fluoxetine has been researched along with Alcohol Drinking in 37 studies
Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.
fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.
N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.
Alcohol Drinking: Behaviors associated with the ingesting of ALCOHOLIC BEVERAGES, including social drinking.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Here, we utilized a rat model of 14-daily administration of the SSRI fluoxetine (10 mg/kg/day) along alcohol self-administration deprivation to study the effects of fluoxetine cessation on neuroinflammation after resuming alcohol drinking." | 8.02 | Sudden cessation of fluoxetine before alcohol drinking reinstatement alters microglial morphology and TLR4/inflammatory neuroadaptation in the rat brain. ( Alén, F; Aranda, J; Fernández-Arjona, MDM; Pavón, FJ; Rivera, P; Rodríguez de Fonseca, F; Rubio, L; Serrano, A; Serrano-Castro, PJ; Smith-Fernández, I; Suárez, J, 2021) |
| "The selective serotonergic agonist fluoxetine has demonstrated efficacy in the treatment of depression and has possible efficacy in the treatment of nondepressed and depressed alcoholics." | 5.08 | Preliminary report: double-blind, placebo-controlled study of fluoxetine in depressed alcoholics. ( Black, A; Cornelius, JR; Cornelius, MD; Ehler, JG; Jarrett, PJ; Levin, RL; Mann, JJ; Perel, JM; Salloum, IM, 1995) |
| "The selective serotonergic medication fluoxetine has demonstrated efficacy in the treatment of major depression and has suggested efficacy in the treatment of alcoholism." | 5.08 | Fluoxetine in depressed alcoholics. A double-blind, placebo-controlled trial. ( Black, A; Cornelius, JR; Cornelius, MD; Ehler, JG; Jarrett, PJ; Perel, JM; Salloum, IM; Thase, ME, 1997) |
| "The effects of fluoxetine, a relatively selective long-acting serotonin uptake inhibitor, on the consumption of alcoholic and nonalcoholic drinks, cigarette smoking, and body weight were assessed in 29 men who were early stage problem drinkers." | 5.06 | Fluoxetine differentially alters alcohol intake and other consummatory behaviors in problem drinkers. ( Kadlec, KE; Naranjo, CA; Sanhueza, P; Sellers, EM; Woodley-Remus, D, 1990) |
| "Naltrexone (NTX) and fluoxetine (FLU) are useful for treating alcoholism and depression, respectively." | 3.69 | Combination of naltrexone and fluoxetine on rats' propensity to take alcoholic beverage. ( Cavallaro, CA; Chattophadyay, S; Gardell, LR; Hubbell, CL; Reid, LD; Whalen, CA, 1997) |
| "fluoxetine treatment induced a long-lasting increase in alcohol consumption during relapse, an effect that was not observed in the case of bupropion treatment." | 1.51 | Bupropion, a possible antidepressant without negative effects on alcohol relapse. ( Alen, F; Antón, M; Arco, R; Ballesta, A; de Fonseca, FR; de Heras, RG; Nogueira-Arjona, R; Orio, L; Pavón, FJ; Ramírez-López, M; Romero-Sanchiz, P; Serrano, A; Suárez, J; Vargas, A, 2019) |
| "Fluoxetine treatment was shown to cause a locomotor sensitized response to a challenge dose of amphetamine (0." | 1.39 | Increased alcohol consumption in rats after subchronic antidepressant treatment. ( Alén, F; de Fonseca, FR; de Heras, RG; Gorriti, MÁ; Orio, L; Pozo, MÁ; Ramírez-López, MT, 2013) |
| "Fluoxetine was associated with an increased risk of isolated ventricular septal defects (adjusted OR 2." | 1.37 | Selective serotonin reuptake inhibitors and risk for major congenital anomalies. ( Artama, M; Gissler, M; Malm, H; Ritvanen, A, 2011) |
| "Treatment with fluoxetine resulted in a dose-dependent decrease in saccharin intake to, but not below, the normal level of their DFI." | 1.30 | Fluoxetine reduces saccharin-induced elevation of fluid intake in alcohol-preferring Fawn-Hooded rats. ( Kampov-Polevoy, AB; Rezvani, AH, 1997) |
