Seismic evidence for a mantle suture and implications for the origin of the Canadian Cordillera.

The origin of the North American Cordillera and its affinity with the bounding craton are subjects of contentious debate. The mechanisms of orogenesis are rooted in two competing hypotheses known as the accretionary and collisional models. The former model attributes the Cordillera to an archetypal accretionary orogen comprising a collage of exotic terranes. The latter, less popular view argues that the Cordillera is a collisional product between an allochthonous ribbon microcontinent and cratonic North America. Here we present new seismic evidence of a sharp and structurally complex Cordillera-craton boundary in the uppermost mantle beneath the southern Canadian Cordillera, which can be interpreted as either a reshaped craton margin or a Late Cretaceous collisional boundary based on the respective hypotheses. This boundary dips steeply westward underneath a proposed (cryptic) suture in the foreland, consisent with the predicted location and geometry of the mantle suture, thus favoring a collisional origin.

Functional Implications of miR-19 in the Migration of Newborn Neurons in the Adult Brain.

Altered microRNA profiles have been implicated in human brain disorders. However, the functional contribution of individual microRNAs to neuronal development and function is largely unknown. Here, we report biological functions for miR-19 in adult neurogenesis. We determined that miR-19 is enriched in neural progenitor cells (NPCs) and downregulated during neuronal development in the adult hippocampus. By manipulating miR-19 in NPCs for gain- and loss-of-function studies, we discovered that miR-19 regulates cell migration by directly targeting Rapgef2. Concordantly, dysregulation of miR-19 in NPCs alters the positioning of newborn neurons in the adult brain. Furthermore, we found abnormal expression of miR-19 in human NPCs generated from schizophrenic patient-derived induced pluripotent stem cells (iPSCs) that have been described as displaying aberrant migration. Our study demonstrates the significance of posttranscriptional gene regulation by miR-19 in preventing the irregular migration of adult-born neurons that may contribute to the etiology of schizophrenia.

In vivo imaging of dendritic pruning in dentate granule cells.

We longitudinally imaged the developing dendrites of adult-born mouse dentate granule cells (DGCs) in vivo and found that they underwent over-branching and pruning. Exposure to an enriched environment and constraint of dendritic growth by disrupting Wnt signaling led to increased branch addition and accelerated growth, which were, however, counteracted by earlier and more extensive pruning. Our results indicate that pruning is regulated in a homeostatic fashion to oppose excessive branching and promote a similar dendrite structure in DGCs.

What is memory? The present state of the engram.

The mechanism of memory remains one of the great unsolved problems of biology. Grappling with the question more than a hundred years ago, the German zoologist Richard Semon formulated the concept of the engram, lasting connections in the brain that result from simultaneous "excitations", whose precise physical nature and consequences were out of reach of the biology of his day. Neuroscientists now have the knowledge and tools to tackle this question, however, and this Forum brings together leading contemporary views on the mechanisms of memory and what the engram means today.

Paradox of pattern separation and adult neurogenesis: A dual role for new neurons balancing memory resolution and robustness.

Hippocampal adult neurogenesis is thought to subserve pattern separation, the process by which similar patterns of neuronal inputs are transformed into distinct neuronal representations, permitting the discrimination of highly similar stimuli in hippocampus-dependent tasks. However, the mechanism by which immature adult-born dentate granule neurons cells (abDGCs) perform this function remains unknown. Two theories of abDGC function, one by which abDGCs modulate and sparsify activity in the dentate gyrus and one by which abDGCs act as autonomous coding units, are generally suggested to be mutually exclusive. This review suggests that these two mechanisms work in tandem to dynamically regulate memory resolution while avoiding memory interference and maintaining memory robustness.

Neural proliferation in the dorsal root ganglia of the adult rat following capsaicin-induced neuronal death.

Glial proliferation is a major component of the nervous system's response to injury. In addition to glial proliferation, injury may induce neuronal proliferation in areas of the adult nervous system not considered neurogenic. We have previously reported increased neural proliferation within adult nodose ganglia following capsaicin-induced neuronal death. However, proliferation within the dorsal root ganglia (DRG) remains to be characterized. We hypothesized that capsaicin-induced neuronal death would increase proliferation of satellite glial cells (SGCs) within the DRG. To test this hypothesis, 6-week-old Sprague-Dawley rats received a neurotoxic dose of capsaicin, and proliferation was quantified and characterized at multiple time points thereafter. Proliferation of satellite glial cells expressing the progenitor cell marker nestin was increased at 1 and 3 days following capsaicin administration as shown by BrdU incorporation. In addition to SGCs was a large population of proliferating resident macrophages, as shown by retrovirally mediated expression of GFP. SGC proliferation at these early time points was followed by recovery of neuronal numbers after a loss of 40% of the neuronal population in the DRG. This recovery in neuronal number correlated with recovery of function as shown by paw withdrawal from a noxious heat source. Further understanding of the role that glial proliferation plays in the recovery of neuronal numbers and function may lead to the development of therapeutic treatments for neurodegenerative conditions.