1,720,973 research outputs found
MiRNA-34 and stress response
Get PDFPsychiatric disorders are known to result from a strong interaction between genetic predisposition and environmental factors, mainly exposure to stressful events. Environmental events can modulate genes expression, possibly via epigenetic mechanisms, and affect onset/expression of a disease [1]. Epigenetic mechanisms include, among others, post-transcriptional regulation by non-coding RNAs such as microRNAs (miRNAs). MiRNAs are small non-coding RNAs predicted to regulate hundreds of targets and to be engaged in every biological process [2]. Thanks to their ability to fine-tune gene expression, miRNAs can control gene expression patterns favoring organism’s adaptation to internal and
environmental (external) factors [3], such as stressful events
Editorial: Long-term effects of early-life manipulations: risks and advantages for neurodevelopment
No full textLong-term effects of early environment on the brain: Lesson from rodent models
No full textThe postnatal period is characterized by extensive neuronal plasticity, synaptic organization, and remod-eling. High neuroplasticity renders the brain sensitive to the remodeling effects induced by environmentalfactors, such as exposure to adversity, which can imprint neurochemical, neuroendocrine, morphological,and behavioral changes.Early experiences that influence developmental trajectories during maturation of the brain can have awide range of long-lasting effects, modulating stress-coping strategies in adult life and inducing vulner-ability or resilience to psychopathologies, depending on the gene × later experience interplay.Future studies will clarify how manipulation of the early environment induces these effects acting ongenetic and epigenetic factors
Linking drug and food addiction: an overview of the shared neural circuits and behavioral phenotype
No full text: Despite a lack of agreement on its definition and inclusion as a specific diagnosable disturbance, the food addiction construct is supported by several neurobiological and behavioral clinical and preclinical findings. Recognizing food addiction is critical to understanding how and why it manifests. In this overview, we focused on those as follows: 1. the hyperpalatable food effects in food addiction development; 2. specific brain regions involved in both food and drug addiction; and 3. animal models highlighting commonalities between substance use disorders and food addiction. Although results collected through animal studies emerged from protocols differing in several ways, they clearly highlight commonalities in behavioral manifestations and neurobiological alterations between substance use disorders and food addiction characteristics. To develop improved food addiction models, this heterogeneity should be acknowledged and embraced so that research can systematically investigate the role of specific variables in the development of the different behavioral features of addiction-like behavior in preclinical models
Interactions between experience, genotype and sex in the development of individual coping strategies
Get PDFCoping strategies, the first line of defense against adversities, develop through experience. There is consistent evidence that both genotype and sex contribute to the development of dysfunctional coping, leading to maladaptive outcomes of adverse experiences or to adaptive coping that fosters rapid recovery even from severe stress. However, how these factors interact to influence the development of individual coping strategies is just starting to be investigated. In the following review, we will consider evidence that experience, sex, and genotype influence the brain circuits and neurobiological processes involved in coping with adversities and discuss recent results pointing to the specific effects of the interaction between early experiences, genotype, and stress in the development of functional and dysfunctional coping styles
Interaction Between Genetic And Environmental Factors Promotes Eating Disorders Altering Expression And Function Of Dopamine, Serotonin And Norepinephrine Receptors
No full textEating disorders are multifactorial conditions involving genetic, metabolic, environmental, and behavioral factors. Although animal studies cannot reproduce the complex psychosomatic features of human eating disorders, can be useful to separately examine the elements of the homeostatic and motivational impairments associated with compulsive eating behaviors.
Drugs of abuse and palatable food intake show behavioral similarities and common neurobiological adaptations have been proposed to be involved in both drug and food related-disorders (Volkow and Wise, 2005). Compulsive drug intake in the face of adverse consequences is a hallmark feature of addiction and compulsive drug seeking has been shown to emerge only following an extended history of drug-taking (Vanderschuren and Everitt, 2004). Similarly, compulsive eating emerges following extended access to a palatable diet (Johnson and Kenny, 2010). Finally, stress exposure influences both the propensity to take drugs and food intake.
Dopamine is a neurotransmitter critically involved in the reward and motivational aspects of feeding and D2 receptors have received particular attention (Wang et al., 2001; Davis et al 2009). However, recent reviews have focused on central monoamine systems in eating disorders, such serotonin and norepinephrine (Hainer et al , 2006; Kaye, 2008).
Here we show that interaction between extended access to chocolate and chronic stress is able to transform adaptive food seeking/intake behavior into compulsive eating in DBA/2J mice (previously shown by Patel and coworkers, 2006, to be characterized by high impulsivity), but not in C57BL/6J mice.
Moreover, we find strong alterations of dopamine, serotonin and norepinephrine receptors expression in three brain areas (medial prefrontal cortex, nucleus accumbens, dorsal striatum) critically involved in food-related motivated behavior.
The animal model proposed here could be a good tool for understanding how environmental factors interact with genetic vulnerability to promote the development of eating disorders altering expression and function of dopamine, serotonin and norepinephrine receptors
Animal models of compulsive eating behavior
Get PDFIn industrialized nations, overeating is a significant problem leading to overweight, obesity, and a host of related disorders; the increase in these disorders has prompted a significant amount of research aimed at understanding their etiology. Eating disorders are multifactorial conditions involving genetic, metabolic, environmental, and behavioral factors. Considering that compulsive eating in the face of adverse consequences characterizes some eating disorders, similar to the way in which compulsive drug intake characterizes drug-addiction, it might be considered an addiction in its own right. Moreover, numerous review articles have recently drawn a connection between the neural circuits activated in the seeking/intake of palatable food and drugs of abuse. Based on this observation, “food addiction” has emerged as an area of intense scientific research and accumulating evidence suggests it is possible to model some aspects of food addiction in animals. The development of well-characterized animal models would advance our understanding of the etiologic neural factors involved in eating disorders, such as compulsive overeating, and it would permit to propose targeted pharmacological therapies. However, to date, little evidence has been reported of continued food seeking and intake despite its harmful consequences in rats and mice
Effects of lack of microRNA-34 on the neural circuitry underlying the stress response and anxiety
Get PDFStress-related psychiatric disorders, including anxiety, are complex diseases that have genetic, and
environmental causes. Stressful experiences increase the release of prefrontal amygdala neurotransmitters,
a response that is relevant to cognitive, emotional, and behavioral coping. Moreover, exposure to
stress elicits anxiety-like behavior and dendritic remodeling in the amygdala. Members of the miR-34
family have been suggested to regulate synaptic plasticity and neurotransmission processes, which
mediate stress-related disorders. Using mice that harbored targeted deletions of all 3 members of the
miR-34-family (miR-34-TKO), we evaluated acute stress-induced basolateral amygdala (BLA)-GABAergic
and medial prefrontal cortex (mpFC) aminergic outflow by intracerebral in vivo microdialysis. Moreover,
we also examined fear conditioning/extinction, stress-induced anxiety, and dendritic remodeling in the
BLA of stress-exposed TKO mice.
We found that TKO mice showed resilience to stress-induced anxiety and facilitation in fear extinction.
Accordingly, no significant increase was evident in aminergic prefrontal or amygdala GABA release, and
no significant acute stress-induced amygdalar dendritic remodeling was observed in TKO mice. Differential
GRM7, 5-HT2C, and CRFR1 mRNA expressionwas noted in the mpFC and BLA between TKO andWT
mice. Our data demonstrate that the miR-34 has a critical function in regulating the behavioral and
neurochemical response to acute stress and in inducing stress-related amygdala neuroplasticity
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