| "Buspirone was without important effects on the high alcohol preferring rats." | 1.29 | Effects of various serotonergic agents on alcohol intake and alcohol preference in Wistar rats selected at two different levels of alcohol preference. ( Meert, TF, 1993) |
| "Body weight was decreased by 12." | 1.28 | Tianeptine, a specific serotonin uptake enhancer, decreases ethanol intake in rats. ( Compagnon, P; Daoust, M; Legrand, E; Mocaër, E, 1992) |
| "Spiroxatrine (4 mg/kg, IP) was without effect on ethanol intake when given alone." | 1.28 | Spiroxatrine augments fluoxetine-induced reduction of ethanol intake by the P line of rats. ( Li, TK; Lumeng, L; McBride, WJ; Murphy, JM, 1989) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 4 (10.81) | 18.7374 |
| 1990's | 22 (59.46) | 18.2507 |
| 2000's | 4 (10.81) | 29.6817 |
| 2010's | 6 (16.22) | 24.3611 |
| 2020's | 1 (2.70) | 2.80 |
| Authors | Studies |
|---|---|
| Aranda, J | 1 |
| Fernández-Arjona, MDM | 1 |
| Alén, F | 3 |
| Rivera, P | 1 |
| Rubio, L | 1 |
| Smith-Fernández, I | 1 |
| Pavón, FJ | 2 |
| Serrano, A | 2 |
| Serrano-Castro, PJ | 1 |
| Rodríguez de Fonseca, F | 1 |
| Suárez, J | 2 |
| Ruiz, P | 1 |
| Calliari, A | 1 |
| Pautassi, RM | 1 |
| Ballesta, A | 1 |
| Orio, L | 2 |
| Arco, R | 1 |
| Vargas, A | 1 |
| Romero-Sanchiz, P | 1 |
| Nogueira-Arjona, R | 1 |
| de Heras, RG | 2 |
| Antón, M | 1 |
| Ramírez-López, M | 1 |
| de Fonseca, FR | 2 |
| Gorriti, MÁ | 1 |
| Ramírez-López, MT | 1 |
| Pozo, MÁ | 1 |
| Koren, G | 1 |
| Mamiya, PC | 1 |
| Matray-Devoti, J | 1 |
| Fisher, H | 4 |
| Wagner, GC | 4 |
| Malm, H | 1 |
| Artama, M | 1 |
| Gissler, M | 1 |
| Ritvanen, A | 1 |
| Martijena, ID | 1 |
| Bustos, SG | 1 |
| Bertotto, ME | 1 |
| Molina, VA | 1 |
| Cornelius, JR | 3 |
| Clark, DB | 1 |
| Bukstein, OG | 1 |
| Birmaher, B | 1 |
| Salloum, IM | 3 |
| Brown, SA | 1 |
| Cornelius, MD | 2 |
| Perel, JM | 2 |
| Ehler, JG | 2 |
| Jarrett, PJ | 2 |
| Levin, RL | 1 |
| Black, A | 2 |
| Mann, JJ | 1 |
| Naranjo, CA | 3 |
| Poulos, CX | 2 |
| Bremner, KE | 1 |
| Lanctot, KL | 1 |
| Kranzler, HR | 2 |
| Burleson, JA | 2 |
| Korner, P | 1 |
| Del Boca, FK | 1 |
| Bohn, MJ | 1 |
| Brown, J | 2 |
| Liebowitz, N | 1 |
| Lu, MR | 3 |
| Meert, TF | 1 |
| Babor, TF | 1 |
| Kampov-Polevoy, AB | 1 |
| Rezvani, AH | 4 |
| Thase, ME | 1 |
| Gardell, LR | 1 |
| Whalen, CA | 1 |
| Chattophadyay, S | 1 |
| Cavallaro, CA | 1 |
| Hubbell, CL | 1 |
| Reid, LD | 1 |
| Ciccocioppo, R | 1 |
| Panocka, I | 1 |
| Polidori, C | 1 |
| Dourish, CT | 1 |
| Massi, M | 1 |
| Zhou, FC | 1 |
| McKinzie, DL | 1 |
| Patel, TD | 1 |
| Lumeng, L | 3 |
| Li, TK | 3 |
| Hendrie, CA | 1 |
| Sairally, J | 1 |
| Starkey, N | 1 |
| Maurel, S | 1 |
| De Vry, J | 1 |
| Schreiber, R | 1 |
| Farren, CK | 1 |
| O'Malley, SS | 1 |
| Lê, AD | 1 |
| Harding, S | 1 |
| Watchus, J | 1 |
| Juzytsch, W | 1 |
| Shaham, Y | 1 |
| Overstreet, DH | 3 |
| Mason, GA | 1 |
| Janowsky, DS | 3 |
| Hamedi, M | 1 |
| Clark, E | 1 |
| Yang, Y | 1 |
| Knoke, DM | 1 |
| Gorelick, DA | 1 |
| Paredes, A | 1 |
| Daoust, M | 1 |
| Compagnon, P | 1 |
| Legrand, E | 1 |
| Mocaër, E | 1 |
| Kadlec, KE | 1 |
| Sanhueza, P | 1 |
| Woodley-Remus, D | 1 |
| Sellers, EM | 1 |
| McBride, WJ | 2 |
| Murphy, JM | 2 |
| Grupp, LA | 1 |
| Perlanski, E | 1 |
| Stewart, RB | 1 |
| Allen, D | 1 |
| Lader, M | 1 |
| Curran, HV | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| 5HT3 Antagonists to Treat Opioid Withdrawal and to Prevent the Progression of Physical Dependence[NCT01549652] | 133 participants (Actual) | Interventional | 2011-04-30 | Completed | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
