Relevant bibliographies by topics / Pharmacology of antidepressants

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Reports

Academic literature on the topic 'Pharmacology of antidepressants'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Pharmacology of antidepressants"

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Dugan, Daniel J. "Antidepressants: Using Pharmacology to Individualize Therapy." Journal of Pharmacy Practice 14, no. 6 (December 2001): 458–66. http://dx.doi.org/10.1177/089719001129040955.

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The pharmacotherapy of depression has undergone significant change in the last two decades. A new generation of antidepressant agents has displaced older drugs as first-line therapies for depression. The clinician that seeks optimal outcomes for treatment of depression must be familiar with all of the available antidepressant agents. This article will discuss the pharmacologic profile of antidepressants currently marketed in the United States, identifying similarities and differences that have clinical relevance in the management of depression. Drug selection with an emphasis on antidepressant receptor affinity will be reviewed.
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Jackson, Cherry W. "Antidepressants in the Treatment of Chronic Pain." Journal of Pharmacy Practice 11, no. 5 (October 1998): 388–93. http://dx.doi.org/10.1177/089719009801100509.

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Antidepressants have been successfully used for chronic pain syndromes for approximately 30 years. One theory is that analgesic action is secondary to the antidepressant effects of the medications. Placebo-controlled trials have documented that antidepressants treat neuropathic pain, musculoskeletal pain, chronic pain, and cancer pain. The most frequently studied antidepressant for pain is amitriptyline. Other antidepressants that have shown analgesic activity include imipramine, citalopram, paroxetine, nortriptyline, desipramine, and mianserin. Fluoxetine and trazodone have not been shown to successfully treat pain syndromes. Venlafaxine, a new antidepressant, most recently was shown to have antidepressant activity in fibromyalgia. More studies need to be done with newer antidepressants to confirm their place in treating pain syndromes.
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Richelson, Elliott. "Pharmacology of antidepressants." Mayo Clinic Proceedings 76, no. 5 (May 2001): 511–27. http://dx.doi.org/10.4065/76.5.511.

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Frazer, Alan. "Pharmacology of Antidepressants." Journal of Clinical Psychopharmacology 17 (April 1997): 2S—18S. http://dx.doi.org/10.1097/00004714-199704001-00002.

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Richelson, Elliott. "Pharmacology of Antidepressants." Psychopathology 20, no. 1 (1987): 1–12. http://dx.doi.org/10.1159/000284517.

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Cohen, Lawrence J., and C. Lindsay DeVane. "Clinical Implications of Antidepressant Pharmacokinetics and Pharmacogenetics." Annals of Pharmacotherapy 30, no. 12 (December 1996): 1471–80. http://dx.doi.org/10.1177/106002809603001216.

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OBJECTIVE: To review available data on pharmacokinetic and pharmacogenetic influences on the response to antidepressant therapy, analyze the mechanisms for and clinical significance of pharmacokinetic and pharmacogenetic differences, and explain the implications of pharmacokinetics and pharmacogenetics for patient care. DATA SOURCES: A MEDLINE search of English-language clinical studies, abstracts, and review articles on antidepressant pharmacokinetics, pharmacogenetics, and drug interactions was used to identify pertinent literature. DATA SYNTHESIS: The pharmacokinetic profiles of selected antidepressants are reviewed and the impact of hepatic microsomal enzymes on antidepressant metabolism is considered. How phenotypic differences influence the metabolism of antidepressant drug therapy is addressed. To evaluate the clinical implications of these pharmacokinetic and pharmacogenetic considerations, the findings of studies designed to elucidate drug interactions involving antidepressant agents are discussed. CONCLUSIONS: Differences in antidepressant plasma concentrations, and possibly safety, are caused by polymorphism in the genes that encode some of the cytochrome P450 isoenzymes that metabolize antidepressants. The isoenzymes 1A2, 2C9/19, 2D6, and 3A4 are the major enzymes that catalyze antidepressant metabolic reactions. Antidepressants can be either substrates or inhibitors of these enzymes, which also metabolize many other pharmacologic agents. Although the cytochrome enzymes that metabolize antidepressants have not been fully characterized, interaction profiles of the newer antidepressants are becoming more clearly defined. Determining patient phenotypes is not practical in the clinical setting, but an awareness of the possibility of genetic polymorphism in antidepressant metabolism may help explain therapeutic failure or toxicity, help predict the likelihood of drug interactions, and help clinicians better manage antidepressant drug therapy.
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Saraghi, Mana, Leonard Golden, and Elliot V. Hersh. "Anesthetic Considerations for Patients on Antidepressant Therapy – Part II." Anesthesia Progress 65, no. 1 (March 1, 2018): 60–65. http://dx.doi.org/10.2344/anpr-65-01-10.

