Erysodine
Erysodine is a blood-brain barrier-permeable nicotinic acetylcholine receptor (nAChR) ligand with high affinity for α4β2 nAChR, Ki = 5 nM, and it blocks nicotine-induced dopamine release and behavioral effects through competitive inhibition. Erysodine is useful for studies on alcohol dependence.
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- CAS No.: 7290-03-1
- Formule: C18H21NO3
- Masse moléculaire:299.37
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
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Activité biologique
Description
IC50 & Target
[4]|
nAChR 5 nM (Ki) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| IMR-32 | IC50 |
7 μM
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Inhibition of (-)-nicotine-induced 86Rb+ efflux from IMR-32 human neuroblastoma cells measured by 86Rb+ efflux assay.
Inhibition of (-)-nicotine-induced 86Rb+ efflux from IMR-32 human neuroblastoma cells measured by 86Rb+ efflux assay.
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7498257 |
In Vitro
Erysodine (3 h) exhibits significantly lower affinity for α-bungarotoxin-sensitive neuronal nicotinic acetylcholine receptor subtypes in rat brain compared to its affinity for the α4β2 subtype labeled by [3H]cytisine, with a Ki value of 4000 nM[1].
Erysodine (7 μM) is a functional antagonist of nicotinic acetylcholine receptor-mediated cation efflux in IMR-32 human neuroblastoma cells[1].
Erysodine is a potent competitive antagonist of the α4β2 nicotinic acetylcholine receptor, with a Ki of 5 nM for the displacement of [3H]-cytisine in brain membrane fractions[4].
Erysodine potently blocks acetylcholine-induced activation of α4β2 nicotinic acetylcholine receptor currents, with an IC50 of 20 nM[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Parmacokinetics
In Vivo
Erysodine (30 μmol/kg; i.p.; administered 5 min before (-)-nicotine challenge) penetrates the blood-brain barrier in Wistar rats and completely blocks the biphasic effects (initial inhibition, subsequent excitation) of (-)-nicotine on locomotor activity and rearing behavior[1].
Erysodine (0.3-10 mg/kg; s.c.; administered 15 min before testing) is a surmountable competitive antagonist of the nicotine discriminative stimulus, producing up to a 9-fold rightward shift in nicotine potency at a dose of 1.0 mg/kg, with minimal disruption of operant response rates[3].
Erysodine (0.32-32 mg/kg; s.c.; administered 15 min before the 90-min test session) dose-dependently and selectively reduces nicotine self-administration behavior under a fixed-ratio 5 schedule, with the maximum effect at the highest tested dose being comparable to full nicotine antagonism[3].
Erysodine (0.1-10 mg/kg; s.c.; administered 15 min before the 3 h test session) dose-dependently reduces the progressive ratio breakpoint for nicotine self-administration, without producing nonspecific effects on response latency during the test session[3].
Erysodine (1.5-8 mg/kg; i.p.; once daily for 3 consecutive days) dose-dependently reduces voluntary ethanol intake and ethanol preference in alcohol-preferring UChB rats, with a daily dose of 8.0 mg/kg decreasing ethanol intake by an average of 66% during the treatment period and the initial post-dosing phase[4].
Erysodine (10 mg/kg; i.p.; single injection) does not alter locomotor activity in healthy male Sprague-Dawley rats, indicating that the previously observed reduction in ethanol intake is not due to a motor-impairing effect of this compound[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD-1 mice (Male, 30-35 g)[1]
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Dosage:3 μmol/kg; 10 μmol/kg; 30 μmol/kg
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Administration:i.p.; 5 min prior to (-)-nicotine challenge
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Result:Showed no significant nicotine-induced hypothermia in mice pretreated with 10 μmol/kg or 30 μmol/kg erysodine.
Attenuated the tendency for (-)-nicotine to reduce locomotor activity at 30 μmol/kg.
Did not alter time spent in the open arms of the elevated plus-maze on its own at 30 μmol/kg, but fully blocked the anxiolytic-like increase in open arm time induced by (-)-nicotine.
Reached 58 ng/g brain levels and 21 ng/mL plasma levels at 15 minutes after 10 μmol/kg i.p. administration.
Reached 92.2 ng/g brain levels and 30.5 ng/mL plasma levels immediately after elevated plus-maze testing.
Showed no obvious toxicities following administration of 30 μmol/kg erysodine.
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Animal Model:Wistar rats (Male, 250-300 g)[1]
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Dosage:30 μmol/kg
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Administration:i.p.; 5 min prior to (-)-nicotine challenge
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Result:Did not significantly alter rearing behavior at the 10 min (maximal nicotine-induced locomotor suppression) or 40 min (maximal nicotine-induced locomotor stimulation) post-nicotine time points.