The Beck Depression Inventory (a 21-item self-report multiple-choice inventory) yields a single summed score between 0 and 63; higher scores indicate more severe depression. Change is from baseline score (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken prior to receiving ondansetron or placebo, at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) |
|---|---|
| Prevention of Opioid Withdrawal | -0.44 |
The VAS is a 0 to 100 millimeter scale where 0 corresponds to no pain and 100 to extreme pain, used by participants to indicated their level of pain over the last two weeks. Change is from baseline score for average level of pain (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken prior to receiving ondansetron or placebo, at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) |
|---|---|
| Prevention of Opioid Withdrawal | -2.68 |
The Roland-Morris Disability Index is a 24-question instrument used to assess level of disability from lower back pain. Scores range from 0-24 with lower scores corresponding to fewer symptoms. Change is from baseline score (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken prior to receiving ondansetron or placebo, at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) |
|---|---|
| Prevention of Opioid Withdrawal | -2.59 |
The Beck Depression Inventory (a 21-item self-report multiple-choice inventory) yields a single summed score between 0 and 63; higher scores indicate more severe depression. Change is from baseline score (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in BDIS (Ondansetron) | Change in BDIS (Placebo) | |
| Prevention of Physical Dependence | -0.6 | 0.2 |
"Originally developed by Handelsman, the Objective Opioid Withdrawal Scale (OOWS) score is a well-characterized measure of opioid withdrawal in humans, calculated as the sum of a 13-item physician assessment documenting physically observable signs of withdrawal, which are rated as present (1) or absent (0) during the observation period. The minimum score of 0 means the patient is not showing any signs of opioid withdrawal. The maximum score of 13 signifies all signs of opioid withdrawal to the largest extent possible.~Immediately prior to ondansetron or placebo administration a baseline OOWS score was taken. 30 minutes later participants received naloxone, then 15 minutes later an OOWS score was taken. If deemed necessary by the clinician, participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an OOWS score was taken. Change from the baseline OOWS score to the score assessed following the last naloxone dose is reported." (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in OOWS (Ondansetron) | Change in OOWS (Placebo) | |
| Prevention of Opioid Withdrawal | 3.6 | 3.6 |
"Originally developed by Handelsman, the OOWS score is a well-characterized measure of opioid withdrawal in humans, calculated as the sum of a 13-item physician assessment documenting physically observable signs of withdrawal, which are rated as present (1) or absent (0) during the observation period. The maximum score is 13 and suggests the patient is showing all signs of opioid withdrawal to the largest extent possible. The minimum score of 0 suggests the patient is not showing any signs of opioid withdrawal.~Immediately prior to ondansetron or placebo administration a baseline OOWS score was taken. 30 minutes later participants received naloxone, then 15 minutes later an OOWS score was taken. If necessary (as deemed by the clinician), participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an OOWS score was taken. Change from the baseline OOWS score to the score assessed following the last naloxone dose is reported." (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in OOWS (Ondansetron) | Change in OOWS (Placebo) | |
