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JournalISSN: 1662-5153

Frontiers in Behavioral Neuroscience 

Frontiers Media
About: Frontiers in Behavioral Neuroscience is an academic journal published by Frontiers Media. The journal publishes majorly in the area(s): Medicine & Biology. It has an ISSN identifier of 1662-5153. It is also open access. Over the lifetime, 3958 publications have been published receiving 95355 citations.


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Journal ArticleDOI
TL;DR: The WAZM can be used to model traumatic memories re-experiencing in rodent models of human stress-related pathologies such as PTSD and the behavioral changes detected were accompanied by changes of c-Fos expression in the amygdala of exposed rats.
Abstract: Often, freezing and startle behaviors in the context of a previously experienced stress are taken as an indication of posttraumatic stress disorder (PTSD)-like symptoms in rats. However, PTSD is characterized by large individual variations of symptoms. In order to take into consideration the complex and long term distinctive variations in effects of trauma exposure additional behavioral measures are required.The current study used a novel behavioral test, the Water Associated Zero Maze (WAZM). This test was planned to enable a formation of an association between the context of the maze and an underwater trauma or swim stress in order to examine the impact of exposure to the context which immediately precedes a stressful or a traumatic experience on rat's complex behavior. Rats were exposed to the WAZM and immediately after to an underwater trauma or short swim. One month later rats were re-exposed to the context of the WAZM while their behavior was video recorded. Furthermore, c-Fos expression in the amygdala was measured 90 min after this exposure.The results of the current study indicate that the WAZM can be used to discern behavioral changes measured a long time after the actual traumatic or stressful events. Furthermore, the behavioral changes detected were accompanied by changes of c-Fos expression in the amygdala of exposed rats. We suggest that the WAZM can be used to model traumatic memories re-experiencing in rodent models of human stress-related pathologies such as PTSD.

582 citations

Journal ArticleDOI
TL;DR: Excess glucocorticoids in early life can permanently alter tissue glucOCorticoid signalling, effects which may have short-term adaptive benefits but increase the risk of later disease.
Abstract: Numerous clinical studies associate an adverse prenatal environment with the development of cardio-metabolic disorders and neuroendocrine dysfunction, as well as an increased risk of psychiatric diseases in later life. Experimentally, prenatal exposure to stress or excess glucocorticoids in a variety of animal models can malprogram offspring physiology, resulting in a reduction in birth weight and subsequently increasing the likelihood of disorders of cardiovascular function, glucose homeostasis, hypothalamic-pituitary-adrenal (HPA) axis activity and anxiety-related behaviours in adulthood. During fetal development, placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) provides a barrier to maternal glucocorticoids. Reduced placental 11β-HSD2 in human pregnancy correlates with lower birth weight and higher blood pressure in later life. Similarly, in animal models, inhibition or knockout of placental 11β-HSD2 lowers offspring birth weight, in part by reducing glucose delivery to the developing fetus in late gestation. Molecular mechanisms thought to underlie the programming effects of early life stress and glucocorticoids include epigenetic changes in target chromatin, notably affecting tissue-specific expression of the intracellular glucocorticoid receptor (GR). As such, excess glucocorticoids in early life can permanently alter tissue glucocorticoid signalling, effects which may have short-term adaptive benefits but increase the risk of later disease.

572 citations

Journal ArticleDOI
TL;DR: The evidence that infection during the perinatal period of life acts as a vulnerability factor for later-life alterations in cytokine production, and marked changes in cognitive and affective behaviors throughout the remainder of the lifespan is reviewed.
Abstract: The immune system is well characterized for its critical role in host defense. Far beyond this limited role however, there is mounting evidence for the vital role the immune system plays within the brain, in both normal, “homeostatic” processes (e.g., sleep, metabolism, memory), as well as in pathology, when the dysregulation of immune molecules may occur. This recognition is especially critical in the area of brain development. Microglia and astrocytes, the primary immunocompetent cells of the CNS, are involved in every major aspect of brain development and function, including synaptogenesis, apoptosis, and angiogenesis. Cytokines such as tumor necrosis factor [TNF]α, interleukin [IL]-1β, and IL-6 are produced by glia within the CNS, and are implicated in synaptic formation and scaling, long-term potentiation, and neurogenesis. Importantly, cytokines are involved in both injury and repair, and the conditions underlying these distinct outcomes are under intense investigation and debate. Evidence from both animal and human studies implicates the immune system in a number of disorders with known or suspected developmental origins, including schizophrenia, anxiety/depression, and cognitive dysfunction. We review the evidence that infection during the perinatal period of life acts as a vulnerability factor for later-life alterations in cytokine production, and marked changes in cognitive and affective behaviors throughout the remainder of the lifespan. We also discuss the hypothesis that long-term changes in brain glial cell function underlie this vulnerability.