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Millions of patients take antidepressant medications in the United States for the treatment of depression or anxiety disorders. Some antidepressants are prescribed off-label to treat problems such as chronic pain, low energy, and menstrual symptoms. Antidepressants are a broad and expansive group of medications, but the more common drug classes include tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and monoamine oxidase inhibitors. A miscellaneous or “atypical” category covers other agents. Some herbal supplements that claim to have antidepressant activity will also be discussed. Part I of this series reviewed antidepressant pharmacology, adverse effects, and drug interactions with adrenergic agonists. In part II, drug–drug interactions with sedation and general anesthetics, bleeding effects, and serotonin syndrome will be discussed.
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Gers, Lynn, Mirko Petrovic, Stany Perkisas, and Maurits Vandewoude. "Antidepressant use in older inpatients: current situation and application of the revised STOPP criteria." Therapeutic Advances in Drug Safety 9, no. 8 (May 28, 2018): 373–84. http://dx.doi.org/10.1177/2042098618778974.

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Objectives: Antidepressant use increases as age rises. Moreover, older patients are more sensitive to side effects and drug interactions. This descriptive study aims to map antidepressant use among patients at the geriatrics department of a university hospital and to evaluate whether prescribing happens in an evidence-based manner. Methods: Patients aged 75 years and over, admitted to the geriatrics department of the Middelheim Hospital in Antwerp between February and July 2017 were included. We checked whether they took antidepressants, which types and doses were prescribed, who prescribed the antidepressants, and whether prescribing was in concordance with the revised STOPP (Screening Tool of Older People’s Prescriptions) criteria. Results: Out of the 239 included patients, 61 were found to use antidepressants, with depression being the most important indication. General practitioners appeared to be the most frequent prescribers. Trazodone was the most prescribed antidepressant and was often used for sleeping disorders. Antidepressants were taken longer than recommended in almost one out of five cases. Patients with diabetes and renal insufficiency were prescribed antidepressants less frequently. Only 2.8% of the study participants were prescribed antidepressants for anxiety disorders. Conclusion: We can conclude that prescription of antidepressants in older patients at the geriatrics department is often not evidence based. Clear guidelines may offer a solution; therefore more studies are needed on antidepressant use in older patients.
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Saraghi, Mana, Leonard R. Golden, and Elliot V. Hersh. "Anesthetic Considerations for Patients on Antidepressant Therapy—Part I." Anesthesia Progress 64, no. 4 (December 1, 2017): 253–61. http://dx.doi.org/10.2344/anpr-64-04-14.

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Millions of patients take antidepressant medications in the United States for the treatment of depression or anxiety disorders. Some antidepressants are prescribed off-label to treat problems such as chronic pain, low energy, and menstrual symptoms. Antidepressants are a broad and expansive group of medications, but the more common drug classes include tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and monoamine oxidase inhibitors. A miscellaneous or “atypical” category covers other agents. Some herbal supplements that claim to have antidepressant activity will also be discussed. In Part I of this review, antidepressant pharmacology, adverse effects, and drug interactions with adrenergic agonists will be discussed. In part II, drug interactions with sedation and general anesthetics will be reviewed. Bleeding effects and serotonin syndrome implications in anesthetic practice will also be highlighted.
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Cyr, Monica, and Candace S. Brown. "Nefazodone: Its Place among Antidepressants." Annals of Pharmacotherapy 30, no. 9 (September 1996): 1006–12. http://dx.doi.org/10.1177/106002809603000916.

