Tail-flick test response in 3×Tg-AD mice at early and advanced stages of disease

Baeta-Corral, Raquel; Defrin, R.; Pick, Chagi G.

doi:10.1016/j.neulet.2015.06.007

Cited by 11 publications

(7 citation statements)

References 29 publications

(39 reference statements)

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“…The present results showing preservation of pain sensitivity to a hot stimulus through aging and AD processes complement those previously reported by our laboratory in the tail-flick test (Baeta-Corral et al, 2015 ). The nociceptive response to a cold stimulus was studied in male 3xTg-AD mice from early to advanced stages of disease (7 and 11 months of age, respectively) and found preserved.…”

Section: Discussionsupporting

confidence: 93%

“…In fact, this animal model of Alzheimer’s disease progressively develops βA plaques and neurofibrillary tangles with a temporal-and regional- specific profile that closely mimics their development in the human AD brain (Barrot, 2012 ). Synaptic dysfunction manifests in an age-dependent manner starting at 6 months of age but before plaque (12 months of age) and tangle (15 months of age) hallmark neuropathology (Belfiore et al, 2019 ) and severe cognitive impairment (Chapman et al, 1985 ; Giménez-Llort et al, 2007 ; Baeta-Corral et al, 2015 ). 3xTg-AD mice show diminished curiosity and apathy (exploration) in the open-field and lack of ability to cope with mild stressors (novelty) with increased emotionality (freezing behavior, defecation, and urination) in most of the behavioral tests (Oddo et al, 2003a , b ; Billings et al, 2005 ; Giménez-Llort et al, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

“…3xTg-AD mice show diminished curiosity and apathy (exploration) in the open-field and lack of ability to cope with mild stressors (novelty) with increased emotionality (freezing behavior, defecation, and urination) in most of the behavioral tests (Oddo et al, 2003a , b ; Billings et al, 2005 ; Giménez-Llort et al, 2007 ). At early and advanced stages of the disease, male 3xTg-AD show preserved tail flicking withdrawal response to a cold stimulus and presented a correlation with the immediate response exhibited in a sort of environments differing in the anxiogenic levels (Baeta-Corral et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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Preserved Thermal Pain in 3xTg-AD Mice With Increased Sensory-Discriminative Pain Sensitivity in Females but Affective-Emotional Dimension in Males as Early Sex-Specific AD-Phenotype Biomarkers

Cañete

2021

Front. Aging Neurosci.

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The increase of the aging population, where quite chronic comorbid conditions are associated with pain, draws growing interest across its investigation and the underlying nociceptive mechanisms. Burn injuries associated problems might be of relevance in the older adult’s daily life, but in people with dementia, exposure to high temperatures and heat sources poses a significantly increased risk of burns. In this brief report, the hind paws and tail pain withdrawal reflexes and the emotional responses to thermal nociception in 3xTg-AD mice were characterized for the first time in the plantar test and compared to their non-transgenic (NTg) counterparts. We studied a cohort of male and female 3xTg-AD mice at asymptomatic (2 months), early (6 months), middle (9 months), and advanced (12 and 15 months) stages of the disease and as compared to sex- and age-matched NTg control mice with normal aging. At 20 and 40W intensities, the sensorial-discriminative thresholds eliciting the withdrawal responses were preserved from asymptomatic to advanced stages of the disease compared to NTg counterparts. Moreover, 3xTg-AD females consistently showed a greater sensory-discriminative sensitivity already at premorbid ages, whereas increased emotionality was shown in males. False-negative results were found in “blind to sex and age” analysis, warning about the need to study sexes independently. The current results and previous report in cold thermal stimulation provide two paradigms unveiling sex-specific early AD-phenotype nociceptive biomarkers to study the mechanistic underpinnings of sex-, age- and AD-disease-dependent thermal pain sensitivity.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Preserved Thermal Pain in 3xTg-AD Mice With Increased Sensory-Discriminative Pain Sensitivity in Females but Affective-Emotional Dimension in Males as Early Sex-Specific AD-Phenotype Biomarkers

Cañete

2021

Front. Aging Neurosci.

