Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

Veniaminova, Ekaterina; Cespuglio, Raymond; Чернуха, И. М.; Schmitt-Boehrer, Angelika G.; Морозов, С. В.; Kalueff, Allan V.; Kuznetsova, Oxana; Anthony, Daniel C.; Lesch, Klaus‐Peter; Strekalova, Tatyana

doi:10.3389/fnins.2020.00024

Cited by 23 publications

(39 citation statements)

References 85 publications

(117 reference statements)

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“…Compared with rats that were fed normal chow, HFD rats had significantly higher levels of TPH1 (tryptophan hydroxylase 1), the enzyme involved in serotonin synthesis, and lower SERT (serotonin transporter) protein expression, although this was not statistically significant. In an interesting study, researchers simulated a western diet (high fat, high cholesterol, calorie‐dense) in mice of three different genotypes: Sert ‐/‐, Sert +/‐, and Sert +/+ (Veniaminova et al., 2020). Here, the heterozygous mice showed remarkable resilience to the negative physiological changes induced by the western diet, namely glucose intolerance, neuroinflammation, and disturbed expression of the serotonin autoreceptors and heteroreceptors, Htr2a, Htr1b, and Htr2c, compared with SERT knockout and wild‐type mice.…”

Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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Diabetes increases the likelihood of developing depression and vice versa. Research on this bidirectional association has somewhat managed to delineate the interplay among implicated physiological processes. Still, further exploration is required in this context. This review addresses the comorbidity by investigating suspected common pathophysiological mechanisms. One such factor is psychological stress which disturbs the hypothalamic–pituitary–adrenal axis causing hormonal imbalance. This includes elevated cortisol levels, a common biomarker of both depression and diabetes. Disrupted insulin signaling drives the hampered neurotransmission of serotonin, dopamine, and norepinephrine. Also, adipokine hormones such as adiponectin, leptin, and resistin and the orexigenic hormone, ghrelin, are involved in both depression and T2DM. This disarray further interferes with physiological processes encompassing sleep, the gut–brain axis, metabolism, and mood stability. Behavioral coping mechanisms, such as unhealthy eating, mediate disturbed glucose homeostasis, and neuroinflammation. This is intricately linked to oxidative stress, redox imbalance, and mitochondrial dysfunction. However, interventions such as psychotherapy, physical exercise, fecal microbiota transplantation, and insulin‐sensitizing agents can help to manage the distressing condition. The possibility of glucagon‐like peptide 1 possessing a therapeutic role has also been discussed. Nonetheless, there stands an urgent need for unraveling new correlating targets and biological markers for efficient treatment.

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Section: Physiological Factors That Play Key Roles In the Comorbiditymentioning

confidence: 99%

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Subba

Sandhir

Singh

et al. 2021

Eur J of Neuroscience

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“…In Study 1, FUS-tg mice at the age of 9 weeks corresponding to a pre-symptomatic stage of the ALS model alone with wild type littermates, were studied for motor functions in the Cat-walk, Wire test, Grip-test, Pole test and Rotarod model with 1-hour inter-test interval as described elsewhere (Veniaminova et al, 2020;; see below) to verify the absence of any motor deficits during three days prior the experiment (Fig. 1A, data now shown).…”

Section: Methodsmentioning

confidence: 99%

“…Mice were placed on constantly rotting rod of rotarod (Columbus Instruments, Columbus, OH, USA; speed 10 rpm) for 600s. Latency to fall and the number and percent of mice with falling events (latency<200s) were registered in three runs as described elsewhere (Veniaminova et al, 2020;.…”

Section: Rotarodmentioning

confidence: 99%

“…Mice were allowed to grip a horizontal wire (diameter 0.3 cm, height above the surface 60 cm) for 180s. The latency of falling and the number and percent of mice with falling events (latency<20s) were recorded as described elsewhere (Veniaminova et al, 2020;.…”

Section: Wire Testmentioning

confidence: 99%

“…Mice were placed on a top of the vertical bar (diameter 1.1 cm, height 60 cm) and allowed to climb down to a horizontal surface. The latency of descending the bar and the number and percent of mice with sliding events (latency to descend<50s) were scored as described elsewhere (Veniaminova et al, 2020;.…”

Section: Pole Testmentioning

confidence: 99%

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The patient's own bone marrow-derived stromal cells

Munter¹

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Molecular signature of excessive female aggression: study of stressed mice with genetic inactivation of neuronal serotonin synthesis

Strekalova,

Moskvin,

Jain

et al. 2023

J Neural Transm

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Aggression is a complex social behavior, critically involving brain serotonin (5-HT) function. The neurobiology of female aggression remains elusive, while the incidence of its manifestations has been increasing. Yet, animal models of female aggression are scarce. We previously proposed a paradigm of female aggression in the context of gene x environment interaction where mice with partial genetic inactivation of tryptophan hydroxylase-2 (Tph2+/− mice), a key enzyme of neuronal 5-HT synthesis, are subjected to predation stress resulting in pathological aggression. Using deep sequencing and the EBSeq method, we studied the transcriptomic signature of excessive aggression in the prefrontal cortex of female Tph2+/− mice subjected to rat exposure stress and food deprivation. Challenged mutants, but not other groups, displayed marked aggressive behaviors. We found 26 genes with altered expression in the opposite direction between stressed groups of both Tph2 genotypes. We identified several molecular markers, including Dgkh, Arfgef3, Kcnh7, Grin2a, Tenm1 and Epha6, implicated in neurodevelopmental deficits and psychiatric conditions featuring impaired cognition and emotional dysregulation. Moreover, while 17 regulons, including several relevant to neural plasticity and function, were significantly altered in stressed mutants, no alteration in regulons was detected in stressed wildtype mice. An interplay of the uncovered pathways likely mediates partial Tph2 inactivation in interaction with severe stress experience, thus resulting in excessive female aggression.

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Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

Cited by 23 publications

References 85 publications

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

Pathophysiology linking depression and type 2 diabetes: Psychotherapy, physical exercise, and fecal microbiome transplantation as damage control

The patient's own bone marrow-derived stromal cells

Molecular signature of excessive female aggression: study of stressed mice with genetic inactivation of neuronal serotonin synthesis

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