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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Community studies indicate that 19% of men and 31% of women will develop some type of anxiety disorder during their lifetime. The impact of gender is profound in that it increases the likelihood of developing an anxiety disorder by 85% in women compared to men. Sex difference in prevalence rates are apparent as early as age 6, when girls are twice as likely as boys to have an anxiety disorder. In the National Comorbidity Survey, the prevalence rates for panic disorder in women and men were 5% and 2%, respectively. Agoraphobia, which often coexists with panic disorder, has a lifetime prevalence rate of 7% in women and 3.5% in men. Prevalence of trauma is increased in young women as well, and is experienced earlier in life; 62% of sexual assaults are inflicted on females < or = 18 years of age, and 29% occur in children < 11 years of age. Comorbidity of anxiety in women complicates other medical conditions as well. For example, panic disorder is highly comorbid with CHD, which remains the leading cause of death in women in developed countries. Fluctuations in reproductive hormone levels during the female life cycle is thought to be responsible for modulating anxiety. This is often implicated in the later age of onset, the more sudden and acute symptom emergence, and the more episodic course of OCD in women, and in the high prevalence(47.4%) of PMDD. Pregnancy appears to be a protective period for some anxiety disorders, including panic, while for others, such as OCD, it may be associated with onset. Hormonal changes during pregnancy, such as increased prolactin, oxytocin, and cortisol, may contribute to the suppression of stress response that occurs during this period. Despite a large and growing body of literature on anxiety disorders in general, the available data relating to women and girls falls short of informing aspects of diagnosis, treatment, and prevention that may entail sex differences. Additional work is required to understand the biological and psychosocial causes of these differences.
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PMID:Women and anxiety disorders: implications for diagnosis and treatment. Proceedings of a conference, November 19-21, 2003, Chantilly, Virginia, USA. 1548 27

Clinically significant separation anxiety disorder in childhood leads to adult panic disorder and other anxiety disorders. The prevailing pathophysiological model of anxiety disorders, which emphasizes extinction deficits of fear-conditioned responses, does not fully consider the role of separation anxiety. Pathological early childhood attachments have far-reaching consequences for the later adult ability to experience and internalize positive relationships in order to develop mental capacities for self-soothing, anxiety tolerance, affect modulation, and individuation. Initially identified in attachment research, the phenomenon of separation anxiety is supported by animal model, neuroimaging, and genetic studies. A role of oxytocin is postulated. Adults, inured to their anxiety, often do not identify separation anxiety as problematic, but those who develop anxiety and mood disorders respond more poorly to both pharmacological and psychotherapeutic interventions. This poorer response may reflect patients' difficulty in forming and maintaining attachments, including therapeutic relationships. Psychotherapies that focus on relationships and separation anxiety may benefit patients with separation anxiety by using the dyadic therapist-patient relationship to recapture and better understand important elements of earlier pathological parent-child relationships.
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PMID:Childhood separation anxiety and the pathogenesis and treatment of adult anxiety. 2412 27

Fear responses play evolutionarily beneficial roles, although excessive fear memory can induce inappropriate fear expression observed in posttraumatic stress disorder, panic disorder, and phobia. To understand the neural machineries that underlie these disorders, it is important to clarify the neural pathways of fear responses. Contextual conditioned fear induces freezing behavior and neuroendocrine responses. Considerable evidence indicates that the central amygdala plays an essential role in expression of freezing behavior after contextual conditioned fear. On the other hand, mechanisms of neuroendocrine responses remain to be clarified. The medial amygdala (MeA), which is activated after contextual conditioned fear, was lesioned bilaterally by infusion of N-methyl-d-aspartate after training of fear conditioning. Plasma oxytocin, ACTH, and prolactin concentrations were significantly increased after contextual conditioned fear in sham-lesioned rats. In MeA-lesioned rats, these neuroendocrine responses but not freezing behavior were significantly impaired compared with those in sham-lesioned rats. In contrast, the magnitudes of neuroendocrine responses after exposure to novel environmental stimuli were not significantly different in MeA-lesioned rats and sham-lesioned rats. Contextual conditioned fear activated prolactin-releasing peptide (PrRP)-synthesizing neurons in the medulla oblongata. In MeA-lesioned rats, the percentage of PrRP-synthesizing neurons activated after contextual conditioned fear was significantly decreased. Furthermore, neuroendocrine responses after contextual conditioned fear disappeared in PrRP-deficient mice. Our findings suggest that the MeA-medullary PrRP-synthesizing neuron pathway plays an important role in neuroendocrine responses to contextual conditioned fear.
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PMID:The medial amygdala-medullary PrRP-synthesizing neuron pathway mediates neuroendocrine responses to contextual conditioned fear in male rodents. 2487 22

In the present chapter, we review the literature focusing on oxytocin (OT)-centered research in anxiety spectrum conditions, comprising separation anxiety disorder, specific phobias, social anxiety disorder (SAD), panic disorder, generalized anxiety disorder, and anxiety-related endophenotypes (e.g., trust behavior, behavioral inhibition, neuroticism, and state/trait anxiety). OT receptor gene (OXTR) polymorphisms have been implicated in gene-environment interactions with attachment style and childhood maltreatment and to influence clinical outcomes, including SAD intensity and limbic responsiveness. Epigenetic OXTR DNA methylation patterns have emerged as a link between categorical, dimensional, neuroendocrinological, and neuroimaging SAD correlates, highlighting them as potential peripheral surrogates of the central oxytocinergic tone. A pathophysiological framework of OT integrating the dynamic nature of epigenetic biomarkers and the summarized genetic and peripheral evidence is proposed. Finally, we emphasize opportunities and challenges of OT as a key network node of social interaction and fear learning in social contexts. In conjunction with multi-level investigations incorporating a dimensional understanding of social affiliation and avoidance in anxiety spectrum disorders, these concepts will help to promote research for diagnostic, state, and treatment response biomarkers of the OT system, advancing towards indicated preventive interventions and personalized treatment approaches.
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PMID:Oxytocin and Anxiety Disorders. 2881 74