Pharmacotherapy of anxious disorders

Bourin, Michel; Lambert, Olivier

doi:10.1002/hup.435

Cited by 34 publications

(15 citation statements)

References 220 publications

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“…Even though it is now well established that selective antidepressants (ADs) possess anxiolytic properties, their underlying neuropharmacological mechanism of action is still not understood (Zohar and Westenberg 2000;Bourin and Lambert 2002;Nemeroff 2003;Vaswani et al 2003). Owing to their 5-HT re-uptake inhibiting effects, SSRIs and SNRIs increase synaptic levels of 5-HT (Fuller 1994;Kreiss and Lucki 1995;Beyer et al 2002;Lambert and Bourin 2002;Ables and Baughman 2003;Felton et al 2003), leading to an increased activation of a multitude of specific postsynaptic serotonin (5-HT) receptors (e.g.…”

Section: Introductionmentioning

confidence: 99%

Implication of 5-HT2 receptor subtypes in the mechanism of action of antidepressants in the four plates test

Dhonnchadha¹,

Ripoll²,

Clénet³

et al. 2004

Psychopharmacology

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Section: Introductionmentioning

confidence: 99%

Implication of 5-HT2 receptor subtypes in the mechanism of action of antidepressants in the four plates test

Dhonnchadha¹,

Ripoll²,

Clénet³

et al. 2004

Psychopharmacology

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“…Other classes of antidepressants, including norepinepherine reuptake inhibitors (NRIs) and monoamine oxidase inhibitors (MAOIs), are ineffective in OCD (1, 4). OCD is the only anxiety disorder showing selective response to SRI antidepressants (5). Furthermore, the mechanisms by which SRIs produce therapeutic effects in OCD remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Essential Role for Orbitofrontal Serotonin 1B Receptors in Obsessive-Compulsive Disorder-Like Behavior and Serotonin Reuptake Inhibitor Response in Mice

Shanahan

Velez

Masten

et al. 2011

Biological Psychiatry

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Background Perseveration and sensorimotor gating deficits are core features of obsessive-compulsive disorder (OCD). Serotonin 1B receptor (5-HT1BR) agonists exacerbate OCD symptoms in patients, and induce perseveration and sensorimotor gating deficits in mice. Serotonin reuptake inhibitors (SRIs), but not noradrenaline reuptake inhibitors (NRIs), reduce OCD symptoms following 4–8 weeks of treatment. Using mice, we compared the effects of chronic SRI versus NRI treatment on 5-HT1BR-induced OCD-like behavior, and 5-HT1BR sensitivity in orbitofrontal-subcortical “OCD circuits”. Furthermore, we localized the 5-HT1BR population that mediates OCD-like behavior. Methods Mice chronically received the SRI clomipramine or the NRI desipramine and were examined for 5-HT1BR-induced OCD-like behavior, or 5-HT1BR binding and G-protein-coupling in caudate-putamen, nucleus accumbens, and orbitofrontal cortex. Separate mice were tested for OCD- or depression-like behavior following 4, 14, 21, 28 or 56 days of SRI treatment. Finally, OCD-like behavior was assessed following intra-orbitofrontal 5-HT1BR agonist infusion, or intra-orbitofrontal 5-HT1BR antagonist infusion coupled with systemic 5-HT1BR agonist treatment. Results Effective, but not ineffective, OCD treatments reduced OCD-like behavior in mice with a time-course that parallels the delayed therapeutic onset in OCD patients, and downregulated 5-HT1BR expression in the orbitofrontal cortex. Intra-orbitofrontal 5-HT1BR agonist infusion induced OCD-like behavior, and intra-orbitofrontal 5-HT1BR antagonist infusion blocked OCD-like effects of systemic 5-HT1BR agonist treatment. Conclusions These results indicate that orbitofrontal 5-HT1BRs are necessary and sufficient to induce OCD-like behavior in mice, and that SRI pharmacotherapy reduces OCD-like behavior by desensitizing orbitofrontal 5-HT1BRs. Our findings suggest an essential role for orbitofrontal 5-HT1BRs in OCD pathophysiology and treatment.

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“…However these drugs reduce heart palpitations and other physical HPA-related symptoms of anxiety and by controlling these feedback signals, the beta blockers offer a relatively new approach to treating some forms of anxiety. Potential side effects include sexual dysfunction, slow pulse, drowsiness, fatigue, dry mouth, numbness or tingling of fingers or toes, dizziness, diarrhea, nausea, weakness, and cold hands and feet [23]. …”

Section: Introductionmentioning

confidence: 99%

Dietary and botanical anxiolytics

Alramadhan

Hanna

et al. 2012

Med Sci Monit

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SummaryDrugs used to treat anxiety have many negative side effects including addiction, depression, suicide, seizures, sexual dysfunction, headaches and more. Anxiolytic medications do not restore normal levels of neurotransmitters but instead manipulate the brain chemistry. For example, selective serotonin reuptake inhibitors (SSRIs) prevent the reuptake of serotonin from the synapse allowing serotonin to remain in the area of activity for a longer period of time but does not correct the lack of serotonin production. Benzodiazepines, such as Valium and Xanax®, stimulate GABA receptors, thus mimicking the calming effects of GABA but again do not fix the lack of GABA production. Often, the brain becomes accustomed to these medications and they often lose their effectiveness, requiring higher doses or different drugs. In contrast to anxiolytic drugs, there are herbs and nutrients which can stimulates neurotransmitter synthesis and more naturally effect and even adjust brain chemistry in the absence of many of the side effects experienced with drugs. Therefore this paper explores several herbal and nutritional approaches to the treatment of anxiety.

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Pharmacotherapy of anxious disorders

Cited by 34 publications

References 220 publications

Implication of 5-HT2 receptor subtypes in the mechanism of action of antidepressants in the four plates test

Implication of 5-HT2 receptor subtypes in the mechanism of action of antidepressants in the four plates test

Essential Role for Orbitofrontal Serotonin 1B Receptors in Obsessive-Compulsive Disorder-Like Behavior and Serotonin Reuptake Inhibitor Response in Mice

Dietary and botanical anxiolytics

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