Anxiety Signals are the complex cascade of neuroendocrine and physiological communications that translate perceived threat or stress into the subjective experience and physical manifestations of anxiety. These signals involve rapid, bidirectional communication between the central nervous system and the endocrine system, leading to a state of heightened arousal and vigilance. Chronic activation of these signals can lead to allostatic overload and systemic hormonal dysregulation.
Origin
The term is rooted in psychoneuroendocrinology, a specialized field studying the interactions between the nervous system and the endocrine system. The clinical understanding of anxiety is intrinsically tied to the stress response system, originating etymologically from the Latin anxietas, denoting distress or trouble of mind. Modern research focuses on quantifying the hormonal and neurotransmitter markers associated with this internal state.
Mechanism
The primary mechanism involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis, where the hypothalamus releases corticotropin-releasing hormone (CRH), stimulating the pituitary to release adrenocorticotropic hormone (ACTH), culminating in the adrenal glands secreting cortisol and catecholamines. These hormonal signals flood the body, increasing heart rate and muscle tension, while also modulating neurotransmitter release, particularly GABA and serotonin, to perpetuate the anxious state within the neural circuits.
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