553 citations

Journal ArticleDOI
TL;DR: Inter-domain analysis revealed significant correlations between mood (FST and SCT) and anxiety-like behavior (NSF, but not EPM), and significant correlations were found between cognitive performance (reverse learning task) and mood(s) and Anxiety-like Behavior (NSf).
Abstract: Depression, a complex mood disorder, displays high comorbidity with anxiety and cognitive disorders. To establish the extent of inter-dependence between these behavioral domains, we here undertook a systematic analysis to establish interactions between mood [assessed with the forced-swimming (FST) and sucrose consumption tests (SCT)], anxiety [elevated-plus maze (EPM) and novelty suppressed feeding (NSF) tests] and cognition (spatial memory and behavioral flexibility tests) in rats exposed to unpredictable chronic-mild-stress (uCMS). Expectedly, uCMS induced depressive-like behavior, a hyperanxious phenotype and cognitive impairment; with the exception of the measure of anxiety in the EPM, these effects were attenuated by antidepressants (imipramine, fluoxetine). Measures of mood by the FST and SCT were strongly correlated, whereas no significant correlations were found between the different measures of anxiety (EPM and NSF); likewise, measures of cognition by spatial memory and behavioral flexibility tests were poorly correlated. Inter-domain analysis revealed significant correlations between mood (FST and SCT) and anxiety-like behavior (NSF, but not EPM). Furthermore, significant correlations were found between cognitive performance (reverse learning task) and mood (FST and SCT) and anxiety-like behavior (NSF). These results demonstrate interactions between different behavioral domains that crosscut the disciplines of psychiatry and neurology.

462 citations

Journal ArticleDOI
TL;DR: The scope of the present research topic is to provide a panoramic view of recent progress in neural circuits underlying emotion and motivation: Insights from optogenetics and pharmacogenetics, with special emphasis on circuit level exploration of emotion, motivation and memory.
Abstract: Over the last 10 years, methods that combine genetics and optics have neuroscientists glowing about the possibilities to study movement, motivation, reinforcement, emotion and abnormal reward seeking processes such as addiction and obesity. From the fruit fly, rodents, to primates, optogenetics sheds light on the previously unanswered questions. With its specificity and high temporal precision, we gained several insights about the brain processes and we were the witnesses of those changes in the field. Search with the key word “Optogenetic” retrieved close to 1500 articles in PubMed, almost more than 90% of them published in the past 5 years with tremendous progress in several areas of Neuroscience research. This includes dissection of neural circuitries combined with a vast array of behavioral procedures while simultaneously obtaining neurotransmitter measurement and electrophysiological signatures. These developments led us to deconstruct a detailed view of circuits underlying neuropsychiatric disorders. From studying reward, aversion, anxiety, associative learning, habit formation, the tools also applied to study the long lasting and persistent memories, which are bad for the healthy brain (for example, fear and addiction). The scope of the present research topic “Neural circuits underlying emotion and motivation: Insights from optogenetics and pharmacogenetics” is to provide a panoramic view of recent progress in this direction, with special emphasis on circuit level exploration of emotion, motivation and memory. A number of topics are covered which are of great interest to a broad readership. These include reinforcement, motivation under the influence of drugs compulsive consumption of food reward, and formation of habits and reactivation memory. Some of the reviews explicitly addressed the problems and the necessity of developing the next generation tools. We believe, leveraging the knowledge obtained from this research topic in Behavioral Neuroscience will help us to gain deeper insights in the future.

424 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
2023209
2022556
2021315
2020265
2019288
2018326