Do challenging behaviors affect staff psychological well-being? Issues of causality and mechanism

Little explicit attention has been given to the potential impact of client challenging behavior on staff psychological well-being. Relevant research was critically reviewed according to criteria required to establish a causal relationship. Reasonable evidence was found for an association between challenging behavior and staff stress, and some evidence for temporal precedence. However, few researchers had analyzed data enabling alternative explanations to be eliminated. Thus, empirical evidence of a causal relationship between challenging behavior and staff stress is weak. A fourth causality criterion was addressed by suggestion of a mechanism by which challenging behavior may have its effects. I propose that staff negative emotional reactions mediate the impact of challenging behaviors on staff stress and evaluate research evidence for this theory.     

Behavior problems of children with autism, parental self-efficacy, and mental health

Self-efficacy has been identified in the general parenting literature as an important variable affecting parent outcomes. In the present study, 26 mothers and 20 fathers of children with autism reported on their self-efficacy, anxiety, and depression. Teachers rated the behavior problems of the children. Regression analyses showed that self-efficacy mediated the effect of child behavior problems on mothers' anxiety and depression, but there was no evidence that it functioned as a mediator for fathers. However, there was evidence that self-efficacy moderated the effect of child behavior problems on fathers' anxiety. No evidence for the moderating effect of self-efficacy was apparent for mothers. Methodological issues and the theoretical and practical implications of these results are discussed.     

Granule neurons generated during development extend divergent axon collaterals to hippocampal area CA3

cAMP is a ubiquitous second messenger, which acts mainly through specific protein kinases that consist of two regulatory and two catalytic subunits. An unsolved problem in cAMP physiology is how it can regulate so many cellular functions through this simple enzymatic cascade. A tentative explanation is related to the different biochemical properties of the four regulatory subunit isoforms (RI alpha and RI beta, RII alpha and RII beta) and to their differential cell and tissue distribution. For example, detergent insoluble aggregates of RI alpha are present in some cholinergic neurons of the adult rat brain. Rat brains, from the embryonic stage to old age, were examined for the presence of highly concentrated clusters of RI alpha. They are present only in some neurons of restricted brain areas, for a limited time span. During development, labeled neurons appear in different brain areas after neuron migration, at a stage of advanced functional maturation. They have their greatest expression after birth but before sexual maturation, and then they slowly decline, persisting only in a few brain areas throughout life. The first appearance, time course, and eventual disappearance is different in the different brain areas: RI alpha clusters appear in brainstem, hypothalamus, and accessory olfactory bulb at a late embryonic stage; in the main olfactory bulb, hippocampus, and medial thalamic nuclei shortly after birth; and in the cortex as late as in the third and fourth postnatal week. During the rat's lifespan, the distribution of these peculiar RI alpha clusters undergo changes that may contribute to shape neuronal responses differentially to agents modifying cAMP levels.     

Identification of the key amino acids of gliai cell line-derived neurotrophic factor family receptor alpha 1 involved in its biological function

Glial cell line-derived neurotrophic factor （GDNF） plays a critical role in neurodevelopment and survival of midbrain dopaminergic and spinal motor neurons in vitro and in vivo. The biological actions of GDNF are mediated by a two-receptor complex consisting of a glycosylphosphatidylinositol-linked cell surface molecule, the GDNF family receptor alpha 1 （GFR alpha 1）, and receptor protein tyrosine kinase Ret. Although structural analysis of GDNF has been extensively examined, less is known about the structural basis of GFR alpha 1 function. In this study, based on evolutionary trace method and relative solvent accessibility prediction of residues, a set of trace residues that are solvent-accessible was selected for site-directed mutagenesis. A series of GFR alpha 1 mutations was made, and PC12 cell lines stably expressing different GFR alpha 1 mutants were generated. According to the survival and differentiation responses of these stable PC12 cells upon GDNF stimulation and the GDNF- GFR alpha 1-Ret interaction assay, residues 152NN153, Arg259, and 316SNS318 in the GFR alpha 1 central region were found to be critical for GFR alpha 1 binding to GDNF and eliciting downstream signal transduction. The single mutation R259A in the GFR alpha 1 molecule simultaneously lost its binding ability to GDNF and Ret. However N152A/N153A or S316A/N317A/ S318A mutation in the GFR alpha 1 molecule still retained the ability to bind with Ret. These findings suggest that distinct structural elements in GFR alpha 1 may be involved in binding to GDNF and Ret.