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This article discusses the role of the amygdala and hippocampus in emotional imagery. It challenges the notion that the amygdala is consistently activated during emotional processing, suggesting that conflicting results may be due to variations in task design and the proximity of the amygdala to other activated regions. The article presents evidence that the anterior hippocampus, rather than the amygdala, may play a key role in emotional processing in some contexts. The authors recommend including an amygdala perceptual localizer task and using sagittal views in future studies to accurately assess and confirm amygdala involvement. [Extracted from the article]

Stress is one of the major factors in drug abuse, particularly in relapse and drug-seeking behavior. However, the mechanisms underlying the interactions between stress and drug abuse are unclear. For many years, studies have focused on the role of the dopaminergic reward system in drug abuse. Our results, for example, show that increased dopaminergic activity is induced by drug sensitization and different stressors via potentiation of the ventral subiculum-nucleus accumbens (NAc) pathway. Although the role of the norepinephrine (NE) system in stress is well known, its involvement in drug abuse has received less attention. This review explores the different mechanisms by which stressors can modulate the ventral subiculum-accumbens pathway, and how these modulations can induce alterations in the behavioral response to drug administration. In particular, we will focus on two main afferents to the NAc, the basolateral amygdala and the ventral subiculum of the hippocampus, and their interactions with the locus coeruleus-norepinephrine system. [ABSTRACT FROM AUTHOR]

The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation ( allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions ( allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load. [ABSTRACT FROM AUTHOR]

Adolescence is a developmental period characterized by suboptimal decisions and actions that are associated with an increased incidence of unintentional injuries, violence, substance abuse, unintended pregnancy, and sexually transmitted diseases. Traditional neurobiological and cognitive explanations for adolescent behavior have failed to account for the nonlinear changes in behavior observed during adolescence, relative to both childhood and adulthood. This review provides a biologically plausible model of the neural mechanisms underlying these nonlinear changes in behavior. We provide evidence from recent human brain imaging and animal studies that there is a heightened responsiveness to incentives and socioemotional contexts during this time, when impulse control is still relatively immature. These findings suggest differential development of bottom-up limbic systems, implicated in incentive and emotional processing, to top-down control systems during adolescence as compared to childhood and adulthood. This developmental pattern may be exacerbated in those adolescents prone to emotional reactivity, increasing the likelihood of poor outcomes. [ABSTRACT FROM AUTHOR]

The amygdala and orbitofrontal cortex (OFC) are often thought of as components of a neural circuit that assigns affective significance—or value—to sensory stimuli so as to anticipate future events and adjust behavioral and physiological responses. Much recent work has been aimed at understanding the distinct contributions of the amygdala and OFC to these processes, but a detailed understanding of the physiological mechanisms underlying learning about value remains lacking. To gain insight into these processes, we have focused initially on characterizing the neural signals of the primate amygdala, and more recently of the primate OFC, during appetitive and aversive reinforcement learning procedures. We have employed a classical conditioning procedure whereby monkeys form associations between visual stimuli and rewards or aversive stimuli. After learning these initial associations, we reverse the stimulus-reinforcement contingencies, and monkeys learn these new associations. We have discovered that separate populations of neurons in the amygdala represent the positive and negative value of conditioned visual stimuli. This representation of value updates rapidly upon image value reversal, as fast as monkeys learn, often within a single trial. We suggest that representations of value in the amygdala may change through multiple interrelated mechanisms: some that arise from fairly simple Hebbian processes, and others that may involve gated inputs from other brain areas, such as the OFC. [ABSTRACT FROM AUTHOR]

