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Mauricette Brocco - One of the best experts on this subject based on the ideXlab platform.
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The Vogel conflict test: procedural aspects, gamma-aminobutyric acid, glutamate and monoamines.
European journal of pharmacology, 2003Co-Authors: Mark J Millan, Mauricette BroccoAbstract:A multitude of mechanisms are involved in the control of emotion and in the response to stress. These incorporate mediators/targets as diverse as gamma-aminobutyric acid (GABA), excitatory amino acids, monoamines, hormones, neurotrophins and various neuropeptides. Behavioural models are indispensable for characterization of the neuronal substrates underlying their implication in the Etiology of Anxiety, and of their potential therapeutic pertinence to its management. of considerable significance in this regard are conflict paradigms in which the influence of drugs upon conditioned (trained) behaviours is examined. For example, the Vogel conflict test, which was introduced some 30 years ago, measures the ability of drugs to release the drinking behaviour of water-deprived rats exposed to a mild aversive stimulus ("punishment"). This model, of which numerous procedural variants are discussed herein, has been widely used in the evaluation of potential anxiolytic agents. In particular, it has been exploited in the characterization of drugs interacting with GABAergic, glutamatergic and monoaminergic networks, the actions of which in the Vogel conflict test are summarized in this article. More recently, the effects of drugs acting at neuropeptide receptors have been examined with this model. It is concluded that the Vogel conflict test is of considerable utility for rapid exploration of the actions of anxiolytic (and anxiogenic) drugs. Indeed, in view of its clinical relevance, broader exploitation of the Vogel conflict test in the identification of novel classes of anxiolytic agents, and in the determination of their mechanisms of action, would prove instructive.
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The Vogel conflict test: procedural aspects, γ-aminobutyric acid, glutamate and monoamines
European Journal of Pharmacology, 2003Co-Authors: Mark J Millan, Mauricette BroccoAbstract:Abstract A multitude of mechanisms are involved in the control of emotion and in the response to stress. These incorporate mediators/targets as diverse as γ-aminobutyric acid (GABA), excitatory amino acids, monoamines, hormones, neurotrophins and various neuropeptides. Behavioural models are indispensable for characterization of the neuronal substrates underlying their implication in the Etiology of Anxiety, and of their potential therapeutic pertinence to its management. of considerable significance in this regard are conflict paradigms in which the influence of drugs upon conditioned (trained) behaviours is examined. For example, the Vogel conflict test, which was introduced some 30 years ago, measures the ability of drugs to release the drinking behaviour of water-deprived rats exposed to a mild aversive stimulus (“punishment”). This model, of which numerous procedural variants are discussed herein, has been widely used in the evaluation of potential anxiolytic agents. In particular, it has been exploited in the characterization of drugs interacting with GABAergic, glutamatergic and monoaminergic networks, the actions of which in the Vogel conflict test are summarized in this article. More recently, the effects of drugs acting at neuropeptide receptors have been examined with this model. It is concluded that the Vogel conflict test is of considerable utility for rapid exploration of the actions of anxiolytic (and anxiogenic) drugs. Indeed, in view of its clinical relevance, broader exploitation of the Vogel conflict test in the identification of novel classes of anxiolytic agents, and in the determination of their mechanisms of action, would prove instructive.
Mark J Millan - One of the best experts on this subject based on the ideXlab platform.
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The Vogel conflict test: procedural aspects, gamma-aminobutyric acid, glutamate and monoamines.
European journal of pharmacology, 2003Co-Authors: Mark J Millan, Mauricette BroccoAbstract:A multitude of mechanisms are involved in the control of emotion and in the response to stress. These incorporate mediators/targets as diverse as gamma-aminobutyric acid (GABA), excitatory amino acids, monoamines, hormones, neurotrophins and various neuropeptides. Behavioural models are indispensable for characterization of the neuronal substrates underlying their implication in the Etiology of Anxiety, and of their potential therapeutic pertinence to its management. of considerable significance in this regard are conflict paradigms in which the influence of drugs upon conditioned (trained) behaviours is examined. For example, the Vogel conflict test, which was introduced some 30 years ago, measures the ability of drugs to release the drinking behaviour of water-deprived rats exposed to a mild aversive stimulus ("punishment"). This model, of which numerous procedural variants are discussed herein, has been widely used in the evaluation of potential anxiolytic agents. In particular, it has been exploited in the characterization of drugs interacting with GABAergic, glutamatergic and monoaminergic networks, the actions of which in the Vogel conflict test are summarized in this article. More recently, the effects of drugs acting at neuropeptide receptors have been examined with this model. It is concluded that the Vogel conflict test is of considerable utility for rapid exploration of the actions of anxiolytic (and anxiogenic) drugs. Indeed, in view of its clinical relevance, broader exploitation of the Vogel conflict test in the identification of novel classes of anxiolytic agents, and in the determination of their mechanisms of action, would prove instructive.
