Modifying biased attention towards food stimuli in binge eating disorder: A multi-session training study.

Individuals with binge eating disorder (BED) exhibit a biased attention towards food stimuli. Against this backdrop, the present study with pre-registered design (ID: DRKS00012984) tested whether (a) a training designed to reduce attentional food processing indeed modifies this bias, (b) this reduction is evident in several measures of food-related attention and (c) this is associated with reductions in craving, binge frequency over the past 28 days and calories eaten in a laboratory based bogus taste test. Individuals with BED were randomly allocated to four sessions of either an attentional bias modification training (ABMT; n = 39) or a comparable no-modification control training (CT; n = 27). In all measures assessed via eye-tracking - dwell time bias, dwell time bias variability and first fixation bias - food-related bias decreased in the ABMT relative to the CT. Against our hypothesis, no differential between-group effects were found for reaction time (RT) bias and its variability as well as for calories consumed in a bogus taste test. By contrast, reductions in binge frequency and subjective craving were found for both groups. Taken together, the tendency to preferentially process food seems a modifiable phenomenon in individuals with BED. However, modifying this selective viewing pattern does not seem a prerequisite for a successful reduction of binge frequency.

Optogenetic and chemogenetic insights into the neurocircuitry of depression-like behaviour: A systematic review.

Major depressive disorder (MDD) and its treatment are challenges for global health. Optogenetics and chemogenetics are driving MDD research forward by unveiling causal relations between cell-type-specific control of neurons and depressive-like behaviour in rodents. Using a systematic search process, in this review, a set of 43 original studies applying optogenetic or chemogenetic techniques in rodent models of depression was identified. Our aim was to provide an examination of all available studies elucidating central neuronal mechanisms leading to depressive-like behaviour in rodents and thereby unveiling the most promising routes for future research. A complex interacting network of relevant structures, in which central circuitries causally related to depressive-like behaviour are implicated, has been identified. As most relevant structures emerge: medial prefrontal cortex, anterior cingulate cortex, amygdala, nucleus accumbens, ventral tegmental area, hippocampus and raphe nuclei. Further evidence, though examined by only few studies, emerges for structures like the lateral habenula, or medial dorsal thalamus. Most of the identified brain areas have previously been associated with MDD neuropathology, but now evidence can be provided for causal pathological mechanisms within a complex cortico-limbic reward circuitry. However, the studies also show conflicting results concerning the mechanisms underlying the causal involvement of specific circuitries. Comparability of studies is partly limited since even small deviations in methodological approaches lead to different outcomes. Factors influencing study outcomes were identified and need to be considered in future studies (e.g. frequency used for stimulation, time and duration of stimulation, limitations of applied animal models of MDD).