Selecting an Appropriate Animal Model of Depression

Hao, Yuanzheng; Ge, Huixiang; Sun, Mengyun; Gao, Yun

doi:10.3390/ijms20194827

Cited by 174 publications

(134 citation statements)

References 112 publications

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“…The depletion of catecholamines (norepinephrine, epinephrine, and dopamine) and serotonin (5-HT) leads to morphological changes in the brain of tested animals and has good face validity due to the appearance of the depression-like phenotype [ 145 , 146 , 147 , 148 , 157 ]. This model is widely used in preclinical studies to evaluate the antidepressant effect of new developing drugs and plant compounds [ 149 , 150 , 151 , 152 , 153 , 154 ] due to the short-term time and good predictive validity [ 147 , 155 ]. However, reserpine treatment produces motor impairments mimicking Parkinson disease dyskinesia, increased nociceptive sensitization and hypothermia and has high mortality rate [ 148 , 155 , 156 , 157 ].…”

Section: Models Of Depressionmentioning

confidence: 99%

“…This model is widely used in preclinical studies to evaluate the antidepressant effect of new developing drugs and plant compounds [ 149 , 150 , 151 , 152 , 153 , 154 ] due to the short-term time and good predictive validity [ 147 , 155 ]. However, reserpine treatment produces motor impairments mimicking Parkinson disease dyskinesia, increased nociceptive sensitization and hypothermia and has high mortality rate [ 148 , 155 , 156 , 157 ].…”

Section: Models Of Depressionmentioning

confidence: 99%

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Animal Models of Depression: What Can They Teach Us about the Human Disease?

2021

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Depression is apparently the most common psychiatric disease among the mood disorders affecting about 10% of the adult population. The etiology and pathogenesis of depression are still poorly understood. Hence, as for most human diseases, animal models can help us understand the pathogenesis of depression and, more importantly, may facilitate the search for therapy. In this review we first describe the more common tests used for the evaluation of depressive-like symptoms in rodents. Then we describe different models of depression and discuss their strengths and weaknesses. These models can be divided into several categories: genetic models, models induced by mental acute and chronic stressful situations caused by environmental manipulations (i.e., learned helplessness in rats/mice), models induced by changes in brain neuro-transmitters or by specific brain injuries and models induced by pharmacological tools. In spite of the fact that none of the models completely resembles human depression, most animal models are relevant since they mimic many of the features observed in the human situation and may serve as a powerful tool for the study of the etiology, pathogenesis and treatment of depression, especially since only few patients respond to acute treatment. Relevance increases by the fact that human depression also has different facets and many possible etiologies and therapies.

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Section: Models Of Depressionmentioning

confidence: 99%

Section: Models Of Depressionmentioning

confidence: 99%

Animal Models of Depression: What Can They Teach Us about the Human Disease?

2021

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“…The inhibition percentage was calculated according to the Eq. 6 [34][35][36]. Accordingly, mice were gently placed in a transparent Plexiglas cylinder (30 cm height × 20 cm width) filled with water (15 cm from the bottom), set at room temperature (23-25°C).…”

Section: Marble-burying Testmentioning

confidence: 99%

QbD-driven development of intranasal lipid nanoparticles for depression treatment

