PlexinD1 signaling controls morphological changes and migration termination in newborn neurons

Newborn neurons maintain a very simple, bipolar shape, while they migrate from their birthplace toward their destinations in the brain, where they differentiate into mature neurons with complex dendritic morphologies. Here, we report a mechanism by which the termination of neuronal migration is maintained in the postnatal olfactory bulb (OB). During neuronal deceleration in the OB, newborn neurons transiently extend a protrusion from the proximal part of their leading process in the resting phase, which we refer to as a filopodium‐like lateral protrusion (FLP). The FLP formation is induced by PlexinD1 downregulation and local Rac1 activation, which coincide with microtubule reorganization and the pausing of somal translocation. The somal translocation of resting neurons is suppressed by microtubule polymerization within the FLP. The timing of neuronal migration termination, controlled by Sema3E‐PlexinD1‐Rac1 signaling, influences the final positioning, dendritic patterns, and functions of the neurons in the OB. These results suggest that PlexinD1 signaling controls FLP formation and the termination of neuronal migration through a precise control of microtubule dynamics.     

The Sodium Hypochlorite Solution for the Removal of Lichen from Vertebrate Track Surfaces

The removal of extraneous biological materials from vertebrate ichnological specimens may be necessary if they have been exposed to subaerial processes in the field for long periods of time. It is not uncommon for fossil track specimens to be found nearly completely covered with lichen colonies, especially those recovered from alpine areas. This paper describes a technique using a sodium hypochlorite solution (bleach) to remove lichen from a track surface containing numerous avian prints and small theropod prints with skin impressions.     

Rescue of neurogenesis and age-associated cognitive decline in SAMP8 mouse: Role of transforming growth factor-alpha

Neuropathological aging is associated with memory impairment and cognitive decline, affecting several brain areas including the neurogenic niche of the dentate gyrus of the hippocampus (DG). In the healthy brain, homeostatic mechanisms regulate neurogenesis within the DG to facilitate the continuous generation of neurons from neural stem cells (NSC). Nevertheless, aging reduces the number of activated neural stem cells and diminishes the number of newly generated neurons. Strategies that promote neurogenesis in the DG may improve cognitive performance in the elderly resulting in the development of treatments to prevent the progression of neurological disorders in the aged population. Our work is aimed at discovering targeting molecules to be used in the design of pharmacological agents that prevent the neurological effects of brain aging. We study the effect of age on hippocampal neurogenesis using the SAMP8 mouse as a model of neuropathological aging. We show that in 6-month-old SAMP8 mice, episodic and spatial memory are impaired; concomitantly, the generation of neuroblasts and neurons is reduced and the generation of astrocytes is increased in this model. The novelty of our work resides in the fact that treatment of SAMP8 mice with a transforming growth factor-alpha (TGFα) targeting molecule prevents the observed defects, positively regulating neurogenesis and improving cognitive performance. This compound facilitates the release of TGFα in vitro and in vivo and activates signaling pathways initiated by this growth factor. We conclude that compounds of this kind that stimulate neurogenesis may be useful to counteract the neurological effects of pathological aging.     

The endocannabinoid system in normal and pathological brain ageing

The role of endocannabinoids as inhibitory retrograde transmitters is now widely known and intensively studied. However, endocannabinoids also influence neuronal activity by exerting neuroprotective effects and regulating glial responses. This review centres around this less-studied area, focusing on the cellular and molecular mechanisms underlying the protective effect of the cannabinoid system in brain ageing. The progression of ageing is largely determined by the balance between detrimental, pro-ageing, largely stochastic processes, and the activity of the homeostatic defence system. Experimental evidence suggests that the cannabinoid system is part of the latter system. Cannabinoids as regulators of mitochondrial activity, as anti-oxidants and as modulators of clearance processes protect neurons on the molecular level. On the cellular level, the cannabinoid system regulates the expression of brain-derived neurotrophic factor and neurogenesis. Neuroinflammatory processes contributing to the progression of normal brain ageing and to the pathogenesis of neurodegenerative diseases are suppressed by cannabinoids, suggesting that they may also influence the ageing process on the system level. In good agreement with the hypothesized beneficial role of cannabinoid system activity against brain ageing, it was shown that animals lacking CB1 receptors show early onset of learning deficits associated with age-related histological and molecular changes. In preclinical models of neurodegenerative disorders, cannabinoids show beneficial effects, but the clinical evidence regarding their efficacy as therapeutic tools is either inconclusive or still missing.     