| Prevention of Physical Dependence | 4.5 | 4.2 |
The VAS is a 0 to 100 millimeter scale where 0 corresponds to no pain and 100 to extreme pain, used by participants to indicated their level of pain over the last two weeks. Change is from baseline score for average level of pain (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in VAS Score (Ondansetron) | Change in VAS Score (Placebo) | |
| Prevention of Physical Dependence | -2.9 | -2.8 |
The Roland-Morris Disability Index is a 24-question instrument used to assess level of disability from lower back pain. Scores range from 0-24 with lower scores corresponding to fewer symptoms. Change is from baseline score (taken at the beginning of the first study visit, prior to beginning of titration into morphine) to the score taken after taking morphine for 30 days (score taken at the beginning of second study visit). (NCT01549652)
Timeframe: 2 study days 1 month apart (at the start of each study visit)
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in RMDI (Ondansetron) | Change in RMDI (Placebo) | |
| Prevention of Physical Dependence | -4.6 | -2.0 |
The Subjective Opioid Withdrawal Score (SOWS) score is calculated as the sum of 16 subjective patient-reported symptom scores rated on a scale of 0 to 4 (0=not at all, 4=extremely) based on what subjects were experiencing at the time of testing. A maximum score of 64 would suggest the patient is experiencing the symptoms of withdrawal to the maximum extent possible while the lowest score of 0 would suggest the patient is not experiencing any of the symptoms of withdrawal. Immediately prior to ondansetron or placebo administration a baseline SOWS score was taken. 30 minutes later participants received naloxone, then 15 minutes later an SOWS score was taken. If necessary (as deemed by the clinician), participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an SOWS score was taken. Change from the baseline SOWS score to the score assessed following the last naloxone dose is reported (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in SOWS (Ondansetron) | Change in SOWS (Placebo) | |
| Prevention of Opioid Withdrawal | 12.5 | 12.2 |
The SOWS score is composed of 16 subjective symptoms rated on a scale of 0 to 4 (0=not at all, 4=extremely) based on what subjects were experiencing at the time of testing. A maximum score of 64 would suggest the patient is experiencing the symptoms of withdrawal to the maximum extent possible while the lowest score of 0 would suggest the patient is not experiencing any of the symptoms of withdrawal. Immediately prior to ondansetron or placebo administration a baseline SOWS score was taken. 30 minutes later participants received naloxone, then 15 minutes later an SOWS score was taken. If necessary (as deemed by the clinician), participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an SOWS score was taken. Change from the baseline SOWS score to the score assessed following the last naloxone dose is reported (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in SOWS (Ondansetron) | Change in SOWS (Placebo) | |
| Prevention of Physical Dependence | 16.4 | 12.0 |
