Yohimbine

CAS# 146-48-5

Yohimbine

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Quality Control of Yohimbine

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Chemical structure

Yohimbine

3D structure

Chemical Properties of Yohimbine

Cas No. 146-48-5 SDF Download SDF
PubChem ID 8969 Appearance Cryst.
Formula C21H26N2O3 M.Wt 354.44
Type of Compound Alkaloids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name methyl (1S,15R,18S,19R,20S)-18-hydroxy-1,3,11,12,14,15,16,17,18,19,20,21-dodecahydroyohimban-19-carboxylate
SMILES COC(=O)C1C(CCC2C1CC3C4=C(CCN3C2)C5=CC=CC=C5N4)O
Standard InChIKey BLGXFZZNTVWLAY-SCYLSFHTSA-N
Standard InChI InChI=1S/C21H26N2O3/c1-26-21(25)19-15-10-17-20-14(13-4-2-3-5-16(13)22-20)8-9-23(17)11-12(15)6-7-18(19)24/h2-5,12,15,17-19,22,24H,6-11H2,1H3/t12-,15-,17-,18-,19+/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Yohimbine

The peel of Corynante yohimbe

Biological Activity of Yohimbine

DescriptionYohimbine is a potent and relatively nonselective alpha 2-adrenergic receptor (AR) antagonist, with IC50 of 0.6 μM. Yohimbine may augment extinction learning without significant side effects, and as a therapeutic augmentation strategy for exposure therapy in social anxiety disorder. Yohimbine can be used as antagonistic agents against medetomidine-induced diuresis in healthy cats; it inhibits ATP-sensitive K+ channels in mouse pancreatic beta-cells.
Targetsalpha 2-adrenergic receptor | ATPase | Potassium Channel
In vitro

Phentolamine and yohimbine inhibit ATP-sensitive K+ channels in mouse pancreatic beta-cells.[Pubmed: 2282453 ]

Br J Pharmacol. 1990 Sep;101(1):115-20.

1. The effects of phentolamine and Yohimbine on adenosine 5'-triphosphate (ATP)-sensitive K+ channels were studied in normal mouse beta-cells.
METHODS AND RESULTS:
2. In the presence of 3 mM glucose, many ATP-sensitive K+ channels are open in the beta-cell membrane. Under these conditions, phentolamine inhibited 86Rb efflux from the islets. This inhibition was faster with 100 than with 20 microM phentolamine but its steady-state magnitude was similar with both concentrations. Yohimbine (20-100 microM) also inhibited the efflux rate but was not as potent as phentolamine. 3. In the presence of 6 mM glucose, most ATP-sensitive K+ channels are closed in the beta-cell membrane. Their opening by 100 microM diazoxide caused a marked acceleration of 86Rb efflux from the islets. This acceleration was almost entirely prevented by 20 microM phentolamine. It was barely affected by 20 microM Yohimbine and reduced by 50% by 100 microM Yohimbine. 4. ATP-sensitive K+ currents were studied in single beta-cells by the whole cell patch-clamp technique. Phentolamine (20-100 microM) caused a progressive but almost complete and irreversible inhibition of the current. The effects of Yohimbine were faster but smaller; the inhibition was still incomplete with 100 microM Yohimbine. 5. The increase in ATP-sensitive K+ current produced by 100 microM diazoxide was prevented by 100 microM phentolamine but only partially attenuated by 100 microM Yohimbine.
CONCLUSIONS:
6. It is concluded that phentolamine inhibits ATP-sensitive K+ channels in pancreatic beta-cells. This novel effect of phentolamine resembles that of hypoglycaemic sulphonylureas. It may account for previously unexplained effects of the drug. These observations also call for reinterpretation of many studies in which phentolamine was used as an allegedly specific blocker of alpha-adrenoceptors.

In vivo

Yohimbine enhancement of exposure therapy for social anxiety disorder: a randomized controlled trial.[Pubmed: 24237691]

Biol Psychiatry. 2014 Jun 1;75(11):840-6.