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OBJECTIVE: To review the pharmacology, pharmacokinetics, efficacy, adverse effects, and drug interactions of nefazodone, as well as to determine its place among currently available antidepressants. DATA SOURCES: A search of European and American literature using EMBASE and MEDLINE was completed. Nefazodone was the search term. DATA SYNTHESIS: Nefazodone is an antidepressant that blocks serotonin type 2 (5-HT2) receptors in addition to inhibiting the reuptake of serotonin and norepinephrine. In double-blind, placebo-controlled studies, nefazodone demonstrates antidepressant activity at dosages ranging from 400 to 600 mg/d. Sedation, dry mouth, nausea, and dizziness are the more common adverse effects of nefazodone. Nefazodone, an analog of trazodone, has not been associated with priapism at this time, and may have fewer sexual adverse effects than other antidepressants. More studies are needed to determine the potential role of nefazodone in treating anxiety, pain, and premenstrual syndrome. STUDY SELECTION: Only double-blind, placebo-controlled studies designed to establish the efficacy of nefazodone as an antidepressant were reviewed. CONCLUSIONS: Based on placebo-controlled, double-blind, comparative trials, nefazodone demonstrates greater efficacy than placebo, and equivalent efficacy to imipramine. Somnolence, dry mouth, nausea, dizziness, and constipation are the most common adverse effects. Nefazodone appears to have a milder adverse effect profile than the tricyclic antidepressants, causes fewer sexual dysfunctions than the serotonin selective reuptake inhibitors, and may cause less dizziness than trazodone. Nefazodone at dosages of at least 300 mg/d provides another option for the treatment of depression.
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Dissertations / Theses on the topic "Pharmacology of antidepressants"

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Ordway, Gregory A. "Molecular Pharmacology of Antidepressants." Digital Commons @ East Tennessee State University, 2006. https://dc.etsu.edu/etsu-works/8657.

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Wang, Haiyan. "Manipulation of ion channel function and its effects on the neuropharmacology of 5-hydroxytryptamine." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279930.

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Maurya, Manisha. "The effect of antidepressants on rodent brain glucocorticoid systems." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368872.

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Janger, Darren S. "The Collective Overuse of Antidepressants as a Psychological Defense Inhibiting Soul Opportunities." Thesis, Pacifica Graduate Institute, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10750296.

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It is not the existence of depressive symptomology, but understanding the function and effect that should be central in how to best support patients. Even in cases of milder depression, phase-of-life issues, or adjustment-related depressive episodes, the myth of a magical pill, here an antidepressant, appeals to the human desire for cessation of whatever unpleasantness may be arising. As a collective, clinicians may be placating clients’ psychological defenses and natural desire to suppress or dissociate at the expense of allowing a soulful opportunity to work through and resolve challenges. Utilizing a primarily hermeneutic approach, the author contemplates various studies supporting psychotherapy, psychopharmacology, and combined therapies. Ultimately, the case is made for decision-making processes that place higher value on the greater context of potential soul opportunities for resolution and healing as well as individuation and growth.

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Nomikos, George Goulielmos. "In vivo neurochemical effects of antidepressant treatments studied by microdialysis." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/31076.

