Generalization of beneficial exposure effects to untreated stimuli from another fear category.

Previous research has shown that fear associated with one stimulus often spreads to other stimuli with similar perceptual features as well as across different stimulus categories. Exposure is considered as the most effective intervention to attenuate exaggerated fear. The extent to which exposure treatment effects can generalize to fears not targeted during treatment remains elusive. Previous studies on possible generalization of beneficial effects of exposure used stimuli sharing the same stimulus category and/or stimuli having high perceptual similarity. The current study examined whether exposure treatment generalization can be achieved for untreated stimuli which do not share any perceptual resemblance and belong to a different fear category. An analogue sample of fifty participants with fear of spiders (animal-related fears) and heights (natural environment-related fears) was tested. Participants have been randomly assigned to either an exposure treatment (n = 24) or a control condition (n = 26). Exposure treatment was designed to only target participants' fear of spiders, leaving their fear of heights untreated. Results demonstrated that the effects of exposure treatment generalized to fear of heights, as indicated by a reduction in behavioral avoidance, as well as self-reported acrophobia symptoms. The present study confutes the assumption that generalization of exposure effects to untreated fears is based on perceptual similarity. Clearly, further research is required to determine the decisive factors, in order to expand the generalization effect permanently to any given type of fear.

A fatal alliance: Glial connexins, myelin pathology and mental disorders.

Mature oligodendrocytes are myelin forming glial cells which are responsible for myelination of neuronal axons in the white matter of the central nervous system. Myelin pathology is a major feature of severe neurological disorders. Oligodendrocyte-specific gene mutations and/or white matter alterations have also been addressed in a variety of mental disorders. Breakdown of myelin integrity and demyelination is associated with severe symptoms, including impairments in motor coordination, breathing, dysarthria, perception (vision and hearing), and cognition. Furthermore, there is evidence indicating that myelin sheath defects and white matter pathology contributes to the affective and cognitive symptoms of patients with mental disorders. Oligodendrocytes express the connexins GJC2; mCx47 [human (GJC2) and mouse (mCx47) connexin gene nomenclature according to Söhl and Willecke (2003)], GJB1; mCx32, and GJD1; mCx29 in both white and gray matter. Preclinical findings indicate that alterations in connexin expression in oligodendrocytes and astrocytes can induce myelin defects. GJC2; mCx47 is expressed at early embryonic stages in oligodendrocyte precursors cells which precedes central nervous system myelination. In adult humans and animals GJC2, respectively mCx47 expression is essential for oligodendrocyte function and ensures adequate myelination as well as myelin maintenance in the central nervous system. In the past decade, evidence has accumulated suggesting that mental disorders can be accompanied by changes in connexin expression, myelin sheath defects and corresponding white matter alterations. This dual pathology could compromise inter-neuronal information transfer, processing and communication and eventually contribute to behavioral, sensory-motor, affective and cognitive symptoms in patients with mental disorders. The induction of myelin repair and remyelination in the central nervous system of patients with mental disorders could help to restore normal neuronal information propagation and ameliorate behavioral and cognitive symptoms in individuals with mental disorders.