Psychoneuroendocrinology
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Psychoneuroendocrinology · Jul 2009
Chronic stress increases pituitary adenylate cyclase-activating peptide (PACAP) and brain-derived neurotrophic factor (BDNF) mRNA expression in the bed nucleus of the stria terminalis (BNST): roles for PACAP in anxiety-like behavior.
Exposure to chronic stress has been argued to produce maladaptive anxiety-like behavioral states, and many of the brain regions associated with stressor responding also mediate anxiety-like behavior. Pituitary adenylate cyclase activating polypeptide (PACAP) and its specific G protein-coupled PAC(1) receptor have been associated with many of these stress- and anxiety-associated brain regions, and signaling via this peptidergic system may facilitate the neuroplasticity associated with pathological affective states. Here we investigated whether chronic stress increased transcript expression for PACAP, PAC(1) receptor, brain-derived neurotrophic factor (BDNF), and tyrosine receptor kinase B (TrkB) in several nuclei. ⋯ Related vasoactive intestinal peptide (VIP) and VPAC receptor, and other stress peptide transcript levels were not altered compared to controls. Moreover, acute PACAP38 infusion into the dBNST resulted in a robust dose-dependent anxiogenic response on baseline startle responding that persisted for 7 days. PACAP/PAC(1) receptor signaling has established trophic functions and its coordinate effects with chronic stress-induced dBNST BDNF and TrkB transcript expression may underlie the maladaptive BNST remodeling and plasticity associated with anxiety-like behavior.
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Psychoneuroendocrinology · Jul 2009
Pre-pubertal stress exposure affects adult behavioral response in association with changes in circulating corticosterone and brain-derived neurotrophic factor.
Early-life stress produces a cascade of neurobiological events that cause enduring changes in neural plasticity and synaptic efficacy that appear to play pivotal roles in the pathophysiology of post-traumatic stress disorder (PTSD). Brain-derived neurotrophic factor (BDNF) has been implicated in the neurobiological mechanisms of these changes, in interaction with components of the stress response, such as corticosterone. This study examined the consequences of juvenile stress for behavior during adulthood in association with circulating corticosterone levels and BDNF expression. ⋯ The consequences of adult stress exposure were more severe in rats were exposed to the same stressor as juveniles, indicated increased vulnerability. The results suggest that juvenile stress has resounding effects in adulthood reflected in behavioral responses. The concomitant changes in BDNF and corticosterone levels may mediate the changes in neural plasticity and synaptic functioning underlying clinical manifestations of PTSD.
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Psychoneuroendocrinology · May 2009
Comparative StudySalivary cortisol and psychological mechanisms in patients with acute versus chronic low back pain.
This study was designed to explore whether the basal adrenocortical activity is related with pain-related coping, nonverbal pain behavior, depressive mood, and fatigue in patients with acute and chronic nonspecific low back pain. 19 patients with acute low back pain (ALBP) and 24 with chronic low back pain (CLBP) participated in the study. The adrenocortical activity was assessed through the cortisol awakening response. All participants provided five saliva samples (0, 15, 30, 45, and 60min after waking) on two consecutive days off work. ⋯ Among CLBP patients, FAC, NPB, depressive mood, and fatigue were negatively associated with the cortisol awakening response, whereas EC tended to be positively associated with it. The results indicate that pain-related coping strategies which are expected to be successful appear to lower the adrenocortical activity among ALBP patients, whereas affective distress may enhance the level of cortisol in this group. Among CLBP patients, long-term maladaptive coping strategies might contribute to hypocortisolism.
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Psychoneuroendocrinology · Apr 2009
BDNF Val66Met polymorphism is associated with HPA axis reactivity to psychological stress characterized by genotype and gender interactions.
A key protein in maintaining neuronal integrity throughout the life span is brain-derived neurotrophic factor (BDNF). The BDNF gene is characterized by a functional polymorphism, which has been associated with stress-related disorders such as anxiety-related syndromes and depression, prompting us to examine individual responses by Genotype and Sex to a standardized social stress paradigm. Gender differences in BDNFxstress responses were posited because estrogen induces synthesis of BDNF in several brain regions. ⋯ These results indicate that a common, functionally significant polymorphism in the BDNF gene modulates HPA axis reactivity and regulation during the TSST differently in men and women. Findings may be related to gender differences in reactivity and vulnerability to social stress.
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Psychoneuroendocrinology · Feb 2009
Randomized Controlled TrialSleep architecture in Sheehan's syndrome before and 6 months after growth hormone replacement therapy.
To characterize the sleep parameters in patients with growth hormone (GH) deficiency in Sheehan's syndrome adults and to assess the effects of 6-month GH replacement therapy (GHRT). ⋯ GH deficiency has sleep disturbing effects on Sheehan's syndrome patients under baseline conditions.