|Cheng, Heng Wei|
Submitted to: Journal of Neuroscience
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/14/2005
Publication Date: N/A
Interpretive Summary: In the modern poultry industry, chickens are housed in different environments, such as battery cage, enriched cage, pen, and free rage. The capability of birds to adapt their environments directly and/or indirectly affects their well-being and productivity. Previous studies have shown that the nervous system, especially, the central nervous system, plays important roles in controlling animal’s adaptability. This study further evidenced that the functions of the central nervous system can be regulated differently based on the types of stimuli. The findings proved a new sign to study the cellular mechanisms that underlie the capability of birds to adapt different housing environments, such as battery cages vs. enriched cages. This method can be adopted by other scientists to study environmental effects on animal well-being by examining the functional changes of the central nervous system, which is stressor-dependent.
Technical Abstract: Investigation of the elements underlying synapse replacement after brain injury is essential for predicting the neural compensation that can be achieved after various types of damage. The growth-associated proteins superior cervical ganglion-10 and growth-associated protein-43 have previously been linked with structural changes in the corticostriatal system in response to unilateral deafferentation. To examine the regulation of this response, unilateral cortical aspiration lesion was carried out in combination with ipsilateral 6-hydroxydopamine lesion of the substantia nigra, and the time course of the contralateral cortical molecular response was followed. Unilateral cortical aspiration lesion in rats corresponds with an upregulation of superior cervical ganglion-10 mRNA at 3 and 10 days post-lesion, and protein, sustained from three to at least 27 days following lesion. With the addition of substantia nigra lesion, the response shifts to an upregulation of growth-associated protein-43 mRNA at 3 and 10 days post-lesion, and protein after 10 days. Nigral lesion alone does not alter contralateral expression of either gene. Likewise, motor function assessment using the rotorod test revealed no significant long-term deficits in animals that sustained only nigrostriatal damage, but cortical lesion was associated with a temporary deficit which was sustained when nigrostriatal input was also removed. Growth-associated protein-43 and superior cervical ganglion-10, two presynaptic genes that are postulated to play roles in lesion-induced sprouting, are differentially upregulated in corticostriatal neurons after cortical versus combined cortical/nigral lesions. The shift in contralateral gene response from superior cervical ganglion-10 to growth-associated protein-43 upregulation and associated behavioral deficit following combined cortical and nigral denervation suggest that nigrostriatal afferents regulate cortical lesion-induced gene expression and ultimate functional outcome.