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“…When it was stable, 1/3rd of the tail was placed in hot water at 52°C. The tail-flick latency (from the tail entering the water to exiting) was measured with a stopwatch (accuracy: 0.01 s) for 4 consecutive times each with an interval of 1 min [21]. Each tail was measured in triplicate, and the average value was calculated.…”

Section: Thermal Tail-flick Testmentioning

confidence: 99%

NLRP3 inflammasome inhibitor MCC950 attenuates primary dysmenorrhea in mice via the NF-κB/COX-2/PG pathway

et al. 2020

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Background: Primary dysmenorrhea (PD) constitutes a common gynecological disease among young women. The NLRP3 inflammasome may be activated and expressed in PD, but the mechanistic link between NLRP3 inflammasome activation and PD is still unclear. Methods: To investigate the potential role of NLRP3 inflammasome activation in the pathogenesis of PD, 30 female Kunming mice without pregnancy were used for experiments. The PD mouse model was constructed by 11 days of successive co-treatment with estradiol and oxytocin. MCC950, a potent and specific small-molecule inhibitor of the NLRP3 inflammasome, was used to treat PD mice. The disease level was assessed by the writhing response and hot water tail-flick test. The levels of prostaglandin E 2 (PGE 2) and prostaglandin F 2 alpha (PGF 2α) in the uterine tissues of mice were detected by ELISA. The expression levels of protein and cytokines, including NLRP3, cysteine aspartic acid-specific protease 1 (caspase-1), interleukin (IL)-1β, IL-18, nuclear factor kappa B (NF-κB) p65, phospho-NF-κB p65, and cyclooxygenase-2 (COX-2) were revealed by western blot analysis. Results: MCC950 greatly ameliorated the writhing response induced by the combination of oxytocin and estradiol, with an increasing length of tail-flick latency. MCC950 also significantly decreased the levels of PGF 2α and PGE 2 , and the expressions of NLRP3, caspase-1, IL-1β, IL-18, phospho-NF-κB p65, NF-κB p65, and COX-2 in the uterus. Conclusions: MCC950 markedly alleviated the pain and pathological damage in PD mice by inhibiting NLRP3 activation. The underlying mechanism may be related to hypoactive uterine inflammation via suppression of NLRP3 activation and the NF-κB/COX-2/PG pathway in uteruses of PD mice.

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“…When it was stable, 1/3rd of the tail was placed in hot water at 52°C. The tail-flick latency (from the tail entering the water to exiting) was measured with a stopwatch (accuracy: 0.01 s) for 4 consecutive times each with an interval of 1 min [16]. Each tail was measured in triplicate, and the average value was calculated.…”

Section: Thermal Tail-flick Testmentioning

confidence: 99%

NLRP3 inflammasome inhibitor MCC950 attenuates primary dysmenorrhea in mice via the NF-κB/COX-2/PG pathway

Tang

Liu

Chen

et al. 2020

Preprint

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Background: Primary dysmenorrhea (PD) constitutes a common gynecological disease among young women. The NLRP3 inflammasome may be activated and expressed in PD, but the mechanistic link between NLRP3 inflammasome activation and PD is still unclear.Methods: To investigate the potential role of NLRP3 inflammasome activation in the pathogenesis of PD, thirty female Kunming mice without pregnancy were used for experiments. The PD mouse model was constructed by 11 days of successive co-treatment with estradiol and oxytocin. MCC950, a potent and specific small-molecule inhibitor of the NLRP3 inflammasome, was used to treat PD mice. The disease level was assessed by the writhing response and hot water tail-flick test. The levels of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2α) in the uterine tissues of mice were detected by ELISA. The expression levels of protein and cytokines, including NLRP3, cysteine aspartic acid-specific protease 1 (caspase-1), interleukin (IL)-1β, IL-18, nuclear factor kappa B (NF-κB) p65, phospho-NF-κB p65, and cyclooxygenase-2 (COX-2) were revealed by western blot analysis.Results: MCC950 greatly ameliorated the writhing response induced by the combination of oxytocin and estradiol, with an increasing length of tail-flick latency. MCC950 also significantly decreased the levels of PGF2α and PGE2, and the expressions of NLRP3, caspase-1, IL-1β, IL-18, phospho-NF-κB p65, NF-κB p65, and COX-2 in the uterus.Conclusions: MCC950 markedly alleviated the pain and pathological damage in PD mice by inhibiting NLRP3 activation. The underlying mechanism may be related to hypoactive uterine inflammation via suppression of NLRP3 activation and the NF-κB/COX-2/PG pathway in uteruses of PD mice.

show abstract

Tail-flick test response in 3×Tg-AD mice at early and advanced stages of disease

Cited by 11 publications

References 29 publications

Preserved Thermal Pain in 3xTg-AD Mice With Increased Sensory-Discriminative Pain Sensitivity in Females but Affective-Emotional Dimension in Males as Early Sex-Specific AD-Phenotype Biomarkers

Preserved Thermal Pain in 3xTg-AD Mice With Increased Sensory-Discriminative Pain Sensitivity in Females but Affective-Emotional Dimension in Males as Early Sex-Specific AD-Phenotype Biomarkers

NLRP3 inflammasome inhibitor MCC950 attenuates primary dysmenorrhea in mice via the NF-κB/COX-2/PG pathway

NLRP3 inflammasome inhibitor MCC950 attenuates primary dysmenorrhea in mice via the NF-κB/COX-2/PG pathway

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