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Early life stressors

Coplan JD, Andrewa MW, Rosenblum LA, Owens MJ, Freidman S, Gorman JM, Nemeroff CB (1996) Persistent elevations of cerebrospinal fluid concentrations of corticotropinreleasing factor in adult nonhuman primates exposed to early-life stressors implications for the pathophysiology of mood and anxiety disorders. Proc Natl Acad Sci USA 93 1619-... [Pg.62]

Coplan JD, Rosenblum LA, Andrews M, et al Persistent elevations of CSF CRF, somatostatin, HVA and 5-HIAA in grown nonhuman primates exposed to early life stressors. Paper presented at the annual meeting of the American College of Neuropsychopharmacology, San Juan, Puerto Rico, December 1994... [Pg.615]

The concept of stress sensidzation , whereby early life stressors can induce an enhanced reactivity to later environmental adversities (review ed in Read et al., 2005), may also be relevant to the etiology of schizophrenia. This phenomenon, w hich results in abnormal activation of the HPA axis, is thought to involve alterations in the mesolimbic dopamine system (review ed in Laruelle, 2000) resulting in excessive release of dopamine, a hallmark of psychotic episodes (Laruelle et al., 1996). Taken together, it appears likely that prenatal developmental abnormalities in limbic stmctures that regulate the HPA axis predispose this system to sensitivity to stressors in early childhood and adolescent maturation. This predisposition may then play a key role in the precipitation of psychotic episodes, as well as the deterioration of brain function that accompanies the progression of the disease. [Pg.483]

The sympathetic nervous system (SNS) and the hypothalamic-pituitary axis work together as important modulators of the immune system after exposure to stressors. Norepinephrine (NE) and epinephrine (EPI) (catecholamines from the SNS) and neuroendocrine hormones modulate a range of immune cell activities, including cell proliferation, cytokine and antibody production, lytic activity, and migration. This chapter will focus on these two major pathways of brain-immune signaling, briefly summarizing the evidence for SNS and hypothalamic-pituitary-adrenal (HPA) modulation of immune function, their influence on immune-mediated diseases, immune modulation in aging, and early life influences on these pathways. [Pg.490]

Anisman, H., Zaharia, M.D., Meaney, M.J., and Merali, Z. (1998) Do early-life events permanently alter behavioral and hormonal responses to stressors Int] Dev Neurosci 16 149-64. Arborelius. L, Owens, M.J., Plotsky, P.M., and Nemeroff, C.B. [Pg.120]

Animal studies have also provided insights into the mechanisms underlying the preeminent role of stressors in early life. Plotsky and Meaney [1993] showed that daily handling and maternal separation of rat pups produces in-... [Pg.22]

Brief Psychotic Disorder. This disorder occurs in the immediate aftermath of a markedly stressful event (or series of events). It is marked by emotional turmoil in conjunction with one or more psychotic symptoms such as delusions, hallucinations, disorganization, or catatonia. On presentation, a brief psychotic disorder can be difficult to distinguish from psychotic depression or mania. The presence of a precipitating stressor is not always helpful, because episodes of psychotic mood disorders (especially early in the course of illness) are also commonly triggered by stressful life events. Careful evaluation for symptoms of emerging depression or... [Pg.75]

If the weakest links of a plant s life cycle to a range of environmental stressors are early seedUng establishment (e.g., particularly the transition from heterotrophic to the autotrophic stage), and reproduction (e.g., flower initiation, pollination, and seed and fmit development), then the greatest effects of phenolic acids, like all other stressors, will occur at these life cycle stages. [Pg.160]


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See also in sourсe #XX -- [ Pg.57 ]




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Early life

Stressors

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