An extensive scientific literature exists on the connections between stress and anxiety, the result of significant research efforts by numerous teams seeking to understand the underpinnings of this highly prevalent neurological condition. Current treatments for anxiety are focused on altering the concentration, persistence, or action of synaptic neurotransmitters such as GABA and the monoamines: serotonin, norepinephrine, and dopamine. Despite this established connection, a limited number of studies have investigated structural modifications to the synapse that occur with the development of anxiety, and extremely few have examined synaptic changes that are induced by exposure to stress and may underlie or contribute to an anxiety phenotype.
The goal of this proposed collection of research articles is to identify potential mechanistic links in the brain through which stress exposure may predispose an individual to develop anxiety, or may worsen a pre-existing anxiety state. Data from the World Health Organization indicate that more than 250 million individuals worldwide suffer from some type of anxiety disorder, most commonly young adults and adolescents, which poses a significant health problem for the future. Mental health in general has also been negatively impacted by the SARS-CoV-2 pandemic, which has further increased stress levels and the incidence of anxiety, in particular.
Links between stress and anxiety have commonly focused on neural pathways and projections, neuroendocrine consequences of activating the hypothalamic-pituitary-adrenocortical axis or the sympathetic nervous system, and specific brain regions including the amygdala, hypothalamus, hippocampus, and prefrontal cortex. Recent electrophysiological studies have identified functional changes at the level of the neuron and synapse that inform our understanding of anxiety-associated dysfunction in the brain. How exposure to stress might facilitate or exacerbate changes of this type, however, is an important and largely unexplored question.
Contributors to this collection will employ established stress models in their research methodology, and assess both neurological and behavioral outcomes in their results. The stress paradigms utilized may include, but are not limited to, acute or chronic applications, early life stress, chronic variable stress, physical stressors such as restraint or footshock, or social stressors such as predator stress or resident-intruder stress. Behavioral measures should evaluate anxiety or anxiety-like behavior; we do not wish to focus on depression as an outcome for this collection. Neurological assessments should be focused on the synapse, with structural or functional analyses that evaluate neurotransmitters and/or their receptors, components of neurotransmitter regulation, or synaptic architecture.
Article types that are welcome include: Original Research, Review, Mini Review, Hypothesis and Theory, or Perspective.
An extensive scientific literature exists on the connections between stress and anxiety, the result of significant research efforts by numerous teams seeking to understand the underpinnings of this highly prevalent neurological condition. Current treatments for anxiety are focused on altering the concentration, persistence, or action of synaptic neurotransmitters such as GABA and the monoamines: serotonin, norepinephrine, and dopamine. Despite this established connection, a limited number of studies have investigated structural modifications to the synapse that occur with the development of anxiety, and extremely few have examined synaptic changes that are induced by exposure to stress and may underlie or contribute to an anxiety phenotype.
The goal of this proposed collection of research articles is to identify potential mechanistic links in the brain through which stress exposure may predispose an individual to develop anxiety, or may worsen a pre-existing anxiety state. Data from the World Health Organization indicate that more than 250 million individuals worldwide suffer from some type of anxiety disorder, most commonly young adults and adolescents, which poses a significant health problem for the future. Mental health in general has also been negatively impacted by the SARS-CoV-2 pandemic, which has further increased stress levels and the incidence of anxiety, in particular.
Links between stress and anxiety have commonly focused on neural pathways and projections, neuroendocrine consequences of activating the hypothalamic-pituitary-adrenocortical axis or the sympathetic nervous system, and specific brain regions including the amygdala, hypothalamus, hippocampus, and prefrontal cortex. Recent electrophysiological studies have identified functional changes at the level of the neuron and synapse that inform our understanding of anxiety-associated dysfunction in the brain. How exposure to stress might facilitate or exacerbate changes of this type, however, is an important and largely unexplored question.
Contributors to this collection will employ established stress models in their research methodology, and assess both neurological and behavioral outcomes in their results. The stress paradigms utilized may include, but are not limited to, acute or chronic applications, early life stress, chronic variable stress, physical stressors such as restraint or footshock, or social stressors such as predator stress or resident-intruder stress. Behavioral measures should evaluate anxiety or anxiety-like behavior; we do not wish to focus on depression as an outcome for this collection. Neurological assessments should be focused on the synapse, with structural or functional analyses that evaluate neurotransmitters and/or their receptors, components of neurotransmitter regulation, or synaptic architecture.
Article types that are welcome include: Original Research, Review, Mini Review, Hypothesis and Theory, or Perspective.