Protective effect of propranolol and nadolol on social defeat-induced behavioral impairments in rats

Zaidi, Safiyya; Atrooz, Fatin; Valdez, Daniel; Liu, Hesong; Kochi, Camila; Bond, Richard A.; Salim, Samina

doi:10.1016/j.neulet.2020.134892

Cited by 8 publications

(7 citation statements)

References 64 publications

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“…Besides, various social defeat stress rat models have been developed in recent years, including the CSDS and psychosocial witness stress rat model (Patki, Solanki, & Salim, 2014). Existing studies have shown that behavioral and physiologic characteristics of these rat models are similar to those in mouse models (Arora et al, 2018;Finnell et al, 2018;Giacobbo et al, 2020;Kochi et al, 2017;Morais-Silva et al, 2019;Zaidi et al, 2020), which further confirms the feasibility of CSDS-induced behavioral deficits among different strains.…”

Section: Perspectivementioning

confidence: 77%

Chronic social defeat stress mouse model: Current view on its behavioral deficits and modifications.

Wang

Liu

Duan

et al. 2021

Behavioral Neuroscience

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Stress is the main cause of mood disorders such as depression and posttraumatic stress disorder. Individuals respond to stress differently, as some develop depressive symptoms, whereas others successfully cope with adversity, but it remains unclear what makes some particularly vulnerable to stress. The chronic social defeat stress (CSDS) mouse model, an ethologically valid rodent model that exhibits long-term physiological and behavioral phenotypes similar to depression and anxiety, can imitate individual differences in stress responses in humans. In this review, we not only summarize various behavioral deficits of the CSDS mouse model that were reported since its establishment but also concentrate on modified CSDS mouse models that have been developed in recent years, aiming at providing useful information for future research and application of this model.

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Section: Perspectivementioning

confidence: 77%

Chronic social defeat stress mouse model: Current view on its behavioral deficits and modifications.

Wang

Liu

Duan

et al. 2021

Behavioral Neuroscience

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“…SD rats pretreated with propranolol or nadolol spent more time in the lit area of the LDB and in the open arms of the EPM after social defeat, suggesting anxiolytic‐like behavior. 84 The pretreatment of mice with propranolol before social defeat reduced anxiety‐like behavior with increased time to enter the dark zone and decreased total time spent in the dark zone in the LDB. 85 However, the results of these studies are not equivocal and vary from hopeful to negative.…”

Section: Cardiovascular Drugs and Anxietymentioning

confidence: 99%

Cardiovascular therapeutics: A new potential for anxiety treatment?

Repova

Aziriova

Krajcirovicova

et al. 2022

Medicinal Research Reviews

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Besides the well-recognized risk factors, novel conditions increasing cardiovascular morbidity and mortality are emerging.Undesirable emotions and behavior such as anxiety and depression, appear to participate in worsening cardiovascular pathologies. On the other hand, deteriorating conditions of the heart and vasculature result in disturbed mental and emotional health. The pathophysiological background of this bidirectional

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“…Beta blockers such as propranolol and nadolol (non-selective beta1/2 antagonists), metoprolol and atenolol (beta1), and butoxamine (beta2) can exhibit antidepressant-like activity in the FST (Chopra et al, 1988 ; Beĭer, 1994 ; Aisa et al, 2008 ; Park et al, 2012 ; Zaidi et al, 2020 ), including potentiation of sub-effective doses of other putative antidepressants such as baclofen (Aley and Kulkarni, 1990 ), or antagonizing depression-like effects of other agents (Parale et al, 1987 ). A mouse study of propranolol and nadolol found that whereas these two drugs did not exhibit therapeutic effects in the TST, propranolol did show an antidepressant-like decrease in TST-induced hyperthermia (Liu et al, 2003 ).…”

Section: Beta Blockersmentioning

confidence: 99%

“…In contrast to these potentially therapeutic properties of beta blockers, it has also been suggested that these drugs can promote depression-like behavior in rodents (Abel and Hannigan, 1994 ; Stone and Quartermain, 1999 ; Al-Tubuly et al, 2008 ) including in the presence of other putative antidepressants (Zhang et al, 2009 ; Gu et al, 2012 ), or under some circumstances, they have no substantial effect either alone or when co-administered with other putative antidepressants (Danysz et al, 1986 ; Evangelista et al, 1987 ; Finnegan et al, 1987 ; Teste et al, 1990 ; Beĭer, 1994 ; Detke et al, 1995 ; Pesarico et al, 2014 ; Sekio and Seki, 2015 ; Zaidi et al, 2020 ). A number of studies also suggest that the beta3 agonist amibegron (also called SR58611A) has antidepressant-like properties in rodents (Consoli et al, 2007 ; Overstreet et al, 2008 ; Stemmelin et al, 2008 , 2010 ; Tamburella et al, 2010 ), and it may achieve these effects by modulating serotonergic and noradrenergic signaling that is triggered by activation of beta3 receptors (Claustre et al, 2008 ).…”

Section: Beta Blockersmentioning

confidence: 99%

Are Noradrenergic Transmission Reducing Drugs Antidepressants?

Fitzgerald

2021

Front. Behav. Neurosci.

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Major depressive disorder (MDD) remains a significant public health problem worldwide, and revised treatment strategies are therefore urgently needed, including the creation of novel antidepressant compounds or using existing molecular entities in new ways. Etiologic theories of MDD from decades ago have suggested that synaptic deficiencies of monoaminergic neurotransmitters play a causative role in this neuropsychiatric disorder, and that boosting monoamines with drugs such as SSRIs, SNRIs, TCAs, and MAOIs has antidepressant effects and in some individuals can even induce hypomania or mania. While other factors, such as various intracellular molecular pathways and hippocampal neurogenesis, undoubtedly also play a role in MDD, monoaminergic boosting drugs nonetheless have clearly demonstrated antidepressant properties. There is also, however, a body of studies in the preclinical literature suggesting that monoaminergic transmission reducing drugs, including noradrenergic ones, also have antidepressant-like behavioral properties in rodents. Given that there is increasing evidence that the monoamines have u-shaped or Janus-faced dose-response properties, in which a mid-range value is “optimal” in a variety of behavioral and physiological processes, it is plausible that either too much or too little synaptic norepinephrine in key circuits may exacerbate MDD in some individuals. Here we briefly review rodent depression-related behavioral data, focusing on the forced swim test, from three major classes of noradrenergic transmission reducing drugs (alpha2 agonists, beta blockers, alpha1 antagonists), and find much support for the hypothesis that they have antidepressant-like properties. Whether these drugs are antidepressants in human subjects remains to be determined.

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Protective effect of propranolol and nadolol on social defeat-induced behavioral impairments in rats

Cited by 8 publications

References 64 publications

Chronic social defeat stress mouse model: Current view on its behavioral deficits and modifications.

Chronic social defeat stress mouse model: Current view on its behavioral deficits and modifications.

Cardiovascular therapeutics: A new potential for anxiety treatment?

Are Noradrenergic Transmission Reducing Drugs Antidepressants?

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