Brain injury results in lower levels of melatonin receptors subtypes MT1 and MT2. (22nd May 2017)

• Record Type: Journal Article
• Authors: Osier, Nicole D.; Pham, Lan; Pugh, Bunny J.; Puccio, Ava; Ren, Dianxu; Conley, Yvette P.; Alexander, Sheila; Dixon, C. Edward
• Is Part Of: Neuroscience letters. Volume 650(2017)
• Page Start: 18
• Page End: 24
• Publication Date: 2017-05-22
• Subjects: Traumatic brain injury (TBI) -- Brain trauma -- Controlled cortical impact (CCI) -- Rat -- Melatonin -- Receptors; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.03.053
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Traumatic brain injury in rats results in lower levels of melatonin receptors. In the frontal cortex, MT1 and MT2 were reduced at 24 h after TBI (vs. sham). In the hippocampus, MT1 and MT2 were reduced at 6- and 24 h after TBI. MT1 and MT2 receptor decreases after TBI may affect response to melatonin therapy. Abstract: Background: Traumatic brain injury (TBI) is a devastating and costly acquired condition that affects individuals of all ages, races, and geographies via a number of mechanisms. The effects of TBI on melatonin receptors remain unknown. Purpose: The purpose of this study is to explore whether endogenous changes in two melatonin receptor subtypes (MT1 and MT2) occur after experimental TBI. Sample: A total of 25 adult male Sprague Dawley rats were used with 6 or 7 rats per group. Methods: Rats were randomly assigned to receive either TBI modeled using controlled cortical impact or sham surgery and to be sacrificed at either 6- or 24-h post-operatively. Brains were harvested, dissected, and flash frozen until whole cell lysates were prepared, and the supernatant fluid aliquoted and used for western blotting. Primary antibodies were used to probe for melatonin receptors (MT1 and MT2), and beta actin, used for a loading control. ImageJ and Image Lab software were used to quantify the data which was analyzed using t -tests to compare means. Results: Melatonin receptor levels were reduced in a brain region- and time point- dependent manner. Both MT1 and MT2 were reduced in the frontal cortex at 24 h and in the hippocampus at both 6 h and 24 h. Discussion: MT1 and MT2 are less abundant after injury, which may alter response to MEL therapy. Studies characterizing MT1 and MT2 after TBI are needed, including exploration of the time course and regional patterns, replication in diverse samples, and use of additional variables, especially sleep-related outcomes. Conclusion: TBI in rats resulted in lower levels of MT1 and MT2; replication of these findings is necessary as is evaluation of the consequences of lower receptor levels.