The effect of comorbid anxiety disorder on the length of index MDD depended on the presence of other clinical features, but it did not seem to affect the risk of subsequent MDD or the course of DD or ADDM.
Anxiety and depression symptom scores from the SCL-90 questionnaire were observed in a large sample of nuclear families, and the effects of genes or family environment were estimated.
Anxiety and depression symptom scores from the SCL-90 questionnaire were observed in a large sample of nuclear families, and the effects of genes or family environment were estimated.
Anxiety and depression symptom scores from the SCL-90 questionnaire were observed in a large sample of nuclear families, and the effects of genes or family environment were estimated.
DBI and its processing products, ODN and TTN, are present in high concentrations in the hypothalamus and in the amygdala, two areas of the brain that are important in regulating behavioral patterns associated with conflict situations, anxiety and stress.
DBI and its processing products, ODN and TTN, are present in high concentrations in the hypothalamus and in the amygdala, two areas of the brain that are important in regulating behavioral patterns associated with conflict situations, anxiety and stress.
We investigated the effect of tetrahydroprogesterone on corticotropin-releasing hormone-induced anxiety, the basal and methoxamine-stimulated release of corticotropin-releasing hormone from hypothalamic organ explants in vitro, and adrenalectomy-induced up-regulation of the gene expression of corticotropin-releasing hormone in the hypothalamic paraventricular nucleus in rats.
Because of previous findings that parents of children with autistic disorder may be at increased risk for anxiety disorders and/or mood disorders, the Center for Epidemiological Studies-Depression (CES-D) Scale and the Modified Maudsley Obsessive-Compulsive Inventory (MMOCI) were administered to parents of children with autistic disorder and parents of children with Down's syndrome.
This paper reports the effects on grooming, related behaviors and levels of anxiety induced by the hypophysiotropic peptides corticotropin-releasing hormone (CRH, 1 microgram, 0.2 nmol, icv), thyrotropin-releasing hormone (TRH, 100 micrograms, 275 nmol, icv) and luteinizing hormone-releasing hormone (LHRH, 1.5 micrograms, 1.3 nmol, icv) administered into the lateral ventricle of the brain (icv) of adult male rats of a Holtzman-derived colony (N = 15, each group).
These data indicate that CRF receptor antagonists may be useful for the treatment of the disease states where CRF is elevated such as anxiety and depression, anorexia nervosa and stroke and that ligand inhibitors of CRF-BP may be used to elevate brain levels of 'free' urocortin and other CRF-related peptides.
This study demonstrates that when applied concomitantly with the stressful challenge, the steroid GABA(A) receptor agonist 3,21-dihydropregnan-20-one (tetrahydrodeoxycorticosterone, THDOC) can attenuate the behavioral and neuroendocrine consequences of repeated maternal separation during early life, e.g., increased anxiety, an exaggerated adrenocortical secretory response to stress, impaired responsiveness to glucocorticoid feedback, and altered transcription of the genes encoding corticotropin-releasing hormone (CRH) in the hypothalamus and glucocorticoid receptors in the hippocampus.
The present studies examined the potential functional significance of the CRF2 receptor in relation to the CRF1 receptor using two animal models of anxiety and endocrine reactivity to a stressor.
Hu-bcl-2 transgenic mice showed a decrease in anxiety and neophobia, indicating that, for this particular behavior, supernumerary neurons elicit the same modification as that observed after neuronal destruction.
Rather than being incidental, the REM disturbances in the foregoing studies appear consistently on consecutive nights of polysomnography in the subthreshold affective group; this was not the case for patients with non-affective personality and anxiety disorders.
In the present study we replicated the relationship of SLC6A4*C to anxiety by sibpair linkage analysis but found no evidence of association, raising the question of whether SLC6A4*C locus is itself affecting anxiety or is linked to another still unknown functional variant.
A polymorphism in the promoter region of the gene (SLC6A4) encoding this protein, was recently reported to affect protein expression and to be associated with measures of anxiety and depression and with autism (using a family-controlled transmission disequilibrium test (TDT) design).
Because of the widespread distribution of NPY, it has been implicated in the modulation of a variety of behaviors, including, but not limited to, circadian rhythms /1/, memory retention /33/, feeding /19,56/, sympathetic control of cardiovascular function /89/ and anxiety /42,43/.
Expression of oncogene sequences in gonadotropin-releasing hormone neurons has allowed the development of cell lines from the resulting tumors, overproduction of corticotropin-releasing factor has produced animal models of anxiety and obesity, and directed ectopic expression of growth hormone has generated a potentially useful rat model of dwarfism.
These results demonstrate that 5-HT1A receptors are involved in the modulation of exploratory and fear-related behaviors and suggest that reductions in 5-HT1A receptor density due to genetic defects or environmental stressors might result in heightened anxiety.
These results demonstrate that 5-HT1A receptors are involved in the modulation of exploratory and fear-related behaviors and suggest that reductions in 5-HT1A receptor density due to genetic defects or environmental stressors might result in heightened anxiety.
In addition, homozygous COMT-deficient female (but not male) mice displayed impairment in emotional reactivity in the dark/light exploratory model of anxiety.