Illumination conditions appear to influence working efficacy in everyday life. In the present study, we obtained electroencephalogram (EEG) correlates of working-memory load, and investigated how these waveforms are modulated by illumination conditions. We hypothesized that illumination conditions may affect cognitive performance. We designed an EEG study to monitor and record participants' EEG during the Sternberg working memory task under 4 different illumination conditions. Illumination conditions were generated with a factorial design of 2 color-temperatures (3000 K and 7100 K) by 2 illuminance levels (150 lx and 700 lx). During a working memory task, we observed that high illuminance led to significantly lower frontal EEG theta activity than did low illuminance. These differences persisted despite no significant difference in task performance between illumination conditions. We found that the latency of an early event-related potential (ERP) component, such as N1, was significantly modulated by the illumination condition. The fact that the illumination condition affects brain activity but not behavioral performance suggests that the lighting conditions used in the present study did not influence the performance stage of behavioral processing. Nevertheless, our findings provide objective evidence that illumination conditions modulate brain activity. Further studies are necessary to refine the optimal lighting parameters for facilitating working memory.

It is widely known that prenatal stress (PS) exposure causes depression-like behaviour to offspring, as well as maladaptive responses including neurobiological and physiological changes. However, the underlying mechanism of PS induced juvenile-onset depression remains largely unravelled. The inadequacies of monoamine deficiency hypothesis, the emerging evidence of altered glutamate neurotransmission in mood disorders, as well as our previous studies inspired us to assess the potential role of glutamatergic system in the pathogenesis of juvenile depression. In this research, we examined the expression of phosphorylated GluR1 subunit of ionotropic receptor AMPAR, the Na+ dependent glutamate transporters EAAT2 and EAAT3 in the hippocampus, striatum and frontal cortex of one month rat offspring after mid and late prenatal stress exposure. Prenatally stressed offspring rats showed significantly prolonged duration of immobility and shortened immobility latency in tail suspension test. We also detected that prenatal stress significantly altered the expression of glutamate receptor and glutamate transporters of these depressed rats. In brief, the changes of pGluR1 protein level in hippocampus and frontal cortex, as well as markedly decreased EAAT2 mRNA expression in hippocampus, striatum and frontal cortex and EAAT3 mRNA expression in hippocampus of stressed rats were both observed. These results underpinned that glutamate receptors and glutamate transporters might be involved in the progress of depression-like behaviour in juvenile rat offspring induced by prenatal stress.

OBJECTIVE:

Step initiation can be modified by environmental stimulations, suggesting the involvement of stimulus-driven attention. Therefore, we assessed the influence of attentional status during step preparation.

METHODS:

Fourteen healthy, young subjects were presented with an auditory oddball paradigm in which an infrequent "target" stimulus was presented among frequent "standard" stimuli. An imperative visual "Go" signal for step initiation was presented 1.4 s after the auditory stimulus. Both the P300 event-related potential (associated with the auditory attention task) and the trajectory of the centre of pressure (associated with step initiation) were recorded.

RESULTS:

When presented before the visual "Go" signal, the auditory stimuli prompted the early release of low-amplitude anticipatory postural adjustments, not followed by step execution. They occurred twice as frequently in the "target" condition as they did in the "standard" condition. P300 component was greater after presentation of the target stimulus than after presentation of the standard stimulus.

CONCLUSION:

Stimulus-driven attention can modify the release of anticipatory postural adjustments.

SIGNIFICANCE:

The cortical integration of an auditory stimulus (as evidenced by the P300 component) in a subject conditioned to initiate gait appears to release postural adjustments via two different attentional mechanisms: an "alerting effect" and an "orienting effect".

BACKGROUND:

In Drosophila, male flies require the expression of the male-specific Fruitless protein (FRUM) within the developing pupal and adult nervous system in order to produce male courtship and copulation behaviors. Recent evidence has shown that specific subsets of FRUM neurons are necessary for particular steps of courtship and copulation. In these neurons, FRUM function has been shown to be important for determining sex-specific neuronal characteristics, such as neurotransmitter profile and morphology.

RESULTS:

We identified a small cohort of FRUM interneurons in the brain and ventral nerve cord by their co-expression with the transcription factor Engrailed (En). We used an En-GAL4 driver to express a fruM RNAi construct in order to selectively deplete FRUM in these En/FRUM co-expressing neurons. In courtship and copulation tests, these males performed male courtship at wild-type levels but were frequently sterile. Sterility was a behavioral phenotype as these En-fruMRNAi males were less able to convert a copulation attempt into a stable copulation, or did not maintain copulation for long enough to transfer sperm and/or seminal fluid.