Preclinical and clinical trials suggest that Yohimbine may augment extinction learning without significant side effects. However, previous clinical trials have only examined adults with specific phobias. Yohimbine has not yet been investigated in the augmentation of exposure therapy for other anxiety disorders.
METHODS AND RESULTS:
Adults (n = 40) with a DSM-IV diagnosis of social anxiety disorder were randomized to placebo or Yohimbine HCl (10.8 mg) 1 hour before each of four exposure sessions. Outcome measures were collected at baseline, each treatment session, posttreatment, and 1-month follow-up. Yohimbine was well tolerated. Yohimbine augmentation, relative to placebo augmentation, resulted in faster improvement and better outcomes on self-report measures of social anxiety disorder severity (Liebowitz Social Anxiety Scale, d = .53) and depressed mood severity (Beck Depression Inventory, d = .37) but not on the clinician-rated measures (Clinical Global Impressions-Severity Scale, d = .09; Clinical Global Impressions-Improvement Scale, d = .25). Between-group differences on the Liebowitz Social Anxiety Scale were moderated by the level of fear reported at the end of an exposure exercise (end fear), such that the advantage of Yohimbine over placebo was only evident among patients who reported low end fear.
CONCLUSIONS:
The results provide moderate support for Yohimbine as a therapeutic augmentation strategy for exposure therapy in social anxiety disorder, one that may be especially effective when coupled with successful exposure experiences. Beneficial effects for Yohimbine were readily evident for self-report measures but not for clinician-rated outcomes of social anxiety severity and improvement.

The CRF1 receptor antagonist antalarmin attenuates yohimbine-induced increases in operant alcohol self-administration and reinstatement of alcohol seeking in rats.[Pubmed: 17705061 ]

Psychopharmacology (Berl). 2007 Dec;195(3):345-55.

Yohimbine is an alpha-2 adrenoreceptor antagonist that provokes stress- and anxiety-like responses in both humans and laboratory animals. In rats, Yohimbine increases operant alcohol self-administration and reinstates alcohol seeking. In this study, we assess whether these effects of Yohimbine are attenuated by systemic injections of the corticotrotropin-releasing factor 1 (CRF1) receptor antagonist antalarmin.
METHODS AND RESULTS:
In Exp. 1, we trained rats to lever press for alcohol solutions (12% w/v, 1 h/day) over several weeks; during training, the response requirement was increased from a fixed-ratio-1 (FR-1) to a fixed-ratio-3 (FR-3) reinforcement schedule. We then tested the effect of antalarmin (10 or 20 mg/kg) on Yohimbine (1.25 mg/kg)-induced increases in operant alcohol self-administration (FR-3 reinforcement schedule). Subsequently, we assessed the effect of antalarmin on Yohimbine-induced increases in plasma corticosterone levels in the previously self-administering rats. In Exp. 2, we trained the rats to self-administer alcohol as in Exp. 1, and after extinction of the alcohol-reinforced lever responding over 13 days, we tested antalarmin's effect on Yohimbine-induced reinstatement of alcohol seeking. Yohimbine increased operant alcohol self-administration and reinstated alcohol seeking after extinction. These effects of Yohimbine were attenuated by antalarmin. Antalarmin injections in the absence of Yohimbine had no effect on either operant alcohol self-administration or extinction responding. Antalarmin had no effect on Yohimbine-induced corticosterone release in alcohol-experienced rats.
CONCLUSIONS:
These results suggest that extrahypothalamic CRF1 receptors are involved in the effect of Yohimbine on operant alcohol self-administration and on relapse to alcohol seeking and support the notion that CRF1 receptor antagonists should be considered in alcohol addiction treatment.

Protocol of Yohimbine

Animal Research

Antagonistic effects of atipamezole, yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats.[Pubmed: 25356000]

Can J Vet Res. 2014 Oct;78(4):304-15.

