doi: 10.1038/nn1104-1167pmid: 15508009
The perception of a stimulus can result in an emotional response, as we all know, but modulation of perception by emotion has been more difficult to demonstrate. A new study combines imaging and patient data to point to an anatomical substrate for such an effect, raising important implications regarding how sensory-processing impairments might arise in affective disorders.
Samuels, Benjamin Adam; Tsai, Li-Huei
doi: 10.1038/nn1104-1169pmid: 15508010
Newborn neurons in the cerebellum migrate along radial glial processes through a series of distinct steps. A report in this issue uses live imaging to grant us a close-up view of the cytoskeletal structures and regulating proteins involved in this migration.
Morris, Richard G M; Rugg, Michael D
doi: 10.1038/nn1104-1171pmid: 15508011
In humans, recollection and familiarity represent qualitatively distinct kinds of memory. A recent study in Nature applied methods commonly used in human research to rats and suggests that their recognition memory may consist of similarly distinct components.
Ullsperger, Markus; von Cramon, D Yves
doi: 10.1038/nn1104-1173pmid: 15508012
The rostral cingulate zone and the orbitofrontal cortex are active when people monitor the consequences of adaptively changing behavior. A new fMRI study distinguishes their functions, implicating them in situations with different contexts and timing.
Crabbe, John C; Morris, Richard G M
doi: 10.1038/nn1343pmid: 15508013
A recent perspective discussed high-throughput behavioral analysis using mice, giving the overall impression that this area is lagging behind in neuroscience and biomedical research. Not only are we more optimistic about the current state of the art in behavioral neuroscience and its promise, but we also have reservations about whether high-throughput analysis is always an appropriate goal for most behavioral studies. We argue that behavioral studies should be carried out with clear goals and more regard to the intellectual context in which they have developed. In addition, behavioral studies can be performed quite easily, but this does not ensure the required validity or reliability of the particular tests used. Finally, high throughput may not always be an appropriate goal. We discuss the role of automated data collection and unique data-mining algorithms, and the question of the ethological relevance of behavioral tests.
Tsai, Julia; Grutzendler, Jaime; Duff, Karen; Gan, Wen-Biao
doi: 10.1038/nn1335pmid: 15475950
Amyloid plaques are a hallmark of Alzheimer disease, but their importance in its pathogenesis is controversial. By neuronal labeling and transcranial two-photon imaging, we show in a transgenic mouse model of Alzheimer disease that dendrites passing through or near fibrillar amyloid deposits undergo spine loss and shaft atrophy, and nearby axons develop large varicosities, together leading to neurite breakage and large-scale, permanent disruption of neuronal connections. Thus, fibrillar amyloid deposition is more detrimental to neuronal circuitry than previously thought, underscoring the importance of prevention and early clearance of plaques.
Cristo, Graziella Di; Wu, Caizhi; Chattopadhyaya, Bidisha; Ango, Fabrice; Knott, Graham; Welker, Egbert; Svoboda, Karel; Huang, Z Josh
doi: 10.1038/nn1334pmid: 15475951
Distinct classes of GABAergic synapses target restricted subcellular domains, thereby differentially regulating the input, integration and output of principal neurons, but the underlying mechanism for such synapse segregation is unclear. Here we show that the distributions of two major classes of GABAergic synapses along the perisomatic and dendritic domains of pyramidal neurons were indistinguishable between primary visual cortex in vivo and cortical organotypic cultures. Therefore, subcellular synapse targeting is independent of thalamic input and probably involves molecular labels and experience-independent forms of activity.
Yeo, Giles S H; Connie Hung, Chiao-Chien; Rochford, Justin; Keogh, Julia; Gray, Juliette; Sivaramakrishnan, Shoba; O'Rahilly, Stephen; Farooqi, I Sadaf
doi: 10.1038/nn1336pmid: 15494731
An 8-year-old male with a complex developmental syndrome and severe obesity was heterozygous for a de novo missense mutation resulting in a Y722C substitution in the neurotrophin receptor TrkB. This mutation markedly impaired receptor autophosphorylation and signaling to MAP kinase. Mutation of NTRK2, which encodes TrkB, seems to result in a unique human syndrome of hyperphagic obesity. The associated impairment in memory, learning and nociception seen in the proband reflects the crucial role of TrkB in the human nervous system.
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