CONCLUSIONS:

We have identified a population of interneurons necessary for successful copulation in Drosophila. These data confirm a model in which subsets of FRUM neurons participate in independent neuronal circuits necessary for individual steps of male behavior. In addition, we have determined that these neurons in wild-type males have homologues in females and fru mutants, with similar placement, projection patterns, and neurochemical profiles.

BACKGROUND:

The mechanisms that underlie autophagy in cerebral ischemia remain poorly defined. Myeloid cell leukemia-1 (Mcl1), an anti-apoptotic member of the Bcl-2 family of proteins, regulates the balance between autophagy and apoptosis. However, little is known regarding its expression profile and contribution to cell fate in the brain following ischemic stroke.

RESULTS:

In this study, we investigated the expression profile and cellular distribution of Mcl1 in brains from transient middle cerebral artery occlusion (MCAO) model rats. Brain slices from sham-operated control rats showed minimal immunoreactivity for Mcl1. Mcl1 was mainly produced in neurons. Immunoreactivity for Mcl1 increased as early as 4 hours after MCAO, peaked at 24 hours, and then declined, but still remained high, at 72 hours. Mcl1 positive cells never colocalized with either cleaved caspase-3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells. Both microtubule-associated protein 1 light chain 3 (LC3) and beclin-1 were evident in ischemic brain between 4 and 72 hours after MCAO. Most cells with strong LC3 staining were also labeled with beclin-1. Beclin-1 did colocalize with caspase-3 or Mcl1. Beclin-1/caspase-3 positive cells displayed the characteristic features of apoptosis including cell shrinkage and pyknotic nuclei, whereas beclin-1/Mcl1 positive cells had normal morphology. Pretreatment with 3-methyladenine attenuated autophagy without affecting the level of Mcl1 protein.

CONCLUSIONS:

These findings demonstrate that the expression of Mcl1 is involved in the survival of neuronal cells. In addition, the coexpression of Mcl1 with beclin-1 may attenuate beclin-1-dependent autophagy during ischemic stroke in rats.

Abstract One of the major pathological characteristics of Alzheimer's disease (AD) is the presence of enhanced deposits of beta-amyloid peptide (Aβ). The neuropeptide galanin (GAL) and its receptors are overexpressed in degenerating brain regions in AD. The functional consequences of galaninergic systems plasticity in AD are unclear. The objective of the present study was to investigate whether exogenous galanin could attenuate spatial memory impairment and hippocampal Aβ aggregation in rat model of Alzheimer's disease. The effects of Aβ, galanin, galanin receptor 1 agonist M617 and galanin receptor 2 agonist AR-M1896 on spatial memory were tested by Morris water maze. The effects of Aβ, galanin, M617 and AR-M1896 on hippocampal Aβ protein expression were evaluated by western blot assay. The expression of galanin, galanin receptors 1 and 2 in rats hippocampus were detected by real time PCR and western blot assay. The results showed that (1) Galanin administration was effective in improving the spatial memory and decreasing hippocampal Aβ levels after intracerebroventricular injection of Aβ; (2) AR-M1896 rather than M617 could imitate these effects of galanin; (3) GAL and GALR2 mRNA and protein levels increased significantly in hippocampus after Aβ administration, while GALR1 mRNA and protein levels did not change; (4) GAL, AR-M1896 and M617 administration did not show significant effect on GAL, GalR1 and GalR2 mRNA and protein levels in hippocampus after Aβ administration. These results implied that galanin receptor 2, but not receptor 1 was involved in the protective effects against spatial memory impairment and hippocampal Aβ aggregation.

The richness of perceptual experience, as well as its usefulness for guiding behaviour, depends on the synthesis of information across multiple senses. Recent decades have witnessed a surge in our understanding of how the brain combines sensory cues. Much of this research has been guided by one of two distinct approaches: one is driven primarily by neurophysiological observations, and the other is guided by principles of mathematical psychology and psychophysics. Conflicting results and interpretations have contributed to a conceptual gap between psychophysical and physiological accounts of cue integration, but recent studies of visual-vestibular cue integration have narrowed this gap considerably.

NMDA receptors (NMDARs) are glutamate-gated ion channels and are crucial for neuronal communication. NMDARs form tetrameric complexes that consist of several homologous subunits. The subunit composition of NMDARs is plastic, resulting in a large number of receptor subtypes. As each receptor subtype has distinct biophysical, pharmacological and signalling properties, there is great interest in determining whether individual subtypes carry out specific functions in the CNS in both normal and pathological conditions. Here, we review the effects of subunit composition on NMDAR properties, synaptic plasticity and cellular mechanisms implicated in neuropsychiatric disorders. Understanding the rules and roles of NMDAR diversity could provide new therapeutic strategies against dysfunctions of glutamatergic transmission.