This study aimed to investigate and compare the antagonistic effects of atipamezole, Yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats.
METHODS AND RESULTS:
Five cats were repeatedly used in each of the 9 groups. One group was not medicated. Cats in the other groups received 2 mg/kg BW xylazine intramuscularly, and saline (as the control); 160 μg/kg BW prazosin; or 40, 160, or 480 μg/kg BW atipamezole or Yohimbine intravenously 0.5 h later. Urine and blood samples were collected 10 times over 8 h. Urine volume, pH, and specific gravity; plasma arginine vasopressin (AVP) concentration; and creatinine, osmolality, and electrolyte values in both urine and plasma were measured. Both atipamezole and Yohimbine antagonized xylazine-induced diuresis, but prazosin did not. The antidiuretic effect of atipamezole was more potent than that of Yohimbine but not dose-dependent, in contrast to the effect of Yohimbine at the tested doses. Both atipamezole and Yohimbine reversed xylazine-induced decreases in both urine specific gravity and osmolality, and the increase in free water clearance. Glomerular filtration rate, osmolar clearance, and plasma electrolyte concentrations were not significantly altered. Antidiuresis of either atipamezole or Yohimbine was not related to the area under the curve for AVP concentration, although the highest dose of both atipamezole and Yohimbine increased plasma AVP concentration initially and temporarily, suggesting that this may in part influence antidiuretic effects of both agents. The diuretic effect of xylazine in cats may be mediated by α2-adrenoceptors but not α1-adrenoceptors.
CONCLUSIONS:
Atipamezole and Yohimbine can be used as antagonistic agents against xylazine-induced diuresis in clinically normal cats.

Structure Identification
J AOAC Int. 2015 Mar-Apr;98(2):330-5.

Characterization and quantitation of yohimbine and its analogs in botanicals and dietary supplements using LC/QTOF-MS and LC/QQQ-MS for determination of the presence of bark extract and yohimbine adulteration.[Pubmed: 25905738]

The compound Yohimbine HCl has been restricted in Australia and categorized as a scheduled prescription drug in other parts of the world, including the United States where it is monographed as a drug in the U. S. Pharmacopeia. However, the bark of the yohimbe plant and its extract is considered a botanical that can be used as a dietary supplement in some parts of the world. For these reasons, methods to characterize the indole alkaloids of the bark and quantify Yohimbine and its analogs are presented using accurate mass LC/quadrupole time-of-flight (QTOF)-MS and triple quadrupole LC/MS, respectively.
METHODS AND RESULTS:
Samples were extracted with a QuEChERS (Quick, Easy, Cheap, Effective, Rugged, and Safe) method to characterize and quantify the indole alkaloids. With the LC/QTOF-MS in auto MS/MS mode the indole alkaloids were identified, and the isomeric response of each could be used to determine whether the actual bark or extract was in samples of dietary supplements and not adulteration with Yohimbine HCl. Analogs were identified and include yohimbic acid, methyl Yohimbine, and hydroxyl Yohimbine. Many isomers of each were also detected, but identified only by the number of chromatographic peaks. Quantification of Yohimbine and ajmalicine spiked extracts showed recoveries of 99 to 103% with RSD of 3.6% or lower and LODs of less than 100 ppt. Calibration of the two standards gave r(2) = 0.9999 in a range from 0.1 to 100 ppb.
CONCLUSIONS:
Dietary supplements quantified for these two compounds showed a range from not detected to 3x the amounts found in the bark.

Yohimbine Dilution Calculator

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Preparing Stock Solutions of Yohimbine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.8214 mL 14.1068 mL 28.2135 mL 56.427 mL 70.5338 mL
5 mM 0.5643 mL 2.8214 mL 5.6427 mL 11.2854 mL 14.1068 mL
10 mM 0.2821 mL 1.4107 mL 2.8214 mL 5.6427 mL 7.0534 mL
50 mM 0.0564 mL 0.2821 mL 0.5643 mL 1.1285 mL 1.4107 mL
100 mM 0.0282 mL 0.1411 mL 0.2821 mL 0.5643 mL 0.7053 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Yohimbine

Phentolamine and yohimbine inhibit ATP-sensitive K+ channels in mouse pancreatic beta-cells.[Pubmed:2282453]

Br J Pharmacol. 1990 Sep;101(1):115-20.