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The present experiments investigated the effects of different antidepressant treatments on dopamine (DA) transmission by employing in vivo microdialysis in the nucleus accumbens (NAC) and the striatum of freely moving rats. The treatments were: a) the tricyclic antidepressant desipramine (DMI), b) the novel antidepressant drug bupropion, and c) electrically induced seizures (ECS). The following results were obtained: 1) Neither acute (5 mg/kg), nor chronic (5 mg/kg, b.i.d. X 21) DMI influenced basal interstitial concentrations of DA in the NAC or the striatum. Chronic DMI did not influence apomorphine (25 μg/kg, s.c.)-induced decreases in extracellular DA in the NAC. In contrast, d-amphetamine (1.5 mg/kg, s.c.)-induced increases in extracellular DA were significantly enhanced in the NAC (not in striatum) of the chronic DMI group. d-Amphetamine-induced hypermotility was also enhanced in the chronic DMI group. 2) Bupropion (10, 25 and 100 mg/kg, i.p.) increased extracellular striatal DA concentrations in a dose-, time-, and action potential-dependent manner. Bupropion produced similar responses in the NAC. The in vivo neurochemical effects of bupropion were compared with the effects of other DA uptake inhibitors such as d-amphetamine, GBR 12909, cocaine, nomifensine, methylphenidate, and benztropine by direct administration of the drugs to the striatum via the perfusion fluid in increasing concentrations (1 to 1000 μM). The rank order of potency of these drugs as determined by the increases in extracellular DA produced by 10 or 100 μM (following correction for dialysis efficiency of the test compounds in vitro) was: GBR 12909> benztropine> amphetamine= nomifensine= methylphenidate> cocaine> bupropion. Simultaneous in vivo microdialysis in the NAC and striatum was employed to investigate the effects of chronic (10 mg/kg, b.i.d. X 21) bupropion treatment on bupropion (25 mg/kg, i.p.)-induced increases in extracellular DA concentrations. The effect of the challenge bupropion injection was significantly enhanced in the NAC (not in striatum) of the chronic bupropion group. Bupropion-induced hyperlocomotion was also enhanced in the chronic bupropion group. 3) Following a single ECS (150 V, 0.75 sec) interstitial concentrations of DA in the NAC and striatum increased sharply to 130% and 300%, respectively. The ECS-induced DA increase in the striatum was Ca⁺⁺-sensitive, partially TTX-independent, and was not influenced by barbiturate-induced anaesthesia. Seizure activity induced by flurothyl did not influence dialysate DA concentrations from the striatum, but increased dialysate DA from the NAC to 150%. These results suggest that the ECS-induced DA release in the striatum (not in the NAC) is related to the passage of current and not to the seizure activity. A course of ECS (8 treatments, one every second day) did not influence basal extracellular DA concentrations in the striatum or the NAC, while it significantly increased the DA metabolites in the striatum. Chronic ECS did not influence apomorphine (25 μg/kg, s.c.)-induced decreases in extracellular DA in the NAC. d-Amphetamine (1.5 mg/kg s.c.)-induced increases in extracellular DA were significantly enhanced in the NAC of the chronic ECS group. d-Amphetamine-induced hypermotility was also enhanced in the chronic ECS group. These results provide in vivo neurochemical confirmation that chronically administered DMI or ECS do not produce DA autoreceptor subsensitivity. They also demonstrate that chronic DMI- or chronic ECS-induced increases in the locomotor stimulant effects of d-amphetamine are accompanied by a potentiation of its effects on interstitial DA concentrations in the NAC. Moreover, these results demonstrate that chronic bupropion-induced behavioral sensitization is accompanied by a selective potentiation of its effects on interstitial DA concentrations in the NAC. Taken together, the present data provide direct neurochemical evidence that these antidepressant treatments can increase the functional output of the meso-accumbens dopaminergic system.
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Slamon, Noreen Deborah Louise. "Studies on the toxicological and protective responses of cultured astrocytes to antidepressants." Thesis, University of Salford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313910.

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Berggård, Cecilia. "Transcription Factor AP-2 in Relation to Personality and Antidepressant Drugs." Doctoral thesis, Uppsala University, Department of Neuroscience, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4638.

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The CNS monoaminergic systems are considered as the head engine regulating neuropsychiatric functions and personality. Transcription factor AP-2 is known to be essential for the development of the brainstem including the monoaminergic nuclei, and has the ability to regulate many genes in the monoaminergic systems. The ability of transcription factors to regulate specific gene expression, has lately made them hot candidates as drug targets. In this thesis, results indicating a role of AP-2 in the molecular effects of the antidepressant drugs citalopram and phenelzine, are presented.

A polymorphism in the second intron of the gene encoding AP-2ß has previously been associated with anxiety-related personality traits as estimated by the Karolinska Scales of Personality (KSP). In this thesis, results confirming this association, gained by using a larger material and several different personality scales, are presented. Furthermore, data is presented showing an association between the activity of platelet monoamine oxidase, a trait-dependent marker for personality, and the genotype of the AP-2ß intron 2 polymorphism.

