The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Afferent specific localization of muscarinic acetylcholine receptors in cingulate cortex.

The laminar distribution of acetylcholine receptors in rat cingulate cortex and their localization to axons of neurons in the anterior thalamic nuclei (ATN) were evaluated with the muscarinic antagonist [3H]propylbenzilylcholine mustard (PrBCM) in vitro. Specific binding of PrBCM in granular area 29 was heterogeneous, with a 57% variation from the highest binding in layer Ia to the lowest in layer II-III. In contrast, binding in area 24 was homogeneous, with only a 14% variation. The heterogeneity of PrBCM binding almost exactly duplicated the distribution of termination of ATN afferents in layers I to IV of area 29c. Four experiments indicated that 50% of the excess binding in layers Ia and IV was due to axonal receptor sites. First, ATN lesions abolished 41% and 27% of total specific binding in layers Ia and IV, respectively. Second, an undercut procedure that totally deafferented layers I to Va showed changes similar to those following ATN lesions, suggesting that other afferents to these layers may not have muscarinic receptors associated with them. Third, the sequence of losses in receptor binding and acetylcholinesterase (AChE) activity was evaluated 2, 3, 5, 9, and 14 days following ATN lesions. Since AChE was present in ATN axons, as evidenced by early postlesion losses, the correlation of both losses as well as previous analyses of axon degeneration in this cortex confirmed that these receptors were in axons. Fourth, binding peaks in layers Ia and IV remained in area 29c following destruction of virtually all neurons with the neurotoxin ibotenic acid. This is the first evidence that the activity of a major neocortical thalamic afferent may be regulated by axonal acetylcholine receptors.[1]


WikiGenes - Universities