter. The release of acetylcholine results in a postjunctional depolarization which is either above the threshold to induce an action potential and a contraction or below the threshold with no contractile response at all. In contrast to the graduated reactions of the parasympathetic target organs, this is an all or nothing transmission. [Pg.297]

Ramelteon is a hypnotic with melatonin receptor agonist activity targeting melatonin MTj and MT2 receptors. It has not been proven to induce dependence. As with zolpidem and zaleplon, no known anxiolytic properties have been elicited. No appreciable activity on serotonin, dopamine, GABA, or acetylcholine is present with the parent compound, but in vitro studies report that its primary metabolite M-II has weak 5-HT2g receptor agonist activity. [Pg.78]

FIGURE 21.3 Action of class I and II cocaine-displaceable aptamers The effect of cocaine-displaceable aptamers 1-14 and II-3 on carbamoylcholine (lOOpM)-induced stimulation of acetylcholine receptor activity in the absence (control) and presence of cocaine was determined in vitro by fast kinetic electrophysiology. Aptamer 1-14 (0.5 pM) inhibited receptor activity (left panel) aptamer II-3 (5 pM) does not inhibit receptor activity (middle panel) aptamer II-3 (3 pM) alleviates inhibition of receptor function by cocaine (150 pM) (right panel). Prediction of the secondary structure [26] revealed the localization of consensus motifs of class-I and -II aptamers in stem-loop regions (letters in boxes). These stem loops are believed to be necessary for aptamer action. The figure reveals the data published in references [18, 19, 74]. [Pg.509]

The modes of action of different alkaloids are diverse. For example, nicotine binds to and affects nicotinic acetylcholine receptors and shows toxicity. A recent molecular 3D model suggests that both acetylcholine and nicotine bind to the same pocket formed in a nicotinic acetylcholine receptor.15 Morphine binds to and activates opioid receptors, transmembrane-spanning G protein-coupled receptors, in the central nervous system of humans.16 Caffeine, which is structurally similar to adenine, inhibits cyclic AMP phosphodiesterase activity and inhibits the degradation of cAMP, thus exerting a toxic effect on insects 17 in human beings, binding of caffeine to the adenosine A2A receptor induces wakefulness.18 Atropine binds to muscarinic acetylcholine receptors, competing with acetylcholine, and blocks neurotransmission.1... [Pg.340]

Worsening parkinsonism was observed in two patients after treatment with olanzapine 5 mg/day (114). In contrast, coarse tremors induced by fluphenazine or haloper-idol disappeared in three patients within days of the start of treatment with olanzapine (10 mg/day), without discontinuation or reduction in the dosage of fluphenazine or haloperidol (115). Olanzapine is active at muscarinic cholinergic receptors, which may account for the observed suppression of neuroleptic drug-induced tremor however, two of the three patients had been taking ben-zatropine, an antagonist at muscarinic acetylcholine receptors, with little tremor relief, suggesting that olanzapine could suppress tremor by means of an action other than muscarinic blockade. [Pg.310]

The nereistoxin analogs (cartap hydrochloride, bensultap, and thiocyclam) are all proinsecticides that must be activated in vivo to become nereistoxin (see Chapter 4, subsection 4.2.12.8 for nereistoxin structure). Nereistoxin acts as an antagonist of the acetylcholine receptor. Unlike with nicotine, insects treated with nereistoxin are rapidly immobilized without convulsive symptoms, possibly because nereistoxin does not induce depolarization (Corbett et al., 1984). [Pg.131]


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Acetylcholine activation

Acetylcholine activity

Acetylcholine receptor-inducing activity ARIA)

Acetylcholine receptors

Active receptor

Receptor activation

Receptor activity

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