Literature DB >> 24827676

Cortical ablation induces time-dependent changes in rat pituitary somatotrophs and upregulates growth hormone receptor expression in the injured cortex.

Irena Lavrnja1, Vladimir Ajdzanovic, Svetlana Trifunovic, Danijela Savic, Verica Milosevic, Mirjana Stojiljkovic, Sanja Pekovic.   

Abstract

The pituitary appears to be vulnerable to brain trauma, and its dysfunction is a common feature after traumatic brain injury. The role of pituitary growth hormone (GH) in brain repair after injury has been envisaged, but more studies must be performed to understand completely the importance of GH in these processes. Because some of the neuroprotective effects of GH are mediated directly through the GH receptor (GHR), we examined GHR expression in the rat cerebral cortex after sensorimotor cortex ablation. RT-PCR, immunohistochemistry, and double immunofluorescence had been performed to analyze the correlation between GHR expression in the injured cortex and activity of GH cells in the pituitary. Our results showed that the volume of GH-immunopositive cells was reduced at days 2 and 7 postsurgery (dps), and volume density of GH cells was significantly decreased at 14 dps, all compared with appropriate sham controls. At 30 dps all investigated parameters had returned to control level. In the injured cortex, GHR expression was transiently upregulated. Increased GHR immunoreactivity was observed in reactive astrocytes at 7 and particularly at 14 dps. In neuronal cells, an increase of GHR immunoreactivity was seen in neuronal cell bodies and well-defined primary dendrites at 14 and especially at 30 dps. The results presented here suggest that, during recovery from brain injury, changes in activity of pituitary GH cells result in upregulation of GHR that may have a role in neuronal arborization and glial proliferation in the injured cortex.
© 2014 Wiley Periodicals, Inc.

Entities:  

Keywords:  glia scar; growth hormone; growth hormone receptor; pituitary gland; traumatic brain injury

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Year:  2014        PMID: 24827676     DOI: 10.1002/jnr.23408

Source DB:  PubMed          Journal:  J Neurosci Res        ISSN: 0360-4012            Impact factor:   4.164


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