Vitorino

Silva

Gouveia

et al. 2020

European Journal of Pharmaceutics and Biopharmaceutics

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Depression is a life-threatening psychiatric disorder and a multifactorial global public health concern. Current pharmacological treatments present limited efficacy, and are associated with several harmful side effects and development of pharmacoresistance mechanisms. Developing more effective therapeutic options is therefore a priority. This work aims at efficiently designing an antidepressant therapeutic surrogate relying on a dual strategy supported on lipid nanoparticles and intranasal delivery. For that purpose, the formulation was comprehensively optimized following a quality by design perspective. Critical quality attributes (CQAs) ranged from physicochemical to intranasal performance features. The optimized formulation was administered to mice in order to assess the antidepressive and anxiolytic effects by applying the forced swimming and marble-burying tests, respectively. A cross-analysis of the predictive models established for the set of 12 CQAs elicited the formulation containing similar proportion of solid and liquid lipids and lower surfactant concentration as the optimal one. Despite increasing the liquid lipid amount yielded smaller and more homogeneous particle size, and higher release rate, nanostructured lipid carriers (NLCs) provided an earlier and superior pig nasal mucosa permeability than nanoemulsions, along with better stability and cytotoxic profiles. Importantly, the intranasal delivery of the optimal lipid nanoparticle formulation reduced both depressive and anxiety-like behaviors, which positions these intranasal nanosystems in line with the hypothesis of provisioning timely and better acting antidepressant therapies. 1. Introduction Depression is a life-threatening mental disorder and a major public health concern, affecting more than 300 million people of all ages worldwide [1]. It leads to disability, noteworthy health-related costs and decreased quality of life, being considered a prominent risk factor for many other diseases, including neuropsychiatric, cardiovascular, and metabolic conditions [2,3]. Conventional pharmacological treatments for depression are considered relatively well defined. Antidepressant standard-of-care comprises oral selective serotonin reuptake inhibitors (SSRIs, e.g. fluoxetine) and serotonin-norepinephrine reuptake inhibitors (SNRIs, e.g.

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“…Pre-clinical studies conducted on murine model also confirmed this causality. A chronic stress, such as exposure to a long-term inescapable stimulation or a chronic social defeat, is indeed able to induce depressive symptoms in rodents as revealed by specific behavioral tests such as forced swimming test, tail suspension test and sucrose preference test (Hao et al, 2019). Although modeling human depression in animals is challenging and present several limitations, rodent models have been useful in describing specific aspects of mood disturbances in well-designed experimental settings (Hao et al, 2019).…”

Section: Mdd Pathophysiology Hypothesis: the Monoamine Theory And Thementioning

confidence: 99%

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

Bruno

Dolcetti

Rizzo

et al. 2020

Front. Cell. Neurosci.

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In the past years, several theories have been advanced to explain the pathogenesis of Major Depressive Disorder (MDD), a neuropsychiatric disease that causes disability in general population. Several theories have been proposed to define the MDD pathophysiology such as the classic “monoamine-theory” or the “glutamate hypothesis.” All these theories have been recently integrated by evidence highlighting inflammation as a pivotal player in developing depressive symptoms. Proinflammatory cytokines have been indeed claimed to contribute to stress-induced mood disturbances and to major depression, indicating a widespread role of classical mediators of inflammation in emotional control. Moreover, during systemic inflammatory diseases, peripherally released cytokines circulate in the blood, reach the brain and cause anxiety, anhedonia, social withdrawal, fatigue, and sleep disturbances. Accordingly, chronic inflammatory disorders, such as the inflammatory autoimmune disease multiple sclerosis (MS), have been associated to higher risk of MDD, in comparison with overall population. Importantly, in both MS patients and in its experimental mouse model, Experimental Autoimmune Encephalomyelitis (EAE), the notion that depressive symptoms are reactive epiphenomenon to the MS pathology has been recently challenged by the evidence of their early manifestation, even before the onset of the disease. Furthermore, in association to such mood disturbance, inflammatory-dependent synaptic dysfunctions in several areas of MS/EAE brain have been observed independently of brain lesions and demyelination. This evidence suggests that a fine interplay between the immune and nervous systems can have a huge impact on several neurological functions, including depressive symptoms, in different pathological conditions. The aim of the present review is to shed light on common traits between MDD and MS, by looking at inflammatory-dependent synaptic alterations associated with depression in both diseases.

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Selecting an Appropriate Animal Model of Depression

Cited by 174 publications

References 112 publications

Animal Models of Depression: What Can They Teach Us about the Human Disease?

Animal Models of Depression: What Can They Teach Us about the Human Disease?

QbD-driven development of intranasal lipid nanoparticles for depression treatment

Inflammation-Associated Synaptic Alterations as Shared Threads in Depression and Multiple Sclerosis

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