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The Vogel conflict test: procedural aspects, γ-aminobutyric acid, glutamate and monoamines
European Journal of Pharmacology, 2003Co-Authors: Mark J Millan, Mauricette BroccoAbstract:Abstract A multitude of mechanisms are involved in the control of emotion and in the response to stress. These incorporate mediators/targets as diverse as γ-aminobutyric acid (GABA), excitatory amino acids, monoamines, hormones, neurotrophins and various neuropeptides. Behavioural models are indispensable for characterization of the neuronal substrates underlying their implication in the Etiology of Anxiety, and of their potential therapeutic pertinence to its management. of considerable significance in this regard are conflict paradigms in which the influence of drugs upon conditioned (trained) behaviours is examined. For example, the Vogel conflict test, which was introduced some 30 years ago, measures the ability of drugs to release the drinking behaviour of water-deprived rats exposed to a mild aversive stimulus (“punishment”). This model, of which numerous procedural variants are discussed herein, has been widely used in the evaluation of potential anxiolytic agents. In particular, it has been exploited in the characterization of drugs interacting with GABAergic, glutamatergic and monoaminergic networks, the actions of which in the Vogel conflict test are summarized in this article. More recently, the effects of drugs acting at neuropeptide receptors have been examined with this model. It is concluded that the Vogel conflict test is of considerable utility for rapid exploration of the actions of anxiolytic (and anxiogenic) drugs. Indeed, in view of its clinical relevance, broader exploitation of the Vogel conflict test in the identification of novel classes of anxiolytic agents, and in the determination of their mechanisms of action, would prove instructive.
Christian Büchel - One of the best experts on this subject based on the ideXlab platform.
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The role of sleep and sleep deprivation in consolidating fear memories.
NeuroImage, 2013Co-Authors: Mareike M. Menz, Julia S. Rihm, Neda Salari, Jan Born, Raffael Kalisch, Hans-christian Pape, Lisa Marshall, Christian BüchelAbstract:Sleep, in particular REM sleep, has been shown to improve the consolidation of emotional memories. Here, we investigated the role of sleep and sleep deprivation on the consolidation of fear memories and underlying neuronal mechanisms. We employed a Pavlovian fear conditioning paradigm either followed by a night of polysomnographically monitored sleep, or wakefulness in forty healthy participants. Recall of learned fear was better after sleep, as indicated by stronger explicitly perceived Anxiety and autonomous nervous responses. These effects were positively correlated with the preceding time spent in REM sleep and paralleled by activation of the basolateral amygdala. These findings suggest REM sleep-associated consolidation of fear memory in the human amygdala. In view of the critical participation of fear learning mechanisms in the Etiology of Anxiety and post-traumatic stress disorder, deprivation of REM sleep after exposure to distressing events is an interesting target for further investigation.
Janet Woodruff-borden - One of the best experts on this subject based on the ideXlab platform.
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The Associations of Executive Function and Temperament in a Model of Risk for Childhood Anxiety
Journal of Child and Family Studies, 2013Co-Authors: Nicholas W. Affrunti, Janet Woodruff-bordenAbstract:Previous research on the Etiology of Anxiety disorders has implicated temperament as a significant factor. It has been theorized that the expression of temperament may be influenced by cognitive variables, particularly executive function. The current study tested a mediational model to investigate the combined and separate effects of childhood temperament and executive function, specifically the ability to shift cognitive sets, in the relation between parent and child Anxiety. Participants were 102 parent–child dyads recruited from the community. Children were between the ages of 7 and 10 years old (60.7 % male, 93.2 % Caucasian) and most parents were mothers (91.2 %). Parents completed measures of parent Anxiety, child temperament, and child executive function. Children completed a measure of child Anxiety. Overall the data fit the model well. Further analyses indicated that temperament and executive function exerted individual and combined effects on the relation between parent and child Anxiety. Executive function was also found to mediate the relation between temperament and child Anxiety. The results suggest that separately temperament and executive function mediate the link between parent and child Anxiety. Also, executive function may mediate the effect temperament has on child Anxiety. Together, temperament and executive function may represent a specific pathway of risk, by affecting each other and the relation each has on the familial transmission of Anxiety.