The functional importance of the AP-2ß intron 2 polymorphism has not yet been elucidated. Included in this thesis are results showing that the AP-2ß intron 2 polymorphism is not in linkage disequilibrium with the only other described polymorphism in the AP-2ß gene, i.e. in the AP-2ß promoter (-67 G/A). Introns have in several studies been shown to include binding sites for regulatory proteins, and thus, to be important in transcriptional regulation. Results are presented demonstrating that one human brain nuclear protein binds only to the long variant of the AP-2ß intron 2 polymorphism. If this protein is involved in the regulation of the AP-2ß gene, it would affect the expression levels of the AP-2ß protein.

In general, this thesis further establishes the role of transcription factor AP-2 as a regulatory factor of importance for personality and monoaminergic functions.

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Damberg, Mattias. "Transcription Factor AP-2 in Relation to Serotonergic Functions in the Central Nervous System." Doctoral thesis, Uppsala University, Pharmacology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2532.

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Eukaryotic gene transcription plays a regulatory role in mammalian developmental processes. It has been shown that transcriptional control is an important mechanism for specification of neurotransmitter phenotypes. In the mammalian central nervous system, the transcription factor AP-2 family is one of the critical regulatory factors for neural gene expression and neuronal development. It has been shown that several genes in the monoaminergic systems have AP-2 binding sites in regulatory regions, suggesting a regulatory role of AP-2 also in the adult brain. Brainstem monoamines are implicated in the expression of personality traits and imbalances in these systems may give rise to psychiatric disorders.

The gene encoding AP-2β includes a polymorphic region consisting of a tetranucleotide repeat of [CAAA]4-5 in intron 2. Studies on AP-2β genotype in relation to personality and platelet MAO activity, a trait-dependant marker for personality, are presented in this thesis. Furthermore, correlations between brainstem levels of AP-2α and AP-2β and monoamine turnover in projection areas in rat forebrain are reported. These results strengthen the notion that the AP-2 family is important regulators of the monoaminergic systems in the adult brain. Furthermore, two studies are presented in this thesis with analyses indicating a role for AP-2 in the molecular mechanism of antidepressant drugs.

Altogether, this thesis presents data supporting our notion that the transcription factor AP-2 family is involved in the regulation of the monoaminergic systems both pre- and postnatally, and, therefore, might be involved in the pathophysiology of neuropsychiatric disorders.

