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)
 
 
 
 
 

Chronic nicotine exposure during adolescence differentially influences calcium-binding proteins in rat anterior cingulate cortex.

We have recently shown that chronic amphetamine exposure selectively up-regulates parvalbumin (PV) calcium-binding proteins in the anterior cingulate cortex (ACC). In this study, we evaluated the effects of chronic nicotine (NIC) exposure on PV, calbindin D28k (CB) and calretinin (CR) calcium-binding protein immunostaining in ACC GABAergic interneurons. Chronic NIC exposure for 3 weeks in adolescent rats, either via drinking water (the oral group) or by twice daily subcutaneous injections (the injection group), resulted in the expression of high levels of CR proteins in the ACC but not in the parietal cortex. Larger increases in the density of CR-immunoreactive (ir) neurons were noted in the NIC-injected rats at 0-day withdrawal (45% increase) compared with the oral group (26% increase). The larger increases in CR-ir neuron density in the NIC-injected rats were also reflected by prominent CR-ir processes across cortical layers. The density of PV-ir neurons was also increased (37%) at 0-day withdrawal but only in the oral NIC group and no changes in CB-ir neuron density were observed in either NIC group. Combined dual-immunofluorescence and confocal microscopy revealed that somatodendritic alpha4 nicotinic acetylcholine receptors colocalized with cortical neurons stained positively for CR, PV or CB. These results suggest that CR- and/or PV-ir-containing GABA interneurons may be involved in channeling the effects of NIC in the ACC, which is closely associated with the ventral basal ganglia circuit that is linked to brain reward function.[1]

References

  1. Chronic nicotine exposure during adolescence differentially influences calcium-binding proteins in rat anterior cingulate cortex. Liu, J.J., Mohila, C.A., Gong, Y., Govindarajan, N., Onn, S.P. Eur. J. Neurosci. (2005) [Pubmed]
 
WikiGenes - Universities