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Anxiety disorders in children with Williams syndrome, their mothers, and their siblings: Implications for the Etiology of Anxiety disorders
Journal of Neurodevelopmental Disorders, 2009Co-Authors: Ovsanna Leyfer, Janet Woodruff-borden, Carolyn B. MervisAbstract:This study examines the prevalence of Anxiety disorders in children with Williams syndrome (WS), their sibling closest in age, and their mothers as well as the predictors of Anxiety in these groups. The prevalence of Anxiety disorders was assessed and compared to that in the general population. Children with WS had a significantly higher prevalence of specific phobia, generalized Anxiety disorder (GAD), and separation Anxiety in comparison to children in the general population. While mothers had a higher prevalence of GAD than population controls, the excess was accounted for by mothers who had onset after the birth of their WS child. The siblings had rates similar to the general population. This pattern of findings suggests the presence of a gene in the WS region whose deletion predisposes to Anxiety disorders. It is also worthwhile to investigate relations between genes deleted in WS and genes previously implicated in Anxiety disorders.
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Parental Control in the Etiology of Anxiety
Clinical Child and Family Psychology Review, 2006Co-Authors: Natalie Ballash, Ovsanna Leyfer, Amy F. Buckley, Janet Woodruff-bordenAbstract:Anxiety disorders are among the most prevalent forms of adult and childhood psychiatric disorders, and they are highly familial. However, the mechanisms of transmission remain unclear. One familial characteristic that may promote the development of Anxiety is the construct of parental control. This paper provides a conceptual overview of the construct of control in the parenting and Anxiety literatures, reviews existing literature on control in anxious families, and reviews current conceptual models of and developmental approaches to Anxiety. Based on the current empirical literature, an elaborated model that takes child developmental level into consideration is proposed in order to provide a better understanding of the role of parental control in the development of Anxiety.
Anantha Shekhar - One of the best experts on this subject based on the ideXlab platform.
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serotonergic systems Anxiety and affective disorder focus on the dorsomedial part of the dorsal raphe nucleus
Annals of the New York Academy of Sciences, 2008Co-Authors: Christopher A Lowry, Matthew W Hale, Andrew K Evans, Jasper Heerkens, Daniel R Staub, Paul J Gasser, Anantha ShekharAbstract:Depressed suicide patients have elevated expression of neuronal tryptophan hydroxylase 2 (TPH2) mRNA and protein in midbrain serotonergic neurons, as well as increases in brain serotonin turnover. The mechanisms underlying these changes are uncertain, but increased TPH2 expression and serotonin turnover could result from genetic influences, adverse early life experiences, or acute stressful life events, all of which can alter serotonergic neurotransmission and have been implicated in determining vulnerability to major depression. Emerging evidence suggests that there are several different stress-related subsets of serotonergic neurons, each with a unique role in the integrated stress response. Here we review our current understanding of how genetic and environmental factors may influence TPH2 mRNA expression and serotonergic neurotransmission, focusing in particular on the dorsomedial part of the dorsal raphe nucleus. This subdivision of the dorsal raphe nucleus is selectively innervated by key forebrain structures implicated in regulation of Anxiety states, it gives rise to projections to a distributed neural system mediating Anxiety states, and serotonergic neurons within this subdivision are selectively activated by a number of stress- and Anxiety-related stimuli. A better understanding of the anatomical and functional properties of specific stress- or Anxiety-related serotonergic systems should aid our understanding of the neural mechanisms underlying the Etiology of Anxiety and affective disorders.
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Serotonergic Systems, Anxiety, and Affective Disorder
Annals of the New York Academy of Sciences, 2008Co-Authors: Christopher A Lowry, Matthew W Hale, Andrew K Evans, Jasper Heerkens, Daniel R Staub, Paul J Gasser, Anantha ShekharAbstract:Depressed suicide patients have elevated expression of neuronal tryptophan hydroxylase 2 (TPH2) mRNA and protein in midbrain serotonergic neurons, as well as increases in brain serotonin turnover. The mechanisms underlying these changes are uncertain, but increased TPH2 expression and serotonin turnover could result from genetic influences, adverse early life experiences, or acute stressful life events, all of which can alter serotonergic neurotransmission and have been implicated in determining vulnerability to major depression. Emerging evidence suggests that there are several different stress-related subsets of serotonergic neurons, each with a unique role in the integrated stress response. Here we review our current understanding of how genetic and environmental factors may influence TPH2 mRNA expression and serotonergic neurotransmission, focusing in particular on the dorsomedial part of the dorsal raphe nucleus. This subdivision of the dorsal raphe nucleus is selectively innervated by key forebrain structures implicated in regulation of Anxiety states, it gives rise to projections to a distributed neural system mediating Anxiety states, and serotonergic neurons within this subdivision are selectively activated by a number of stress- and Anxiety-related stimuli. A better understanding of the anatomical and functional properties of specific stress- or Anxiety-related serotonergic systems should aid our understanding of the neural mechanisms underlying the Etiology of Anxiety and affective disorders.