Profile of Mood States (POMS) is a 65-question survey of how participants have been feeling over the past week, assessing tension, depression, anger, fatigue, confusion and vigor. Each question is on a 5-point scale: 0 (not at all) to 4 (extremely). Overall score range: 0 to 200 (lower scores corresponding to fewer symptoms), calculated by adding total scores for tension, depression, anger, fatigue and confusing, and subtracting that total score from the total score for vigor. Immediately prior to ondansetron or placebo administration a baseline POMS score was taken. 30 minutes later participants received naloxone, then 15 minutes later a POMS score was taken. If necessary (as deemed by the clinician), participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an POMS score was taken. Change from the baseline POMS score to the score assessed following the last naloxone dose is reported. (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in POMS Score (Ondansetron) | Change in POMS Score (Placebo) | |
| Prevention of Opioid Withdrawal | 29.3 | 28.3 |
(Profile of Mood States) POMS is a 65-question survey of how participants have been feeling over the past week, assessing tension, depression, anger, fatigue, confusion and vigor. Each question is on a 5-point scale: 0 (not at all) to 4 (extremely). Overall score range: 0 to 200 (lower scores corresponding to fewer symptoms), calculated by adding total scores for tension, depression, anger, fatigue and confusing, and subtracting that total score from the total score for vigor. Immediately prior to ondansetron or placebo administration a baseline POMS score was taken. 30 minutes later participants received naloxone, then 15 minutes later a POMS score was taken. If necessary (as deemed by the clinician), participants may have received a second naloxone dose (25 minutes following 1st naloxone dose), then 15 minutes later an POMS score was taken. Change from the baseline POMS score to the score assessed following the last naloxone dose is reported. (NCT01549652)
Timeframe: Baseline; 15 minutes following last naloxone dose
| Intervention | units on a scale (Mean) | |
|---|---|---|
| Change in POMS (Ondansetron) | Change in POMS (Placebo) | |
| Prevention of Physical Dependence | 36.1 | 29.2 |
2 reviews available for fluoxetine and Alcohol Drinking
| Article | Year |
|---|---|
Acute phase and five-year follow-up study of fluoxetine in adolescents with major depression and a comorbid substance use disorder: a review.
Topics: Adolescent; Alcohol Drinking; Alcoholism; Antidepressive Agents, Second-Generation; Combined Modalit | 2005 |
The role of selective serotonin reuptake inhibitors in reducing alcohol consumption.
Topics: Alcohol Drinking; Alcoholism; Animals; Behavior, Addictive; Behavior, Animal; Citalopram; Clinical T | 2001 |
9 trials available for fluoxetine and Alcohol Drinking
| Article | Year |
|---|---|
Preliminary report: double-blind, placebo-controlled study of fluoxetine in depressed alcoholics.
Topics: Adolescent; Adult; Alcohol Drinking; Alcoholism; Depression; Double-Blind Method; Female; Fluoxetine | 1995 |
Fluoxetine attenuates alcohol intake and desire to drink.
Topics: Adult; Alcohol Drinking; Alcoholism; Appetite; Dose-Response Relationship, Drug; Double-Blind Method | 1994 |
Placebo-controlled trial of fluoxetine as an adjunct to relapse prevention in alcoholics.
Topics: Adult; Alcohol Drinking; Alcoholism; Combined Modality Therapy; Comorbidity; Depressive Disorder; Dr | 1995 |
Fluoxetine treatment seems to reduce the beneficial effects of cognitive-behavioral therapy in type B alcoholics.
Topics: Adult; Alcohol Drinking; Alcoholism; Cognitive Behavioral Therapy; Comorbidity; Depressive Disorder; | 1996 |
Fluoxetine in depressed alcoholics. A double-blind, placebo-controlled trial.
Topics: Adult; Alcohol Drinking; Alcoholism; Comorbidity; Depressive Disorder; Diagnosis, Dual (Psychiatry); | 1997 |
Self-medication with alcohol appears not to be an effective treatment for the control of depression.
Topics: Adult; Alcohol Drinking; Antidepressive Agents, Second-Generation; Depression; Female; Fluoxetine; H | 1998 |
Effect of fluoxetine on alcohol consumption in male alcoholics.