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Gurgel, Josà Alves. "AvaliaÃÃo dos efeitos antiinflamatÃrios dos antidepressivos clomipramina, amitriptilina e maprotilina." Universidade Federal do CearÃ, 2002. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1187.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
No presente estudo avaliou-se os efeitos dos antidepressivos, amitriptilina (amt), clomipramina (clm) e maprotilina (mpt) em reaÃÃes inflamatÃrias. Ratos machos Wistar, 150-200g, foram divididos em cinco grupos (n=6), em experimentos de edema de pata (EP) e migraÃÃo de neutrÃfilos (MN) em bolsas de ar subcutÃnea. Amt, mpt (v.o.) e clm (i.p),10, 30 e 90mg/kg, foram administradas previamente ao estÃmulo inflamatÃrio (EI), carragenina (Cg-500 Â g/pata), fMLP (10â6M) ou dextran (Dx-300 Âg/pata). O edema foi aferido por hidropletismometria (Ugo Basile 7140), imediatamente antes (âtempo zeroâ) e 1, 2, 3 e 4h apÃs a aplicaÃÃo de Cg ou Dx. O aumento no volume da pata (volume do edema) foi calculado pela diferenÃa do volume apÃs a injeÃÃo do EI. Os dados demonstraram uma inibiÃÃo dose-dependente nos edemas de pata induzidos por Cg e Dx, na presenÃa dos antidepressivos. Amt, na maior dose, inibiu o EP induzido por Cg em 51,34% (p<0,05), e em 49% (p<0,05) o EP induzido por Dx. Clm, na maior e menor doses, reduziu o EP da Cg em 100% (p<0,001) e 42,45% (p<0,05), respectivamente, e em 97,26% (p<0,001) e 36% (p<0,05) o EP do Dx, respectivamente. A mpt inibiu o EP por Cg, em 60,9% (p<0,05) para a maior dose, e em 57,49% (p<0,01) e 34,42% (p<0,05) nas duas maiores doses, em ordem decrescente, no EP por Dx. Adicionalmente, amt e clm inibiram de forma dose-dependente a MN, na sexta hora, apÃs administraÃÃo de Cg. Amt na maior dose inibiu a MN induzida por Cg em 49,19% (p<0,05) e em 96,31% (p<0,001) a MN induzida por fMLP. A mpt (40 mg/kg, i.p.) inibiu a MN por Cg em 49,26% (p<0,001), e em 92,38% (p<0,001) a migraÃÃo induzida por fMLP. Do mesmo modo, a clm nas doses de 90. 30 e 10 mg/kg (i.p.), inibiu a MN por Cg em 76,46% (p<0,001), 64,4% (p<0,01) e 49,13% (p<0,05), respectivamente, e em 100% (p<0,001) a MN induzida por fMLP, na maior dose. Na avaliaÃÃo do efeito dos AD na degranulaÃÃo de mastÃcitos, observamos que a clm (90 mg/kg/i.p.) e a mpt (40 mg/kg/i.p.) reverteram em 100% a degranulaÃÃo induzida pelo composto 48/80. Amt (90 mg/kg/v.o.) tambÃm reverteu significativamente a degranulaÃÃo de mastÃcitos, alcanÃando 90,19% (p<0,001) de inibiÃÃo. Tais dados sugerem que amt, clm e mpt possuem significativa atividade antiinflamatÃria evidenciada por seus efeitos inibitÃrios na MN e edema
In the present study it was evaluated the effects of antidepressants amitriptiline (amt), clormipramine (clm) and maprotiline (mpt) in the inflammatory reaction. Male Wistar rats, 150-200g, were divided into five groups (n=6) in experiments of hind paw edema (HE) and neutrophils migration (NM) in subcutaneous air pouches. Amt, mpt (v.o.) and clm (i,p), 10, 30 and 90 mg/kg, were administrated before the inflammatory stimulus carragenin (Cg-500 Âg/paw), fMLP (10 â6M) or dextran (Dx-300 Âg/paw). Paw edema was measured with a hydroplethysmometer (Hugo Basile 7140 Plethysmometer) immediately before ( time equal zero ) and 1, 2, 3 and 4 h after the Cg or Dx challenges. The increase in paw volume (edema volume) was obtained by subtracting the paw volume measured before stimulus injection. The results demonstrate that the antidepressants induce a dose dependent reduction in the HE induced by Cg and Dx. Amt in largest dose used, inhibited the Cg-induced HE by 51,34% (p< 0,05), and the Dx-induced HE by 49% (p<0,05). Clm, in biggest and smallest dose, inhibited Cg-induced HE by 100% (p<0,001) and 42,45% (p< 0,05), respectively, and by 97,26% (p< 0,001) and 36% (p<0,05) the Dx-induced HE, respectively. The largest dose of mpt inhibited the Cg-induced HE by 60,9% (p<0,05) and at the two greatest dose, in decreasing order, inhibited the Dx-induced HE, by 57,49% (p<0,01) and 34,42% (p<0,05), respectively. Additionally, amt e clm inhibited the MN in a dose-dependently manner, in the sixth hour after Cg administration. Amt in largest dose (90 mg/kg/v.o.) inhibited the Cg-induced NM by 49,19% (p<0,05) and by 96,31% (p<0,001) the fMLP-induced NM. The mpt (40 mg/kg/i.p.) inhibited the Cg-induced NM by 49,26% (p<0,001), and by 92,38% (p<0,001) the fMLP-induced NM. In the same way, clm at the dose 90, 30 e 10 mg/kg (i.p.) inhibited Cg-induced NM by 76,46% (p< 0.001), 64,4% (p<0,01) and 49,13% (p<0,05), respectively, but the fMLP-induced NM was inhibited just by the biggest dose by 100% (p<0,001). We observed that clm (90 mg/kg/i.p.) and the mpt (40 mg/kg/i.p) completely reverted the mast cell degranulation induced by the compound 48/80. Amt (90 mg/kg/v.o.) also significantly reverted the mast cell degranulation by 90,19% (p<0,001). These data suggest that amt, clm e mpt have a significant antiinflammatory activity demonstrated by their inhibitory effects on NM and edema
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Peters, Eric James. "Pharmacogenetics of antidepressant response." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3251935.