Prevented the early developing (-)-nicotine-induced decrease in both horizontal activity and rearing at 10 min, and also prevented the late developing (-)-nicotine-induced increase in both horizontal activity and rearing at 40 min.
Reached 280 ng/g brain concentrations at 10 min and 306 ng/g at 40 min post-administration, with a corresponding brain:plasma ratio of 1.5 at 10 min.
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Animal Model:Sprague-Dawley rats (adult male, initial weight 250-275 g, held at ~350 g via restricted feeding during training)[3]
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Dosage:0.3 mg/kg; 1.0 mg/kg; 10 mg/kg
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Administration:s.c.; 15 min prior to test sessions
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Result:Produce a dose-dependent, complete blockade of the nicotine discriminative stimulus when co-administered with 0.4 mg/kg nicotine training dose, and 10 mg/kg administered alone does not substitute for nicotine.
Shift the nicotine dose-response curve ~6-fold rightward at 0.3 mg/kg, resulting in a nicotine ED50 of 0.31 mg/kg.
Shift the nicotine dose-response curve ~9-fold rightward at 1.0 mg/kg, resulting in a nicotine ED50 of 0.43 mg/kg.
Cause no substantial reductions in session response rates for most erysodine + nicotine combinations.
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Animal Model:Long-Evans rats (adult male, initial weight 250-275 g)[3]
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Dosage:0.32 mg/kg; 3.2 mg/kg; 32 mg/kg
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Administration:s.c.; 15 min prior to 90-minute test sessions
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Result:Produce a dose-dependent reduction in nicotine self-administration that selectively decreases nicotine-reinforced responding without affecting food-maintained response rates.
Reach a maximal decrease of ~50-60% in nicotine self-administration, matching the level of reduction observed during saline extinction conditions.
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Animal Model:Long-Evans rats (adult male)[3]
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Dosage:0.1 mg/kg; 0.32 mg/kg; 1.0 mg/kg; 3.2 mg/kg; 10 mg/kg
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Administration:s.c.; 15 min prior to 3-hour test sessions
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Result:Produce dose-dependent decreases in progressive-ratio break points relative to vehicle control (mean vehicle break point 54.6), with break points reduced to a mean of 43.1 at 10 mg/kg.
Do not systematically alter latencies to complete the first, fifth, or break-point infusions.
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Animal Model:Wistar-UChB rats (Adult male, 250-300 g body weight, alcohol-preferring, two-bottle 24 h free choice access paradigm)[4]
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Dosage:1.5 mg/kg; 2.0 mg/kg; 4.0 mg/kg; 8.0 mg/kg
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Administration:i.p.; per day; 3 consecutive days
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Result:Produced a dose-dependent reduction in ethanol consumption.
Reduced average 3-day treatment ethanol intake by 23% at 1.5 mg/kg, with reduction in ethanol intake observed only on the third day of treatment.
Reduced average 3-day treatment ethanol intake by 29% at 2.0 mg/kg, with reduction in ethanol intake observed only on the second day of treatment.
Reduced average ethanol intake by 45% over the treatment period and the first post-treatment day at 4.0 mg/kg, with reductions in ethanol preference seen during the second and third treatment days and first post-treatment day.
Reduced average ethanol intake by 66% over the full treatment period and first post-treatment day at 8.0 mg/kg, with reductions in ethanol preference observed across all 3 treatment days and the first post-treatment day.
Showed no observable signs of animal discomfort in treated rats.
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Animal Model:Sprague-Dawley rats (Male, healthy)[4]
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Dosage:10 mg/kg
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Administration:i.p.; single injection
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Result:Showed cumulative total distance traveled and time-course locomotor activity after 10 mg/kg administration equivalent to that of saline-treated control animals.
Chemical Information
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CAS No. 7290-03-1
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Masse moléculaire 299.37
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Formule C18H21NO3
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SMILES
O(C)[C@@H]1C[C@]23C=4C(CCN2CC=C3C=C1)=CC(O)=C(OC)C4
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Structure Classification
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[3]. Mansbach RS, et al. Effects of the competitive nicotinic antagonist erysodine on behavior occasioned or maintained by nicotine: comparison with mecamylamine. Psychopharmacology. 2000 Feb;148(3):234-42. [Content Brief]
[4]. Quiroz G, et al. Erysodine, a competitive antagonist at neuronal nicotinic acetylcholine receptors, decreases ethanol consumption in alcohol-preferring UChB rats. Behavioural brain research. 2018 Sep 03;349:169-176. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Erysodine Related Classifications
HY-N21834 Related Classifications
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