Tyrosine hydroxylase, but not dopamine beta-hydroxylase, is increased in rat frontal cortex after traumatic brain injury

Abstract

Chronic frontal lobe functional deficits after traumatic brain injury (TBI) may be associated with altered catecholamine systems in the frontal cortex. To test this, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) levels were examined by immunohistochemistry and Western blot at 1, 7, 14, and 28 days after TBI or sham surgery. No alterations in DBH levels were observed by Western blot at any time point examined, but there was a significant increase in TH expression 28 days after TBI (optical density 334 +/- 68% or 3.3-fold, ipsilateral and 218 +/- 39% or 2.2-fold, contralateral) relative to the sham controls. The increase in TH may reflect a compensatory response of dopaminergic neurons to upregulate their synthesizing capacity and increase the efficiency of dopamine neurotransmission chronically after TBI.

Delayed increase of tyrosine hydroxylase expression in rat nigrostriatal system after traumatic brain injury

“…Specifically, the TH signal was seen as a single band of approximately 59 kDa ( Fig. 3A and 4A) and is consistent with previous studies (Soriano et al, 1997;Yan et al, 2001). Consistent with the immunohistochemistry findings using this TH antibody (Fig.…”

“…These time points were selected on basis of previous studies of DA systems after TBI (Yan et al, 2001(Yan et al, , 2002. Tissue preparation and immunohistochemistry procedures were as previously reported (Yan et al, 2001).…”

“…Our previous study demonstrates that TBI produced an increase in TH protein in rat frontal cortex that was detectable by both immunohistochemistry and Western blot at 28 days postinjury (Yan et al, 2001). In contrast, dopamine beta hydroxylase (DBH) protein levels were not altered following TBI suggesting that the increase in TH occurred predominantly in dopaminergic axons (Yan et al, 2001).…”

“…In contrast, dopamine beta hydroxylase (DBH) protein levels were not altered following TBI suggesting that the increase in TH occurred predominantly in dopaminergic axons (Yan et al, 2001). The effect of controlled cortical impact (CCI) injury on TH in the nigrostriatal system is currently unknown.…”

Gender associations with chronic methylphenidate treatment and behavioral performance following experimental traumatic brain injury

“…Previous work suggests ongoing regional alterations in tissue catecholaminergic concentrations after experimental TBI [19]. Studies from our laboratory have demonstrated chronic alterations in frontal cortex dopamine (DA) system proteins after experimental TBI, including increased tyrosine hydroxylase [43], a protein critical in the synthesis of DA, and decreased DA transporter (DAT), a protein critical for reuptake of DA into presynaptic terminals [44]. Additional work suggests that striatal DAT levels are decreased in males after TBI [38].…”