1. The effects of phentolamine and Yohimbine on adenosine 5'-triphosphate (ATP)-sensitive K+ channels were studied in normal mouse beta-cells. 2. In the presence of 3 mM glucose, many ATP-sensitive K+ channels are open in the beta-cell membrane. Under these conditions, phentolamine inhibited 86Rb efflux from the islets. This inhibition was faster with 100 than with 20 microM phentolamine but its steady-state magnitude was similar with both concentrations. Yohimbine (20-100 microM) also inhibited the efflux rate but was not as potent as phentolamine. 3. In the presence of 6 mM glucose, most ATP-sensitive K+ channels are closed in the beta-cell membrane. Their opening by 100 microM diazoxide caused a marked acceleration of 86Rb efflux from the islets. This acceleration was almost entirely prevented by 20 microM phentolamine. It was barely affected by 20 microM Yohimbine and reduced by 50% by 100 microM Yohimbine. 4. ATP-sensitive K+ currents were studied in single beta-cells by the whole cell patch-clamp technique. Phentolamine (20-100 microM) caused a progressive but almost complete and irreversible inhibition of the current. The effects of Yohimbine were faster but smaller; the inhibition was still incomplete with 100 microM Yohimbine. 5. The increase in ATP-sensitive K+ current produced by 100 microM diazoxide was prevented by 100 microM phentolamine but only partially attenuated by 100 microM Yohimbine. 6. It is concluded that phentolamine inhibits ATP-sensitive K+ channels in pancreatic beta-cells. This novel effect of phentolamine resembles that of hypoglycaemic sulphonylureas. It may account for previously unexplained effects of the drug. These observations also call for reinterpretation of many studies in which phentolamine was used as an allegedly specific blocker of alpha-adrenoceptors.

Yohimbine enhancement of exposure therapy for social anxiety disorder: a randomized controlled trial.[Pubmed:24237691]

Biol Psychiatry. 2014 Jun 1;75(11):840-6.

BACKGROUND: Preclinical and clinical trials suggest that Yohimbine may augment extinction learning without significant side effects. However, previous clinical trials have only examined adults with specific phobias. Yohimbine has not yet been investigated in the augmentation of exposure therapy for other anxiety disorders. METHODS: Adults (n = 40) with a DSM-IV diagnosis of social anxiety disorder were randomized to placebo or Yohimbine HCl (10.8 mg) 1 hour before each of four exposure sessions. Outcome measures were collected at baseline, each treatment session, posttreatment, and 1-month follow-up. RESULTS: Yohimbine was well tolerated. Yohimbine augmentation, relative to placebo augmentation, resulted in faster improvement and better outcomes on self-report measures of social anxiety disorder severity (Liebowitz Social Anxiety Scale, d = .53) and depressed mood severity (Beck Depression Inventory, d = .37) but not on the clinician-rated measures (Clinical Global Impressions-Severity Scale, d = .09; Clinical Global Impressions-Improvement Scale, d = .25). Between-group differences on the Liebowitz Social Anxiety Scale were moderated by the level of fear reported at the end of an exposure exercise (end fear), such that the advantage of Yohimbine over placebo was only evident among patients who reported low end fear. CONCLUSIONS: The results provide moderate support for Yohimbine as a therapeutic augmentation strategy for exposure therapy in social anxiety disorder, one that may be especially effective when coupled with successful exposure experiences. Beneficial effects for Yohimbine were readily evident for self-report measures but not for clinician-rated outcomes of social anxiety severity and improvement.

Antagonistic effects of atipamezole, yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats.[Pubmed:25356000]

Can J Vet Res. 2014 Oct;78(4):304-15.

This study aimed to investigate and compare the antagonistic effects of atipamezole, Yohimbine, and prazosin on xylazine-induced diuresis in clinically normal cats. Five cats were repeatedly used in each of the 9 groups. One group was not medicated. Cats in the other groups received 2 mg/kg BW xylazine intramuscularly, and saline (as the control); 160 mug/kg BW prazosin; or 40, 160, or 480 mug/kg BW atipamezole or Yohimbine intravenously 0.5 h later. Urine and blood samples were collected 10 times over 8 h. Urine volume, pH, and specific gravity; plasma arginine vasopressin (AVP) concentration; and creatinine, osmolality, and electrolyte values in both urine and plasma were measured. Both atipamezole and Yohimbine antagonized xylazine-induced diuresis, but prazosin did not. The antidiuretic effect of atipamezole was more potent than that of Yohimbine but not dose-dependent, in contrast to the effect of Yohimbine at the tested doses. Both atipamezole and Yohimbine reversed xylazine-induced decreases in both urine specific gravity and osmolality, and the increase in free water clearance. Glomerular filtration rate, osmolar clearance, and plasma electrolyte concentrations were not significantly altered. Antidiuresis of either atipamezole or Yohimbine was not related to the area under the curve for AVP concentration, although the highest dose of both atipamezole and Yohimbine increased plasma AVP concentration initially and temporarily, suggesting that this may in part influence antidiuretic effects of both agents. The diuretic effect of xylazine in cats may be mediated by alpha2-adrenoceptors but not alpha1-adrenoceptors. Atipamezole and Yohimbine can be used as antagonistic agents against xylazine-induced diuresis in clinically normal cats.

