Differential anxiety-related behaviours and brain activation in Tph2-deficient female mice exposed to adverse early environment
Auth C. S., Weidner M. T., Popp S., Strekalova T. V., Schmitt-Böhrer A. G., van d. H. D. L., Lesh K. Yu., Waider J.
European Neuropsychopharmacology
Vol.28, Issue11, P. 1270-1283
Опубликовано: 2018
Тип ресурса: Статья
DOI:10.1016/j.euroneuro.2018.07.103
Аннотация:
Anxiety disorders represent one of the most prevalent mental disorders in today's society and early adversity has been identified as major contributor to anxiety-related pathologies. Serotonin (5-hydroxytryptamine, 5-HT) is implicated in mediating the effects of early-life events on anxiety-like behaviours. In order to further elucidate the interaction of genetic predisposition and adversity in early, developmental stages on anxiety-related behaviours, the current study employed tryptophan hydroxylase 2 (Tph2)–deficient female mice, as a model for lifelong brain 5-HT synthesis deficiency. Offspring of this line were exposed to maternal separation (MS) and tested, in the open-field (OF) or the dark-light box (DLB). Subsequently, neural activity was assessed, using c-Fos immunohistochemistry. In the DLB, MS rescued the observed decrease in activity in the light compartment of homozygous Tph2–deficient mice and furthermore increased the incidence of escape-related jumps in animals of the
Ключевые слова:
Anxiety; Behaviour; c-Fos; Maternal separation; Mouse; Serotonin
protein c fos; serotonin; tryptophan hydroxylase 2; protein c fos; serotonin; Tph2 protein, mouse; tryptophan hydroxylase; animal experiment; animal model; anxiety disorder; Article; basolateral amygdala; brain region; cell density; cohort analysis; controlled study; dorsolateral periaqueductal gray; environmental exposure; escape behavior; female; illumination; immunohistochemistry; jumping; light dark cycle; maternal deprivation; mouse; nonhuman; open field test; post hoc analysis; priority journal; progeny; rearing; amygdala; animal; animal behavior; anxiety; brain; deficiency; genetics; hypothalamic paraventricular nucleus; knockout mouse; metabolism; pathophysiology; periaqueductal gray matter; physiology; Amygdala; Animals; Anxiety; Behavior, Animal; Brain; Female; Maternal Deprivation; Mice; Mice, Knockout; Paraventricular Hypothalamic Nucleus; Periaqueductal Gray; Proto-Oncogene Proteins c-fos; Serotonin; Tryptophan Hydroxylase
Язык текста: Английский
ISSN: 1873-7862
Auth C. S.
Weidner M. T.
Popp S.
Strekalova T. V. Tat`yana Valeryevna 1969-
Schmitt-Böhrer A. G.
van d. H. D. L. den Hove D.L.
Lesh K. Yu. Klaus-Peter Yulius 1957-
Waider J.
Аутх C. С.
Wеиднер М. Т.
Попп С.
Стрекалова Т. В. Татьяна Валерьевна 1969-
Счмитт-Бöхрер А. Г.
ван д. Х. Д. Л. ден Хове Д.Л.
Леш К. Ю. Клаус-Петер Юлиус 1957-
Wаидер Й.
Differential anxiety-related behaviours and brain activation in Tph2-deficient female mice exposed to adverse early environment
Текст визуальный непосредственный
European Neuropsychopharmacology
Elsevier Science Publisher B.V.
Vol.28, Issue11 P. 1270-1283
2018
Статья
Anxiety Behaviour c-Fos Maternal separation Mouse Serotonin
protein c fos serotonin tryptophan hydroxylase 2 protein c fos serotonin Tph2 protein, mouse tryptophan hydroxylase animal experiment animal model anxiety disorder Article basolateral amygdala brain region cell density cohort analysis controlled study dorsolateral periaqueductal gray environmental exposure escape behavior female illumination immunohistochemistry jumping light dark cycle maternal deprivation mouse nonhuman open field test post hoc analysis priority journal progeny rearing amygdala animal animal behavior anxiety brain deficiency genetics hypothalamic paraventricular nucleus knockout mouse metabolism pathophysiology periaqueductal gray matter physiology Amygdala Animals Anxiety Behavior, Animal Brain Female Maternal Deprivation Mice Mice, Knockout Paraventricular Hypothalamic Nucleus Periaqueductal Gray Proto-Oncogene Proteins c-fos Serotonin Tryptophan Hydroxylase
Anxiety disorders represent one of the most prevalent mental disorders in today's society and early adversity has been identified as major contributor to anxiety-related pathologies. Serotonin (5-hydroxytryptamine, 5-HT) is implicated in mediating the effects of early-life events on anxiety-like behaviours. In order to further elucidate the interaction of genetic predisposition and adversity in early, developmental stages on anxiety-related behaviours, the current study employed tryptophan hydroxylase 2 (Tph2)–deficient female mice, as a model for lifelong brain 5-HT synthesis deficiency. Offspring of this line were exposed to maternal separation (MS) and tested, in the open-field (OF) or the dark-light box (DLB). Subsequently, neural activity was assessed, using c-Fos immunohistochemistry. In the DLB, MS rescued the observed decrease in activity in the light compartment of homozygous Tph2–deficient mice and furthermore increased the incidence of escape-related jumps in animals of the