Cover image by Naoki Ihara, Ai Nakashima, Naosuke Hoshina, Yuji Ikegaya and Haruki Takeuchi

The capacity to form associations between neutral and affective information is crucial for generating adaptive responses. In this study, we found that after single association, neutral objects previously encoded in the context of emotional compared to neutral scenes evoked a larger P100 (140–184 ms) over occipital electrodes and larger late positive potentials (LPP) over parietal–occipital electrodes (450–750 ms). The data provide direct evidence for fast emotional associative learning, which could assist in understanding binding mechanisms in stress- and addiction-related disorders.

This study suggests that none of the most frequently used anodal tDCS parameters effectively modify cortical excitability at a group level. Based on an objective classification of response rates, low levels of responders were obtained, with response rates ranging from 20 to 35%. Although none of the baseline measures were related to the magnitude of MEP changes, our result suggest that inter-trial MEP amplitude variability may contribute to variability to response to anodal tDCS.

We investigated how the neural processing of a persons' actions during an economic game is influenced by their reputation. We found significantly greater activation in the left dorsal premotor cortex (dPMC) when participants saw the action of a person with a negative reputation compared to a person with a positive reputation. Our findings show that the processing of observed actions is modulated by an actor's reputation, and suggest a predictive role for the dPMC during action observation.

12–20 Hz beta modulation during auditory-paced finger tapping over parietal and contralateral motor cortex was reduced if sudden movement inhibition was required. Negative mean asynchrony was also reduced indicating more hesitant tapping to the sound. Yet if the beta increase following the last regular tap was relatively high, tapping was more successfully interrupted when required. Elevated beta may thus reflect reduced cognitive load and increased confidence in current performance.

Transcriptome analysis demonstrated that treating neural differentiated SH-SY5Y cells with PGRN and the granulins that the majority of genes were down-regulated, with a role in spliceosome, proteasome and lysosomal function implicated for PGRN.

The changes in cerebrovascular endothelial nitric oxide synthase (eNOS) activity induced by physical exercise and bilateral common carotid occlusion translated into parallel changes in brain-derived neurotrophic factor (BDNF) levels in both the cortex and hippocampus. When induced after vascular occlusion, physical exercise failed to increase eNOS activity and BDNF levels, whereas the exposure of brain slices to a NO donor induces elevation in BDNF and proBDNF levels.

Atorvastatin (AT) increased γ power in a dose-dependent manner. The enhancing effect of AT is associated with the increased interneuron firing and frequency of sIPSCs as well as the activation of PKA, ERK and PI3 kinases.

Exogenous orexin-A increases the firing rate of globus pallidus neurons through both OX₁ and OX₂ receptors. Endogenously released orexins from lateral hypothalamus increase firing rate of pallidal neurons.

Partial inactivation of Gabra5, the gene encoding the GABA_AR α5 subunit causes severe alterations of migration and dendrite development of adult-born dentate gyrus granule cells in mice. In α5-het mice, the deficit could be reversed by retrovirally-mediated overexpression of Cdk5, suggesting that this signalling pathways cooperates with α5-GABA_ARs to regulate neuronal development. In conclusion, minor imbalance of α5-GABA_AR-mediated transmission may have major consequences for neuronal plasticity; calling for caution upon chronic therapeutic use of negative allosteric modulators acting at these receptors.

A hypothetical schema of synaptic vesicle dynamics in the presynaptic terminal. (Upper) Normal dynamics of synaptic vesicles in WT mice. Following the release of glutamate, newly-generated synaptic vesicles are transported directly or indirectly via the endosome to the pool of synaptic vesicles, which may be regulated by CAST. CAST may also regulate membrane fusion of synaptic vesicles. (Lower) Impaired synaptic vesicle dynamics in CAST KO mice or by brefeldin A. The indirect pathway via the endosome is impaired in CAST KO mice or blocked by brefeldin A. The lack of CAST may also impair membrane fusion of synaptic vesicles.