Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship

Abstract

Taurine is considered the most abundant free amino acid in the brain. Even though there are endogenous mechanisms for taurine production in neural cells, an exogenous supply of taurine is required to meet physiological needs. Taurine is required for optimal postnatal brain development; however, its brain concentration decreases with age. Synthesis of taurine in the central nervous system (CNS) occurs predominantly in astrocytes. A metabolic coupling between astrocytes and neurons has been reported, in which astrocytes provide neurons with hypotaurine as a substrate for taurine production. Taurine has antioxidative, osmoregulatory, and anti-inflammatory functions, among other cytoprotective properties. Astrocytes release taurine as a gliotransmitter, promoting both extracellular and intracellular effects in neurons. The extracellular effects include binding to neuronal GABAA and glycine receptors, with subsequent cellular hyperpolarization, and attenuation of N-methyl-D-aspartic acid (NMDA)-mediated glutamate excitotoxicity. Taurine intracellular effects are directed toward calcium homeostatic pathway, reducing calcium overload and thus preventing excitotoxicity, mitochondrial stress, and apoptosis. However, several physiological aspects of taurine remain unclear, such as the existence or not of a specific taurine receptor. Therefore, further research is needed not only in astrocytes and neurons, but also in other glial cells in order to fully comprehend taurine metabolism and function in the brain. Nonetheless, astrocyte’s role in taurine-induced neuroprotective functions should be considered as a promising therapeutic target of several neuroinflammatory, neurodegenerative and psychiatric diseases in the near future. This review provides an overview of the significant relationship between taurine and astrocytes, as well as its homeostatic and neuroprotective role in the nervous system.

Regulation of ethanol‐mediated dopamine elevation by glycine receptors located on cholinergic interneurons in the nucleus accumbens

“…Hence, the reduced taurine response to ethanol might account for the observed decrease of the ethanol‐induced DA response. Even if taurine can be released from both astrocytes and neurons, it is mainly synthesized in astrocytes 41 . The mechanism behind the observed attenuation of ethanol‐induced taurine release is not known.…”

“…Even if taurine can be released from both astrocytes and neurons, it is mainly synthesized in astrocytes. 41 The mechanism behind the observed attenuation of ethanol-induced taurine release is not known. It may be due to CIN depletion.…”

Association between human blood metabolites and cerebral cortex architecture: evidence from a Mendelian randomization study

“…Using in vivo and in vitro mammalian assays demonstrated that the regulation of pyridoxal kinase in thiamine metabolism can affect brain homeostasis ( 34 ). Taurine and hypotaurine have antioxidative, osmoregulatory, and anti-inflammatory functions ( 35 ). Bousquet et al ( 36 ) confirmed that taurine and hypotaurine metabolic pathways have important clinical implications in neurodegenerative diseases by studying key cystamine metabolites, including cysteamine, hypotaurine, taurine, and cysteine.…”

Exercise Alleviates Behavioral Disorders but Shapes Brain Metabolism of APP/PS1 Mice in a Region- and Exercise-Specific Manner

“…Thus, the modification of choline metabolism by exercises could be responsible for protecting against behavioral dysfunction of AD. Taurine is mostly released from astrocytes and has been regarded as an astrocytic biomarker; 70 hence, an increased taurine level in the hypothalamus of AD mice may indicate astrocyte activation and proliferation. 71 Herein a reduced taurine level after exercise especially HIIT suggests that astrocyte dysfunction might be alleviated in the AD brain by HIIT.…”