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    Pictured above: Figure 2 from the article, "Structural organization of the dendritic reticulum linked by gap junctions in layer 4 of the visual cortex." Reconstruction of the gap junction-coupled linkage of PV neurons. All PV neurons shown here are connected to one another through chains of gap junction-coupled dendritic linkage. Different symbols on dendrites indicate sites of gap junctions. Scale bar = 100 μm. (T. Fukuda).

    Established in 1976, Neuroscience is the flagship journal of IBRO and is overseen by the IBRO Publications CommitteeElsevier publishes 28 issues per year. 

    The journal features papers describing the results of original research on any aspect of the scientific study of the nervous system. Any paper, however short, is considered for publication provided that it reports significant, new and carefully confirmed findings with full experimental details.

    READ the current issue of IBRO Neuroscience (vol. 340) published on 6 January 2016. Highlighted findings from this issue include:

    Structural organization of the dendritic reticulum linked by gap junctions in layer 4 of the visual cortex

    (T. Fukuda)

    Neuronal gap junctions are ubiquitous in the brain, but their precise positions in actual neuronal circuits have been uncertain, and their functional roles remain unclear. In this study, I visualized connexin36-immunoreactive gap junctions and examined the structural features of the interconnected dendrites arising from parvalbumin (PV)-positive interneurons in layer 4 of the feline visual cortex. I observed evidence for net-like dense linkages of dendrites among virtually all PV neurons (56/58 cells, 96.6%) in the tissue. This dendritic reticulum established connections among clustered cells and further among remote cells. The latter connectivity exhibited a preference for vertical direction, including translaminar linkages, but was also characterized by lateral continuity. Measurement of the distances from each dendritic gap junction back to the two connected somata revealed that at least one of two somata was within 50 μm from the junction in 77.5% of the cases and within 75 μm in 91.2% of the cases. Thus, distal gap junctions mediated morphologically asymmetrical connection where one soma was close to, but the other soma was far from the connecting junction. This connectivity was typically observed between neurons located apart in the same columnar space, where a long vertical dendrite bridged two neurons through an asymmetrically positioned gap junction. In contrast, gap junctions formed between nearby cells were close to both somata. Thalamocortical afferents established synapses densely on somata of layer 4 PV neurons, indicating the possible involvement of proximal gap junctions in visual stimulus-driven feedforward regulation. These findings provide a new structural basis for cortical investigations.

    Age-induced differences in brain neural activation elicited by visual emotional stimuli: A high-density EEG study

    (A.C. Tsolakia, V.E. Kosmidoub, I. (Yiannis) Kompatsiarisb, C. Papadaniilc, L. Hadjileontiadisc and M. Tsolakie)

    Identifying the brain sources of neural activation during processing of emotional information remains a very challenging task. In this work, we investigated the response to different emotional stimuli and the effect of age on the neuronal activation. Two negative emotion conditions, i.e., ‘anger’ and ‘fear’ faces were presented to 22 adult female participants (11 young and 11 elderly) while acquiring high-density electroencephalogram (EEG) data of 256 channels. Brain source localization was utilized to study the modulations in the early N170 event-related- potential component. The results revealed alterations in the amplitude of N170 and the localization of areas with maximum neural activation. Furthermore, age-induced differences are shown in the topographic maps and the neural activation for both emotional stimuli. Overall, aging appeared to affect the limbic area and its implication to emotional processing. These findings can serve as a step toward the understanding of the way the brain functions and evolves with age which is a significant element in the design of assistive environments.

    Repeated prenatal exposure to valproic acid results in cerebellar hypoplasia and ataxia

    (S.L. Main, R.J. Kulesza)

    Autism spectrum disorder (ASD) is a developmental brain disorder characterized by restricted and repetitive patterns of behavior, social and communication defects, and is commonly associated with difficulties with motor coordination. The etiology of ASD, while mostly idiopathic, has been linked to hereditary factors and teratogens, such as valproic acid (VPA). VPA is used clinically to treat epilepsy, mood disorders, and in the prevention of migraines. The use of VPA during pregnancy significantly increases the risk of ASD in the offspring. Neuropathological studies show decreased cerebellar function in patients with ASD, resulting in gait, balance and coordination impairments. Herein, we have exposed pregnant rats to a repeated oral dose of VPA on embryonic days 10 and 12 and performed a detailed investigation of the structure and function of the cerebellar vermis. We found that throughout all ten lobules of the cerebellar vermis, Purkinje cells were significantly smaller and expression of the calcium binding protein calbindin (CB) was significantly reduced. We also found that dendritic arbors of Purkinje cells were shorter and less complex. Additionally, animals exposed to a repeated dose of VPA performed significantly worse in a number of motor tasks, including beam walking and the rotarod. These results suggest that repeated embryonic exposure to VPA induces significant cerebellar dysfunction and is an effective animal model to study the cerebellar alterations in ASD.

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