It is well known that environmental factors, such as early life events, perinatal damage, and urbanicity, which interact with multiple genes, induces persistent sensitization to stress possibly through an imbalance in interactions between dopaminergic and glutamatergic systems. This stress sensitization may be critical in the development or relapse of schizophrenia. The neural correlates of a negative mood might be impaired, resulting in stress sensitization and difficulties in social adjustment (Dr. Habel). Urbanicity is associated with later schizophrenia. Metabolic stress induces stress sensitization via dysregulation of dopaminergic and/or noradrenergic systems in activated HVA and cortical response (Dr. Marcelis). The glutamatergic regulation activates HPA axis in stress response (Dr. Zelena). Ameloblast activity in human molar's enamel slowed by exposure to stress, and the segment of enamel rods is smaller, making a particular dark line. Stress sensitization may be induced at the age of 10.5 to 11.5 years resulting from severe emotional stress at the age of 10.5 to 11.5 years (Dr. Yui). It has been reported that volume reductions in the amygdala, hippocampus, superior temporal gyrus, and anterior parietal cortex common to both patient groups may represent the vulnerability to schizophrenia, while volume loss of the prefrontal cortex, posterior parietal cortex, cingulate, insula, and fusiform cortex preferentially observed in schizophrenia may be critical for overt manifestation of psychosis (Dr. Suzuki). [ABSTRACT FROM AUTHOR]

It is now well documented that both increased and decreased stress responses can profoundly affect cognition and behavior. This mini review presents possible neural mechanisms subserving stress effects on memory and aggression, particularly focusing on glucocorticoid (GC) hyper- and hypofunction. First, uncontrollable stress impedes hippocampal memory and long-term potentiation (LTP). Because the hippocampus is important for the stability of long-term memory and because LTP has qualities desirable of an information storage mechanism, it has been hypothesized that stress-induced alterations in LTP contribute to memory impairments. Recent evidence suggests a neural–endocrine network comprising amygdala, prefrontal cortex (PFC), and glucocorticoids may be involved in regulating stress effects on hippocampal mnemonic functioning. Second, antisocial aggressiveness correlates with chronically decreased glucocorticoid production, and this condition leads in rats to behavioral–autonomic deficits reminiscent of the human disorder. Glucocorticoid deficiency-induced antisocial aggressiveness results from functional changes in the PFC, medial and central amygdala, and altered serotonin and substance P neurotransmissions. Accordingly, a neurobiological understanding of how stress and glucocorticoid deficiency alter brain, cognition, and behavior is an important challenge facing modern neuroscience with broad implications for individual and social well-being. [ABSTRACT FROM AUTHOR]

Animal research on brain mechanisms involved in psychiatric disorders presents an enormous challenge because it is impossible to precisely model symptoms of a human disorder in a rat or mouse. Nevertheless, there are uses for animal models as long as the limitations are recognized. Animal research related to posttraumatic stress disorder (PTSD) points to acute and chronic stressors, such as restraint or immobilization as being the most relevant stimuli to study how neural and endocrine systems are affected, both immediately and long term. Of particular relevance are the onset and duration of effects of stressors on brain areas subserving emotional memories, such as the amygdala, prefrontal cortex, and hippocampus. The hippocampus plays a role in memory and in vegetative functions of the body. The hippocampus receives input from the amygdala and its function in spatial memory is altered by amygdala activity. Repeated stress in the rat suppresses dentate gyrus neurogenesis and causes dendrites of hippocampal and medial prefrontal cortical neurons to shrink. Conversely, it causes basolateral amygdala neurons to increase in dendritic complexity and sprout new synapses. Repeated stress also increases fear and aggression, reduces spatial memory, and alters contextual fear conditioning. Antidepressants and mood stabilizers have diverse effects on these processes. New data indicate that a single stress episode can cause a delayed alteration in synapse formation in the basolateral amygdala without changing dendritic length and branching. Further studies are examining the structural changes in prefrontal cortex and hippocampus as a result of single traumatic stressors, which may reflect the functional interactions with the amygdala. Together with mechanistic studies of the role of adrenal glucocorticoids and catecholamines, these results may tell us how the brain is shaped by acute and repeated uncontrollable stress in ways that then can be investigated in human anxiety disorders. [ABSTRACT FROM AUTHOR]