Opposing alterations in anxiety and species-typical behaviours in serotonin transporter overexpressor and knockout mice

Line, Samantha J.; Barkus, Christopher; Coyle, Clare; Jennings, Katie A.; Deacon, Robert M. J.; Lesch, Klaus‐Peter; Sharp, Trevor; Bannerman, David M.

doi:10.1016/j.euroneuro.2010.08.005

Cited by 63 publications

(65 citation statements)

References 59 publications

(24 reference statements)

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“…For example, 5-HTT knockout female rats, who have high levels of serotonin throughout life, appear to be protected against late-onset obesity [100,101] and reduced weight, but higher abdominal fat [102].…”

Section: Animal Studiesmentioning

confidence: 99%

Perinatal selective serotonin reuptake inhibitor (SSRI) effects on body weight at birth and beyond: A review of animal and human studies

Hutchison

Mâsse

Pawluski

et al. 2018

Reproductive Toxicology

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. Perinatal selective serotonin reuptake inhibitor (SSRI) effects on body weight at birth and beyond A review of animal and human studies. Reproductive Toxicology, Elsevier, 2018, 77, pp.109-121. 10 Highlights  Our paper reviews our current understanding of the impact of prenatal SSRI exposure on weight and growth using both human and animal findings.  Our review extends the previously published review paper by Grzeskowiak and colleagues in Repro Tox in 2012 by including findings beyond infancy, the impact of maternal mood -pre and post natal, and given that the majority our 5HT is in the gastrointestinal (GI) system we speculate that altering 5HT signaling, via SSRI exposure might have an impact on GI function and later weight gain.  With recent advances in our understanding of the gut-brain axis and the role of 5HT, we raise critical questions about how weight and growth outcomes might be related to SSRI induced changes in the GI microbiome.  Our paper provides an updated review of the literature (e.g., Leuner et al 2014;Nezvalová-Henriksen et al., 2016), with a particular focus on weight related outcomes beyond birth, developmental aspects of SSRI exposure that might also impact weight and growth, as well as provides detailed suggestions for future research. AbstractThe long-term impact of selective serotonin reuptake inhibitor (SSRI) antidepressant treatment during pregnancy and postpartum on offspring outcomes is still not clear. Specifically, perinatal SSRI exposure may have long-term consequences for body weight and related health outcomes in the newborn period and beyond. This review focuses on the impact of perinatal SSRI exposure on weight using human and animal findings. The impact of maternal mood is also explored. We propose potential mechanisms for weight changes, including how early alterations in serotonin signaling may have implications for weight via changes in metabolism and motor development.As the majority of serotonin is in the gastrointestinal (GI) system we also speculate that perinatal SSRI exposure might alter the brain-gut relationship, via the microbiome, leading to changes in feeding behavior and weight.

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Section: Animal Studiesmentioning

confidence: 99%

Perinatal selective serotonin reuptake inhibitor (SSRI) effects on body weight at birth and beyond: A review of animal and human studies

Hutchison

Mâsse

Pawluski

et al. 2018

Reproductive Toxicology

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“…Only anxiety tests have been applied in such mice to-date, including the elevated plus maze test: 5-HTT over-expression led to reduced anxiety (Jennings et al, 2006;Line et al, 2011). Table 1).…”

Section: Mouse Models Informed By the Human Evidence For Polymorphismmentioning

confidence: 99%

Translating the evidence for gene association with depression into mouse models of depression-relevant behaviour: Current limitations and future potential