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Books on the topic "Pharmacology of antidepressants"

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Stahl, S. M. Antidepressants. Cambridge: Cambridge University Press, 2009.

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Stahl, S. M. Antidepressants. Cambridge: Cambridge University Press, 2009.

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Antidepressants: Pharmacology, health effects and controversy. New York: Nova Science Publishers, Inc., 2012.

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Leonard, B. E. Differential effects of antidepressants. London: Martin Dunitz, 1999.

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Psych, Healy David MRC, ed. Differential effects of antidepressants. London: Martin Dunitz, 1999.

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Giorgio, Racagni, and Brunello Nicoletta, eds. Critical issues in the treatment of affective disorders. Basel: Karger, 1994.

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Bennett, Shoshana S. Pregnant on Prozac: The essential guide to making the best decision for you and your baby. Guilford, Conn: GPP Life, 2009.

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Quality, United States Agency for Healthcare Research and. Second-generation antidepressants in the pharmacologic treatment of adult depression: An update of the 2007 comparative effectiveness review : executive Summary. Rockville, Md: Agency for Healthcare Research and Quality, 2011.

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Stahl, S. M. Stahl's essential psychopharmacology: The prescriber's guide. Edited by Stahl, S. M. the prescriber's guide. and Stahl, S. M. the prescriber's guide. 3rd ed. Cambridge: Cambridge University Press, 2009.

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Stahl, S. M. the prescriber's guide. and Stahl, S. M. the prescriber's guide., eds. Stahl's essential psychopharmacology: The prescriber's guide. 3rd ed. Cambridge: Cambridge University Press, 2009.

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Book chapters on the topic "Pharmacology of antidepressants"

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Andrews, John S., and Roger M. Pinder. "Chemistry and pharmacology of novel antidepressants." In Antidepressants, 123–45. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8344-3_9.

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Haefely, Willy. "Preclinical Pharmacology of Antidepressants." In Biological Psychiatry, Higher Nervous Activity, 105–10. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-8329-1_15.

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Efinger, Vanessa, Walter E. Müller, and Kristina Friedland. "Antidepressants: Pharmacology and Biochemistry." In NeuroPsychopharmacotherapy, 1–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-56015-1_26-1.

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Bhandari, Prasan. "Antidepressants." In Pharmacology Mind Maps for Medical Students and Allied Health Professionals, 222–26. Boca Raton, FL : CRC Press/Taylor & Francis, 2020.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429023859-23.

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Sjöqvist, F. "Pharmacogenetics of Antidepressants." In Clinical Pharmacology in Psychiatry, 181–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74430-3_19.

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Ghose, Karabi. "Clinical pharmacology of lithium salts." In Antidepressants for Elderly People, 85–102. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-3436-9_6.

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Ciraulo, Domenic A., Richard I. Shader, and David J. Greenblatt. "Clinical Pharmacology and Therapeuticsof Antidepressants." In Pharmacotherapy of Depression, 33–124. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-435-7_2.

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Ciraulo, Domenic A., Lucy Tsirulnik-Barts, Richard I. Shader, and David J. Greenblatt. "Clinical Pharmacology and Therapeutics of Antidepressants." In Pharmacotherapy of Depression, 33–117. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-792-5_2.

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Vestergaard, P., L. F. Gram, P. Kragh-Sørensen, P. Bech, N. Reisby, and T. G. Bolwig. "Therapeutic Potentials of Recently Introduced Antidepressants." In Clinical Pharmacology in Psychiatry, 190–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78010-3_18.