Topics: Adult; Alcohol Drinking; Alcoholism; Fluoxetine; Hospitalization; Humans; Male; Middle Aged; Single- | 1992 |
Fluoxetine differentially alters alcohol intake and other consummatory behaviors in problem drinkers.
Topics: Adult; Alcohol Drinking; Alcoholism; Analysis of Variance; Appetite; Body Weight; Drinking Behavior; | 1990 |
A comparative study of the interactions of alcohol with amitriptyline, fluoxetine and placebo in normal subjects.
Topics: Alcohol Drinking; Amitriptyline; Arousal; Dose-Response Relationship, Drug; Drug Interactions; Elect | 1988 |
26 other studies available for fluoxetine and Alcohol Drinking
| Article | Year |
|---|---|
Sudden cessation of fluoxetine before alcohol drinking reinstatement alters microglial morphology and TLR4/inflammatory neuroadaptation in the rat brain.
Topics: Alcohol Drinking; Animals; Brain; Ethanol; Fluoxetine; Humans; Microglia; Neuroinflammatory Diseases | 2021 |
Reserpine-induced depression is associated in female, but not in male, adolescent rats with heightened, fluoxetine-sensitive, ethanol consumption.
Topics: Alcohol Drinking; Animals; Depression; Dopamine; Ethanol; Female; Fluoxetine; Male; Rats; Rats, Wist | 2018 |
Bupropion, a possible antidepressant without negative effects on alcohol relapse.
Topics: Alcohol Drinking; Alcoholism; Animals; Antidepressive Agents, Second-Generation; Bupropion; Dopamine | 2019 |
Increased alcohol consumption in rats after subchronic antidepressant treatment.
Topics: Alcohol Drinking; Alcohols; Analysis of Variance; Animals; Antidepressive Agents; Behavior, Addictiv | 2013 |
"Prozac Baby" - 25 years of motherisk research into SSRIs and alcohol in pregnancy.
Topics: Abnormalities, Drug-Induced; Alcohol Drinking; Antidepressive Agents, Second-Generation; Depression; | 2014 |
Mice increased target biting behaviors 24h after co-administration of alcohol and fluoxetine.
Topics: Aggression; Alcohol Drinking; Animals; Behavior, Animal; Brain; Ethanol; Fluoxetine; Frontal Lobe; H | 2017 |
Selective serotonin reuptake inhibitors and risk for major congenital anomalies.
Topics: Abnormalities, Drug-Induced; Adolescent; Adult; Alcohol Drinking; Female; Finland; Fluoxetine; Heart | 2011 |
Antidepressants attenuate both the enhanced ethanol intake and ethanol-induced anxiolytic effects in diazepam withdrawn rats.
Topics: Alcohol Drinking; Analysis of Variance; Animals; Anti-Anxiety Agents; Antidepressive Agents; Anxiety | 2005 |
Ethanol consumption following acute treatment with methysergide, fluoxetine, fenfluramine, and their combination.
Topics: Alcohol Drinking; Animals; Dose-Response Relationship, Drug; Fenfluramine; Fluoxetine; Male; Methyse | 1994 |
Ethanol consumption following acute fenfluramine, fluoxetine, and dietary tryptophan.
Topics: Alcohol Drinking; Animals; Diet; Dose-Response Relationship, Drug; Drinking Behavior; Energy Intake; | 1993 |
Effects of various serotonergic agents on alcohol intake and alcohol preference in Wistar rats selected at two different levels of alcohol preference.
Topics: Alcohol Drinking; Alcoholism; Animals; Buspirone; Chlordiazepoxide; Citalopram; Dose-Response Relati | 1993 |
Fluoxetine reduces saccharin-induced elevation of fluid intake in alcohol-preferring Fawn-Hooded rats.
Topics: Alcohol Drinking; Animals; Antidepressive Agents, Second-Generation; Dose-Response Relationship, Dru | 1997 |
Combination of naltrexone and fluoxetine on rats' propensity to take alcoholic beverage.