Pryce¹,

Klaus

2013

Neuroscience & Biobehavioral Reviews

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Depression is characterised by high prevalence and complex, heterogeneous psychopathology. At the level of aetio-pathology, considerable research effort has been invested to identify specific gene polymorphisms associated with increased depression prevalence. Genome-wide association studies have not identified any risk polymorphisms, and candidate gene case-control studies have identified a small number of risk polymorphisms. It is increasingly recognised that interaction between genotype and environmental factors (G×E), notably stressful life events, is the more realistic unit of depression aetiopathology, with G×E evidence described for a small number of risk polymorphisms. An important complementary approach has been to describe genes exhibiting brain region-specific expression changes in depression. Mouse models of depression informed by the human evidence allow for the study of causality, but to-date have also yielded limited insights into depression aetio-pathology. This review of the translational evidence integrates human and mouse research approaches and evidence. It also makes specific recommendations in terms of how future research in human and mouse should be designed in order to deliver evidence for depression aetio-pathology and thereby to inform the development of novel and improved antidepressant treatments. AbstractDepression is characterised by high prevalence and complex, heterogeneous psychopathology. At the level of aetio-pathology, considerable research effort has been invested to identify specific gene polymorphisms associated with increased depression prevalence. Genome-wide association studies have not identified any risk polymorphisms, and candidate gene case-control studies have identified a small number of risk polymorphisms. It is increasingly recognised that interaction between genotype and environmental factors (GxE), notably stressful life events, is the more realistic unit of depression aetio-pathology, with GxE evidence described for a small number of risk polymorphisms.An important complementary approach has been to describe genes exhibiting brain region-specific expression changes in depression. Mouse models of depression informed by the human evidence allow for the study of causality, but to-date have also yielded limited insights into depression aetiopathology. This review of the translational evidence integrates human and mouse research approaches and evidence. It also makes specific recommendations in terms of how future research in human and mouse should be designed in order to deliver evidence for depression aetio-pathology and thereby to inform the development of novel and improved antidepressant treatments.

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“…In mice, targeted knockout of GAD67 is lethal (Condie et al, 1997); however mice with the GAD65 knockout, which would also alter GABAergic tone, does lead to increases anxiety-related behaviors in the open field test and elevated zero test, which assesses exploratory behaviors in potentially threatening regions that are brightly lit and away from walls or areas lacking walls (Kash et al, 1999). Transgenic knockouts of the 5-HTT gene also increases anxiety-associated behaviors in mice; these mice avoid brightly lit arms in the elevated plus maze and bury fewer marbles in the defensive burying test (Line et al, 2011). Conversely, mice with over-expression of 5-HTT have reduced anxiety-associated behaviors in these same tests (Line et al, 2011).…”

Section: Section 7: Strengths Of Weaknesses Of Animal Models Of Adaptmentioning

confidence: 99%

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

Johnson

Federici

Shekhar

2014

Neuroscience & Biobehavioral Reviews

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Panic disorder (PD) is a severe anxiety disorder that is characterized by recurrent panic attacks (PA), which can be unexpected (uPA, i.e., no clear identifiable trigger) or expected (ePA). Panic typically involves an abrupt feeling of catastrophic fear or distress accompanied by physiological symptoms such as palpitations, racing heart, thermal sensations, and sweating. Recurrent uPA and ePA can also lead to agoraphobia, where subjects with PD avoid situations that were associated with PA. Here we will review recent developments in our understanding of PD, which includes discussions on: symptoms and signs associated with uPA and ePAs; Diagnosis of PD and the new DSM-V; biological etiology such as heritability and gene x environment and gene x hormonal development interactions; comparisons between laboratory and naturally occurring uPAs and ePAs; neurochemical systems that are associated with clinical PAs (e.g. gene associations; targets for triggering or treating PAs), adaptive fear and panic response concepts in the context of new NIH RDoc approach; and finally strengths and weaknesses of translational animal models of adaptive and pathological panic states.

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Opposing alterations in anxiety and species-typical behaviours in serotonin transporter overexpressor and knockout mice

Cited by 63 publications

References 59 publications

Perinatal selective serotonin reuptake inhibitor (SSRI) effects on body weight at birth and beyond: A review of animal and human studies

Perinatal selective serotonin reuptake inhibitor (SSRI) effects on body weight at birth and beyond: A review of animal and human studies

Translating the evidence for gene association with depression into mouse models of depression-relevant behaviour: Current limitations and future potential

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

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