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Rudorfer, M. V., M. Linnoila, and W. Z. Potter. "Accidental Antidepressants: Search for Specific Action." In Clinical Pharmacology in Psychiatry, 157–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71288-3_18.

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Reports on the topic "Pharmacology of antidepressants"

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Viswanathan, Meera, Jennifer Cook Middleton, Alison Stuebe, Nancy Berkman, Alison N. Goulding, Skyler McLaurin-Jiang, Andrea B. Dotson, et al. Maternal, Fetal, and Child Outcomes of Mental Health Treatments in Women: A Systematic Review of Perinatal Pharmacologic Interventions. Agency for Healthcare Research and Quality (AHRQ), April 2021. http://dx.doi.org/10.23970/ahrqepccer236.

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Abstract:
Background. Untreated maternal mental health disorders can have devastating sequelae for the mother and child. For women who are currently or planning to become pregnant or are breastfeeding, a critical question is whether the benefits of treating psychiatric illness with pharmacologic interventions outweigh the harms for mother and child. Methods. We conducted a systematic review to assess the benefits and harms of pharmacologic interventions compared with placebo, no treatment, or other pharmacologic interventions for pregnant and postpartum women with mental health disorders. We searched four databases and other sources for evidence available from inception through June 5, 2020 and surveilled the literature through March 2, 2021; dually screened the results; and analyzed eligible studies. We included studies of pregnant, postpartum, or reproductive-age women with a new or preexisting diagnosis of a mental health disorder treated with pharmacotherapy; we excluded psychotherapy. Eligible comparators included women with the disorder but no pharmacotherapy or women who discontinued the pharmacotherapy before pregnancy. Results. A total of 164 studies (168 articles) met eligibility criteria. Brexanolone for depression onset in the third trimester or in the postpartum period probably improves depressive symptoms at 30 days (least square mean difference in the Hamilton Rating Scale for Depression, -2.6; p=0.02; N=209) when compared with placebo. Sertraline for postpartum depression may improve response (calculated relative risk [RR], 2.24; 95% confidence interval [CI], 0.95 to 5.24; N=36), remission (calculated RR, 2.51; 95% CI, 0.94 to 6.70; N=36), and depressive symptoms (p-values ranging from 0.01 to 0.05) when compared with placebo. Discontinuing use of mood stabilizers during pregnancy may increase recurrence (adjusted hazard ratio [AHR], 2.2; 95% CI, 1.2 to 4.2; N=89) and reduce time to recurrence of mood disorders (2 vs. 28 weeks, AHR, 12.1; 95% CI, 1.6 to 91; N=26) for bipolar disorder when compared with continued use. Brexanolone for depression onset in the third trimester or in the postpartum period may increase the risk of sedation or somnolence, leading to dose interruption or reduction when compared with placebo (5% vs. 0%). More than 95 percent of studies reporting on harms were observational in design and unable to fully account for confounding. These studies suggested some associations between benzodiazepine exposure before conception and ectopic pregnancy; between specific antidepressants during pregnancy and adverse maternal outcomes such as postpartum hemorrhage, preeclampsia, and spontaneous abortion, and child outcomes such as respiratory issues, low Apgar scores, persistent pulmonary hypertension of the newborn, depression in children, and autism spectrum disorder; between quetiapine or olanzapine and gestational diabetes; and between benzodiazepine and neonatal intensive care admissions. Causality cannot be inferred from these studies. We found insufficient evidence on benefits and harms from comparative effectiveness studies, with one exception: one study suggested a higher risk of overall congenital anomalies (adjusted RR [ARR], 1.85; 95% CI, 1.23 to 2.78; N=2,608) and cardiac anomalies (ARR, 2.25; 95% CI, 1.17 to 4.34; N=2,608) for lithium compared with lamotrigine during first- trimester exposure. Conclusions. Few studies have been conducted in pregnant and postpartum women on the benefits of pharmacotherapy; many studies report on harms but are of low quality. The limited evidence available is consistent with some benefit, and some studies suggested increased adverse events. However, because these studies could not rule out underlying disease severity as the cause of the association, the causal link between the exposure and adverse events is unclear. Patients and clinicians need to make an informed, collaborative decision on treatment choices.
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