Topics: Alcohol Deterrents; Alcohol Drinking; Alcoholism; Animals; Dose-Response Relationship, Drug; Drug Sy | 1997 |
Blockade of pre- and post-synaptic 5-HT1A receptors does not modify the effect of fluoxetine or 5-hydroxytryptophan on ethanol and food intake in rats.
Topics: 5-Hydroxytryptophan; Alcohol Drinking; Animals; Drinking; Eating; Fluoxetine; Injections; Male; Pipe | 1997 |
Additive reduction of alcohol drinking by 5-HT1A antagonist WAY 100635 and serotonin uptake blocker fluoxetine in alcohol-preferring P rats.
Topics: Alcohol Drinking; Alcoholism; Animals; Dose-Response Relationship, Drug; Drug Synergism; Female; Flu | 1998 |
Comparison of the effects of the selective serotonin-reuptake inhibitors fluoxetine, paroxetine, citalopram and fluvoxamine in alcohol-preferring cAA rats.
Topics: Alcohol Drinking; Alcoholism; Animals; Citalopram; Disease Models, Animal; Eating; Ethanol; Female; | 1999 |
Occurrence and management of depression in the context of naltrexone treatment of alcoholism.
Topics: Acamprosate; Alcohol Deterrents; Alcohol Drinking; Alcoholism; Comorbidity; Depressive Disorder; Dia | 1999 |
Effects of naltrexone and fluoxetine on alcohol self-administration and reinstatement of alcohol seeking induced by priming injections of alcohol and exposure to stress.
Topics: Alcohol Deterrents; Alcohol Drinking; Animals; Central Nervous System Depressants; Ethanol; Fluoxeti | 1999 |
Combination pharmacotherapy: a mixture of small doses of naltrexone, fluoxetine, and a thyrotropin-releasing hormone analogue reduces alcohol intake in three strains of alcohol-preferring rats.
Topics: Alcohol Drinking; Animals; Drug Therapy, Combination; Fluoxetine; Naltrexone; Narcotic Antagonists; | 2000 |
Ethanol intake of chickens treated with fenfluramine, fluoxetine, and dietary tryptophan.
Topics: Alcohol Drinking; Animals; Body Temperature Regulation; Brain; Chickens; Dose-Response Relationship, | 1992 |
Tianeptine, a specific serotonin uptake enhancer, decreases ethanol intake in rats.
Topics: Alcohol Drinking; Animals; Antidepressive Agents, Tricyclic; Body Weight; Brain; Eating; Fluoxetine; | 1992 |
Drug-induced reductions in ethanol intake in alcohol preferring and Fawn-Hooded rats.
Topics: Alcohol Drinking; Alcoholism; Animals; Buspirone; Drinking Behavior; Ethanol; Feeding Behavior; Fluo | 1991 |
Genetic serotonin deficiency and alcohol preference in the fawn hooded rats.
Topics: Alcohol Drinking; Alcoholism; Animals; Brain; Fluoxetine; Rats; Rats, Inbred Strains; Receptors, Ser | 1990 |
Spiroxatrine augments fluoxetine-induced reduction of ethanol intake by the P line of rats.
Topics: 8-Hydroxy-2-(di-n-propylamino)tetralin; Alcohol Drinking; Animals; Dioxanes; Dioxins; Dopamine Antag | 1989 |
Attenuation of alcohol intake by a serotonin uptake inhibitor: evidence for mediation through the renin-angiotensin system.
Topics: Alcohol Drinking; Animals; Body Weight; Enalapril; Fluoxetine; Male; Rats; Rats, Inbred Strains; Ref | 1988 |
Effects of Ro 15-4513, fluoxetine and desipramine on the intake of ethanol, water and food by the alcohol-preferring (P) and -nonpreferring (NP) lines of rats.
Topics: Alcohol Drinking; Alcoholism; Animals; Azides; Benzodiazepines; Desipramine; Drinking Behavior; Feed | 1988 |