A Uchl1‐Histone2BmCherry:GFP‐gpi BAC transgene for imaging neuronal progenitors

Summary: Uchl1 encodes the protein gene product 9.5 antigen (PGP9.5) that is a widely used to identify migrating neural progenitors in the PNS, mature neurons of the central and peripheral nervous systems, as well as neuroendocrine cells. To facilitate analysis of developing peripheral neurons, we linked regulatory regions of Uchl1 carried within a 160kb bacterial artificial chromosome (BAC) to the dual fluorescent reporter H2BmCherry:GFP‐gpi. The Uchl1‐H2BmCherry:GFP‐gpi transgene exhibits robust expression and allows clear discrimination of individual cells and cellular processes in cranial ganglia, sympathetic chain, the enteric nervous system (ENS), and autonomic ganglia of the urogenital system. The transgene also labels subsets of cells in endocrine tissues where earlier in situ hybridization (ISH) studies have previously identified expression of this deubiquinating enzyme. The Uchl1‐H2BmCherry:GFP‐gpi transgene will be a powerful tool for static and live imaging, as well as isolation of viable neural progenitors to investigate processes of autonomic neurogenesis. genesis 51:852–861. © 2013 Wiley Periodicals, Inc.     

Transcriptional dynamics of delaminating neuroblasts in the mouse otic vesicle

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Relative abundance and species composition of some dung beetles (Coleoptera: Scarabaeinae) in Bangladesh

1. The occurrence and community structure of dung beetle species (Coleoptera: Scarabaeinae) in the faecal deposits of man and some domestic vertebrates varied according to dung type, seasonal conditions and soil type. 2. Of the twenty-four species belonging to six genera, Onthophagus was the prevalent genus and O. ramosellus the most abundant species. 3. Cattle dung was the dominant food type.     

A mineralogical method to determine cyclicity in the taphonomic and diagenetic history of fossilized bones

The study of authigenic minerals within the voids of a fossilized bone can reveal its diagenetic history. When the order of precipitation of minerals is plotted on an Eh/pH diagram any cyclicity in the diagenetic history is revealed. If one cycle is displayed then it can be assumed that the bone has been found in its original bed of deposition; if two cycles or more are revealed then reworking or environmental change may have taken place. This is demonstrated in a case study of two bones from the Wealden Group (Lower Cretaceous) from the Isle of Wight, UK.     

Towards a Knowledge-Based Ethic for Lethal Control of Nuisance Wildlife

ABSTRACT Managers of nuisance wildlife have to rely largely on using lethal methods until such time as nonlethal techniques, such as fertility control, become universally available for a wide range of species. Unfortunately, use of lethal tools has met with opposition from animal welfare and animal rights proponents. Although research has addressed some of the more tractable welfare concerns (e.g., making traps more humane), less tractable ethical issues associated with the justification of killing wildlife remain unresolved. Monistic welfare models or rights-based models have been proposed as ways of addressing these issues, but those that concentrate on the cognitive and conative capabilities of individual animals fail to resolve the ecological and social complexities involved in management of nuisance wildlife. Solutions need to recognize and accept the diversity of values (i.e., within a pluralistic strategy) as well as the uncertainty inherent in many of the systems being managed. Thus, when uncertainty is high in managing wildlife—resource systems, we propose the only ethically defensible action is to apply a knowledge-based ethic that ensures future actions will be carried out with increased understanding. Such an ethic can be made functional within an adaptive management framework that has, as its first tenet, the need to learn and reduce uncertainty. Failure to maximize learning in the presence of uncertainty has the potential to result in increased opposition to even soundly justified operations to manage nuisance wildlife.     

Rin,a novel cell-surface protein that labels reticular neurons early in chick neurogenesis

Rin is a large cell-surface glycoprotein that we have recently purified from chick brain, with a molecular weight of approximately 200 kD. Protein microsequence obtained from immunopurified rin does not match any sequences in the Genbank data base. Based on the sequences information and on its localization in the early chick embryo, rin is a novel cell-surface protein. Rin is expressed on the surface of many, but not all, axons in the developing chick nervous system. In the chick hind-brain, rin is expressed on reticular neurons, the first neurons to extend axons within the brain. Cranial motorneurons, which extend axons just a few stages later, do not express rin. Rin-positive axons pioneer the caudal section of the medial longitudinal fasciculus. The very first rin-positive axons that reach the floorplate do not enter the floorplate, but remain ipsilateral. Some of the next immunopositive axons to reach the floorplate do cross the midline, often with an alteration in trajectory, and often extending within the floorplate for some distance before reaching the other side. The failure of the very first rin-positive axons to cross the floorplate, and the changes in trajectory observed when the next axons extend onto the floorplate, suggests that early differentiating neurons cross the midline with some difficulty. 1994 John Wiley & Sons, Inc.