Potentiation by yohimbine of alpha-adrenoceptor-mediated vasoconstriction in response to clonidine in the rabbit ear vein.[Pubmed:18534573]

Eur J Pharmacol. 2008 Jul 28;589(1-3):201-5.

We investigated the pharmacological profile of the vasoconstrictive response to clonidine in the isolated rabbit ear vein, and compared the characteristics of clonidine with those of noradrenaline and moxonidine. The maximal vasoconstrictive responses to clonidine and moxonidine in the rabbit ear vein were 35.94+/-11.18% and 88.78+/-11.54% of the maximum response to noradrenaline, respectively. Prazosin 0.1 microM inhibited the vasoconstriction induced by lower concentrations of noradrenaline, and the concentration-dependent response curve for noradrenaline was significantly shifted to the right by 1 microM prazosin. Yohimbine (0.1 and 0.5 microM) only decreased the vasoconstrictive response to lower concentrations of noradrenaline, but did not affect the response to higher concentrations. Vasoconstrictive responses to lower but not higher concentrations of clonidine and moxonidine were inhibited by 0.1 microM Yohimbine. In contrast, the same concentration of Yohimbine significantly potentiated the maximal response to a high concentration of clonidine by 24.06%. In isolated rabbit ear vein pretreated with 0.1 microM Yohimbine, prazosin competitively inhibited the concentration-response curve for clonidine with a pA(2) value of 8.05+/-0.06. We conclude that clonidine acts mainly on alpha(2)-adrenoceptors to produce vasoconstriction in the rabbit ear vein; however, in the preparation pretreated with Yohimbine, the clonidine-induced vasoconstriction is mediated via alpha(1)-adrenoceptors and its maximal vasoconstriction is significantly potentiated.

Antagonistic effects of atipamezole, yohimbine and prazosin on medetomidine-induced diuresis in healthy cats.[Pubmed:24107430]

J Vet Med Sci. 2014 Mar 1;76(2):173-82. Epub 2013 Oct 8.

This study aimed to investigate and compare the antagonistic effects of atipamezole, Yohimbine and prazosin on medetomidine-induced diuresis in healthy cats. Five cats were repeatedly used in each of the 9 groups. One group was not medicated. Cats in the other groups received 40 microg/kg medetomidine intramuscularly and saline (as the control), 160 microg/kg prazosin, or 40, 160 or 480 microg/kg atipamezole or Yohimbine intravenously 0.5 hr later. Volume, pH and specific gravity of urine; plasma arginine vasopressin (AVP) level; and creatinine, osmolality and electrolyte levels in both urine and plasma were measured. Both atipamezole and Yohimbine, but not prazosin, antagonized medetomidine-induced diuresis. The antidiuretic effect of atipamezole was more potent than that of Yohimbine, but was not dose dependent, in contrast to the effect of Yohimbine at the tested doses. Both atipamezole and Yohimbine reversed medetomidine-induced decreases in both urine specific gravity and osmolality and increases in plasma osmolality and free-water clearance. Antidiuresis of either atipamezole or Yohimbine was not related to the area under the curve for AVP level, although the highest dose of both atipamezole and Yohimbine initially and temporarily increased plasma AVP levels, suggesting that this may partly influence the antidiuretic effects of both agents. The diuretic effect of medetomidine in cats may be mediated by alpha2-adrenoceptors, but not alpha1-adrenoceptors. Atipamezole and Yohimbine can be used as antagonistic agents against medetomidine-induced diuresis in healthy cats.

