a(MESH:"Dihydro-beta-Erythroidine")

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Name

Dihydro-beta-Erythroidine

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mesh

Namespace Version

20181007

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https://raw.githubusercontent.com/pharmacome/terminology/8ccfed235e418e4c8aa576f9a5ef0f838e794c7f/external/mesh-names.belns

Nicotine self administration is also reduced in rats by dihydro-beta erythroidine (DHbetae), a selective alpha4beta2 antagonist199. in this context, partial agonists may substitute for the desired effects of nicotine and antagonize its reinforcing properties163,200. PubMed:19721446

Nicotine self administration is also reduced in rats by dihydro-beta erythroidine (DHbetae), a selective alpha4beta2 antagonist199. in this context, partial agonists may substitute for the desired effects of nicotine and antagonize its reinforcing properties163,200. PubMed:19721446

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

The up- regulation of nAChRs has also been obtained using nicotinic agonists (cytisine, carbamylcholine and varenicline) [66, 67], antagonists (dihydro-β-erythroidine, mecamylamine) [68-70] and a partial agonist (CC4) PubMed:28901280

For example, DHβE (at nM concentrations) blocks α4β2 and α3β2 nAChRs but is much less potent at α3β4 and α7 nAChRs expressed in Xenopus oocytes (e.g., [134–137]). PubMed:28391535

This conclusion is based on the fact that the stimulus effects of nicotine are convincingly blocked by (a) mecamylamine, a voltage dependent noncompetitive channel blocker at nicotinic receptors (Fig. 3; Table 4) and (b) dihydro-β-erythrodine (DHβE), a nicotinic receptor antagonist that shows high affinity for the nAChR α4β2 subunit (Fig. 3; Table 5) but not by methyllycaconitine (MLA), a α7 nicotinic receptor antagonist (Table 5). PubMed:28391535

Research results summarized in Table 5 indicate that DHβE effectively blocked the stimulus effects of (-)-nicotine in rats or mice (but see exceptions reported by [120, 121]). PubMed:28391535

This conclusion is based on the fact that the stimulus effects of nicotine are convincingly blocked by (a) mecamylamine, a voltage dependent noncompetitive channel blocker at nicotinic receptors (Fig. 3; Table 4) and (b) dihydro-β-erythrodine (DHβE), a nicotinic receptor antagonist that shows high affinity for the nAChR α4β2 subunit (Fig. 3; Table 5) but not by methyllycaconitine (MLA), a α7 nicotinic receptor antagonist (Table 5). PubMed:28391535

This conclusion is based on the fact that the stimulus effects of nicotine are convincingly blocked by (a) mecamylamine, a voltage dependent noncompetitive channel blocker at nicotinic receptors (Fig. 3; Table 4) and (b) dihydro-β-erythrodine (DHβE), a nicotinic receptor antagonist that shows high affinity for the nAChR α4β2 subunit (Fig. 3; Table 5) but not by methyllycaconitine (MLA), a α7 nicotinic receptor antagonist (Table 5). PubMed:28391535

DHβE (Fig. 3) is an alkaloid found in plant seeds of Erythrina and is a competitive nAChR receptor antagonist with a preference for neuronal β2 subtypes PubMed:28391535

DHβE (Fig. 3) is an alkaloid found in plant seeds of Erythrina and is a competitive nAChR receptor antagonist with a preference for neuronal β2 subtypes PubMed:28391535

For example, DHβE (at nM concentrations) blocks α4β2 and α3β2 nAChRs but is much less potent at α3β4 and α7 nAChRs expressed in Xenopus oocytes (e.g., [134–137]). PubMed:28391535

For example, DHβE (at nM concentrations) blocks α4β2 and α3β2 nAChRs but is much less potent at α3β4 and α7 nAChRs expressed in Xenopus oocytes (e.g., [134–137]). PubMed:28391535

For example, DHβE (at nM concentrations) blocks α4β2 and α3β2 nAChRs but is much less potent at α3β4 and α7 nAChRs expressed in Xenopus oocytes (e.g., [134–137]). PubMed:28391535