Evidence has been reviewed which strongly suggests that TRH functions as a neurotransmitter or neuromodulator in the mammalian central nervous system. Both the peptide and its receptor sites are located in the brain. Furthermore, it has protein actions to modify the effects of many neuropharmacological agents and can itself cause alterations in functions mediated by the CNS. Data clearly indicate that many of these actions. of TRH are not dependent on the pituitary- thyroid axis. Various studies of neurotransmitter interactions with TRH have provided evidence that noradrenergic, serotonergic, GABAergic, and cholinergic systems may be influenced by TRH or mediate some of its actions. More than likely, other transmitters will be implicated as the complex actions of TRH are more thoroughly investigated and understood. One set of experiments suggested that TRH may be localized serotonergic fibers. Such findings provide strong support for the view that TRH has a role in the physiology of the CNS. In spite of the progress that has been made, there are several questions to be answered about mechanisms of synthesis, storage, release, and inactivation of TRH. Furthermore, physiological studies would be greatly facilitated if a specific antagonist of TRH actions were available. Controversy still exists about active forms of TRH in situ and the methods by which TRH can be measured in tissue. Future investigations which resolve these difficulties and questions should facilitate our understanding of the role of TRH in brain function and its complex interactions with other neural mechanisms.
|Original language||English (US)|
|Number of pages||18|
|Journal||Progress in clinical and biological research|
|State||Published - 1981|
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