Al Ameen Journal of Medical Sciences (Jan 2010)
Thyroid Hormone Homeostasis in Adult Mammalian Brain: A Novel Mechanism for Functional Preservation of Cerebral T3 Content During Initial Peripheral Hypothyroidism
Abstract
brain is well known. But the action of THs in the adult brain was not widely a focus of study by endocrinologists based on lack of increased energy metabolism and oxygen consumption with changing thyroid status and thus not widely acknowledged. Extensive research has, however, revealed interesting findings like sequestration of T3, possible release of T3 as a neurotransmitter in nerve terminals, identification of specific membrane binding sites of T3 in the synaptosomal fraction of adult rat brain and many non-genomic neurotransmitter-like actions of TH in the adult mammalian brain. Most importantly, thyroid dysfunction is associated with significant disruption of psychobehavioural system in the adult, which can however be reversed with therapeutic hormonal intervention. A complex regulatory network involving transfer of TH through the brain barriers, interactions between neurons and glial cells, and deiodinase expression works synchronously to deliver the appropriate amount of T3 to the neurons. Despite peripheral hypo- or hyper-thyroidism, brain can maintain a normal level of TH up to certain duration. Thus, presence of a novel homeostatic mechanism in the adult mammalian brain (‘central homeostasis for thyroid hormone’) to defend the adverse neuropsychological manifestations commonly associated with peripheral hypothyroidism has been known for a long time. Unfortunately, the exact time course and the mechanism of such central homeostasis were not determined, till we made a pioneering attempt to evaluate the same. The entire phenomenon appeared to be coupled with nuclear mediated genomic processes like mRNA and protein synthesis. Moreover, the effects of THs on some key enzymes and ions related to neurotransmission during the start and end days of this central homeostatic phenomenon point towards a dependency of the enzymes on TH and an involvement of TH in the neurobiochemical events
