Effects of monocular deprivation on the expression pattern of alpha-1 and beta-1 adrenergic receptors in the kitten visual cortex.
To examine how adrenergic receptors are regulated by experimental manipulation of sensory afferents, we performed immunohistochemical analysis on alpha1-, and beta1-adrenergic receptors in the brain of kittens. In normal development, these receptors were similarly expressed in both hemispheres of the occipital and frontal cortices. Notably, monocular deprivation during the sensitive period of ocular dominance plasticity significantly increased beta1-adrenergic receptor immunoreactivity in the visual cortex ipsilateral to the deprived eye. No increase in the intensity of the immunoreactivity for beta1-adrenergic receptors following monocular deprivation was found in the frontal and parietal regions of the cerebral cortex and subcortical structures, including the lateral geniculate nucleus and superior colliculus. Furthermore, such hemispheric change was not found in the alpha1-adrenergic receptor immunoreactivity following monocular deprivation. Comparisons of images, obtained by double staining for microtubule-associated protein-2 or glial fibrillary acidic protein, indicated that the increased immunoreactivity was localized on both apical dendrites of deep layer neurons and glial cells. These results indicate that the monocular deprivation during the sensitive period of ocular dominance plasticity modified beta1-adrenergic receptor immunoreactivity, including that in glial cells. Therefore, it was suggested that beta1-adrenergic receptors in the glial cells also play important roles in the regulation of ocular dominance plasticity.[1]References
- Effects of monocular deprivation on the expression pattern of alpha-1 and beta-1 adrenergic receptors in the kitten visual cortex. Nakadate, K., Imamura, K., Watanabe, Y. Neurosci. Res. (2001) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg