Retarded Formation of the Hippocampal Commissure in Embryos From Mouse Strains Lacking a Corpus Callosum

formation of the hippocampal commissure in embryos from mouse strains lacking a corpus callosum. Hippocampus, 1997, 7, 2- A precise description of the timing and route traveled by axons traversing the telencephalic midline through the ventral hippocampal commissure (HC) is essential for understanding the role it plays in the formation of the corpus callosum (CC). A normal baseline of HC development was described in B6D2F 2 hybrid mice and then compared with two inbred strains of mice displaying callosal agenesis, BALB/cWah1 (50% CC defect) and 129/J (70% CC defect), their F 2 hybrid (C129F 2 -33% CC defect), and a recombinant inbred strain (RI-1-100% CC defect) derived from pairs of C129F 2 mice. Embryos weighing from 0.25 gto0.70 g(E14.5-E17) were collected and fixed by perfusion. Axon tracts were labeled using crystals of the lipophilic dyes DiI and DiA inserted into the hippocampal fimbria and cerebral cortex. HC axons in B6D2F 2 mice first cross the midline at about 0.350 g body weight (E14.8) by traveling over the dorsal septum and along the pia membrane lining the longitudinal fissure. Earlier crossing was prevented by the presence of a deep cleft formed by the longitudinal fissure extending down into the septal region. Subsequent axons fasciculated along existing axons, gradually building the dorsoventral height of the HC to about 200 μm by 0.600 g. The earliest callosal axons from frontal cortex crossed the midline at 0.620 g and were clearly seen fasciculating along and between existing hippocampal axons at the dorsal surface of the HC as they crossed. In the acallosal strains, HC formation was delayed by the continued presence of the cleft deep in the septal region. This delay in time of crossing was correlated with later CC defect expression. Initial HC crossing occurred at about 0.470 g (E1 6.25) in BALB mice and about 0.520 g (E1 6.5) in 129 mice. In the RI-1 embryos, first HC crossing was estimated at about 0.750 g (E1 7.5), although several older embryos showed no crossing. These results show the importance of the HC for successful CC formation and suggest that absent CC arises as a consequence of a developmental defect which affects the formation of the hippocampal commissure prior to arrival of CC axons at midplane

Exploring Pompeii: discovering hospitality through research synergy

Hospitality research continues to broaden through an ever-increasing dialogue and alignment with a greater number of academic disciplines. This paper demonstrates how an enhanced understanding of hospitality can be achieved through synergy between archaeology, the classics and sociology. It focuses on classical Roman life, in particular Pompeii, to illustrate the potential for research synergy and collaboration, to advance the debate on hospitality research and to encourage divergence in research approaches. It demonstrates evidence of commercial hospitality activities through the excavation hotels, bars and taverns, restaurants and fast food sites. The paper also provides an example of the benefits to be gained from multidisciplinary analysis of hospitality and tourism

Restricted Morphological and Behavioral Abnormalities following Ablation of β-Actin in the Brain

The local translation of β-actin is one mechanism proposed to regulate spatially-restricted actin polymerization crucial for nearly all aspects of neuronal development and function. However, the physiological significance of localized β-actin translation in neurons has not yet been demonstrated in vivo. To investigate the role of β-actin in the mammalian central nervous system (CNS), we characterized brain structure and function in a CNS-specific β-actin knock-out mouse (CNS-ActbKO). β-actin was rapidly ablated in the embryonic mouse brain, but total actin levels were maintained through upregulation of other actin isoforms during development. CNS-ActbKO mice exhibited partial perinatal lethality while survivors presented with surprisingly restricted histological abnormalities localized to the hippocampus and cerebellum. These tissue morphology defects correlated with profound hyperactivity as well as cognitive and maternal behavior impairments. Finally, we also identified localized defects in axonal crossing of the corpus callosum in CNS-ActbKO mice. These restricted defects occurred despite the fact that primary neurons lacking β-actin in culture were morphologically normal. Altogether, we identified novel roles for β-actin in promoting complex CNS tissue architecture while also demonstrating that distinct functions for the ubiquitously expressed β-actin are surprisingly restricted in vivo