Characterization and quantitation of yohimbine and its analogs in botanicals and dietary supplements using LC/QTOF-MS and LC/QQQ-MS for determination of the presence of bark extract and yohimbine adulteration.[Pubmed:25905738]

J AOAC Int. 2015 Mar-Apr;98(2):330-5.

The compound Yohimbine HCl has been restricted in Australia and categorized as a scheduled prescription drug in other parts of the world, including the United States where it is monographed as a drug in the U. S. Pharmacopeia. However, the bark of the yohimbe plant and its extract is considered a botanical that can be used as a dietary supplement in some parts of the world. For these reasons, methods to characterize the indole alkaloids of the bark and quantify Yohimbine and its analogs are presented using accurate mass LC/quadrupole time-of-flight (QTOF)-MS and triple quadrupole LC/MS, respectively. Samples were extracted with a QuEChERS (Quick, Easy, Cheap, Effective, Rugged, and Safe) method to characterize and quantify the indole alkaloids. With the LC/QTOF-MS in auto MS/MS mode the indole alkaloids were identified, and the isomeric response of each could be used to determine whether the actual bark or extract was in samples of dietary supplements and not adulteration with Yohimbine HCl. Analogs were identified and include yohimbic acid, methyl Yohimbine, and hydroxyl Yohimbine. Many isomers of each were also detected, but identified only by the number of chromatographic peaks. Quantification of Yohimbine and ajmalicine spiked extracts showed recoveries of 99 to 103% with RSD of 3.6% or lower and LODs of less than 100 ppt. Calibration of the two standards gave r(2) = 0.9999 in a range from 0.1 to 100 ppb. Dietary supplements quantified for these two compounds showed a range from not detected to 3x the amounts found in the bark.

The CRF1 receptor antagonist antalarmin attenuates yohimbine-induced increases in operant alcohol self-administration and reinstatement of alcohol seeking in rats.[Pubmed:17705061]

Psychopharmacology (Berl). 2007 Dec;195(3):345-55.

RATIONALE AND OBJECTIVES: Yohimbine is an alpha-2 adrenoreceptor antagonist that provokes stress- and anxiety-like responses in both humans and laboratory animals. In rats, Yohimbine increases operant alcohol self-administration and reinstates alcohol seeking. In this study, we assess whether these effects of Yohimbine are attenuated by systemic injections of the corticotrotropin-releasing factor 1 (CRF1) receptor antagonist antalarmin. MATERIALS AND METHODS: In Exp. 1, we trained rats to lever press for alcohol solutions (12% w/v, 1 h/day) over several weeks; during training, the response requirement was increased from a fixed-ratio-1 (FR-1) to a fixed-ratio-3 (FR-3) reinforcement schedule. We then tested the effect of antalarmin (10 or 20 mg/kg) on Yohimbine (1.25 mg/kg)-induced increases in operant alcohol self-administration (FR-3 reinforcement schedule). Subsequently, we assessed the effect of antalarmin on Yohimbine-induced increases in plasma corticosterone levels in the previously self-administering rats. In Exp. 2, we trained the rats to self-administer alcohol as in Exp. 1, and after extinction of the alcohol-reinforced lever responding over 13 days, we tested antalarmin's effect on Yohimbine-induced reinstatement of alcohol seeking. RESULTS: Yohimbine increased operant alcohol self-administration and reinstated alcohol seeking after extinction. These effects of Yohimbine were attenuated by antalarmin. Antalarmin injections in the absence of Yohimbine had no effect on either operant alcohol self-administration or extinction responding. Antalarmin had no effect on Yohimbine-induced corticosterone release in alcohol-experienced rats. CONCLUSIONS: These results suggest that extrahypothalamic CRF1 receptors are involved in the effect of Yohimbine on operant alcohol self-administration and on relapse to alcohol seeking and support the notion that CRF1 receptor antagonists should be considered in alcohol addiction treatment.

Description

Yohimbine is a potent and relatively nonselective alpha 2-adrenergic receptor (AR) antagonist, with IC50 of 0.6 μM.

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