Effects of taurine on depolarization-evoked release of amino acids from rat cortical synaptosomes

Kamasaki, Yoshinori; Maeda, Kazuhisa; Ishimura, Masahiko; Omura, Hiromi; Itoh, Tadao

doi:10.1016/0006-8993(93)90318-h

Cited by 41 publications

(14 citation statements)

References 24 publications

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“…It is also possible that Mn may alter some sort of feedback mechanism such as an autoreceptor (e.g., GABA B or GABA A ). Being that taurine is a known modulator of GABA receptors (del Olmo et al, 2000; Kamisaki et al, 1993; Jia et al, 2008; Namima et al, 1982, 1983), perturbations in taurine biology may play a role in GABA homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, the 10-fold increase in taurine after removal of NA may be a compensatory response to help decrease GABA EC concentrations. Taurine binding to GABA A receptors (del Olmo et al, 2000; Jia et al, 2008) and GABA B autoreceptors (Kamisaki et al, 1993; Namima et al, 1982, 1983), may help to regulate GABA release. Enhanced taurine efflux observed in control animals after NA administration could functionally decrease GABA release by activating GABA A and GABA B receptors thereby normalizing GABA EC .…”

Section: Discussionmentioning

confidence: 99%

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Manganese exposure inhibits the clearance of extracellular GABA and influences taurine homeostasis in the striatum of developing rats

et al. 2010

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Manganese (Mn) accumulation in the brain has been shown to alter the neurochemistry of the basal ganglia. Mn-induced alterations in dopamine biology are fairly well understood, but recently more evidence has emerged characterizing the role of γ-aminobutyric acid (GABA) in this dysfunction. The purpose of this study was to determine if the previously observed Mn-induced increase in extracellular GABA (GABA EC ) was due to altered GABA transporter (GAT) function, and whether Mn perturbs other amino acid neurotransmitters, namely taurine and glycine (known modulators of GABA). Extracellular GABA, taurine, and glycine concentrations were collected from the striatum of control (CN) or Mn-exposed Sprague-Dawley rats using in vivo microdialysis, and the GAT inhibitor nipecotic acid (NA) was used to probe GAT function. Tissue and extracellular Mn levels were significantly increased, and the Fe:Mn ratio was decreased 36-fold in the extracellular space due to Mn exposure. NA led to a 2-fold increase in GABA EC of CNs, a response that was attenuated by Mn. Taurine responded inversely to GABA, and a novel 10-fold increase in taurine was observed after the removal of NA in CNs. Mn blunted this response and nearly abolished extracellular taurine throughout collection. Striatal taurine transporter (Slc6a6) mRNA levels were significantly increased with Mn exposure, and Mn significantly increased 3 H-Taurine uptake after 3-minute exposure in primary rat astrocytes. These data suggest that Mn increases GABA EC by inhibiting the function of GAT, and that perturbed taurine homeostasis potentially impacts neural function by jeopardizing the osmoregulatory and neuromodulatory functions of taurine in the brain.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Manganese exposure inhibits the clearance of extracellular GABA and influences taurine homeostasis in the striatum of developing rats

et al. 2010

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“…Since taurine binds both to GABA A and GABA B receptors (Krogsgaard-Larsen et al, 1980;Kontro & Oja, 1990;Frosini et al, 2003), it may affect body temperature by interacting with GABA-ergic systems. However, there is a large body of evidence that taurine elicits a number of neurophysiological effects distinguishable from those afforded by GABA (Hayes et al, 1975;Huxtable, 1989;Kamisaki et al, 1993;Hussy et al, 2001;Tuz et al, 2001). Moreover, taurine desynchronizes while GABA, muscimol and baclofen synchronize motor and limbic cortex activity patterns, suggesting that their effects could depend on the interaction with different neuronal pathways afferent to the cortical areas monitored (Sgaragli et al, 1978;Sesti et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation

Frosini

Sesti

Saponara

et al. 2003

British J Pharmacology

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1 Taurine and GABA are recognized as endogenous cryogens. In a previous study, some structural analogues of taurine, namely 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and (7)cis-2-aminocyclohexane sulfonic acids (CAHS) have been shown to displace [ 3 H]taurine binding from rabbit brain synaptic membrane preparations, without interacting either with GABA-ergic systems, nor with taurine uptake mechanism, thus behaving like direct taurinergic agents. 2 To answer the question whether the role of taurine as an endogenous cryogen depends on the activation of GABA receptors or that of specific taurine receptor(s), taurine or the above structural analogues were injected intracerebroventricularly in conscious, restrained rabbits singularly or in combination and their effects on rectal (RT)-and ear -skin temperature and gross motor behavior (GMB) were monitored. 3 Taurine (1.2 Â 10 À6 -4.8 Â 10 À5 mol) induced a dose-related hypothermia, vasodilation at ear vascular bed and inhibition of GMB. CAHS, at the highest dose tested (4.8 Â 10À5 mol) induced a taurine-like effect either on RT or GMB. On the contrary ISE, injected at the same doses of taurine, induced a dose-related hyperthermia, vasoconstriction and excitation of GMB. AEA and TAG caused a dose-related hyperthermia, but at doses higher than 1.2 Â 10 À7 mol caused death within 24 h after treatment. 4 CAHS (4.8 Â 10 À5 mol) antagonized the hyperthermic effect induced by TAG (1.2 Â 10 À6 mol), AEA (1.2 Â 10 À8 mol) or ISE (4.8 Â 10 À5 mol). 5 In conclusion, these findings may indicate the existence of a recognition site specific for taurine, responsible for its effects on thermoregulation.

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“…In terms of the presynaptic eVects, taurine is reported to increase presynaptic inhibition via GABA B receptors (GABA B Rs) and reduce mitral cell spontaneous activity in the frog olfactory bulb (Chaput et al, 2004). In addition, taurine is reported to reduce GABA release through the activation of presynaptic GABA B Rs (Kamisaki et al, 1996(Kamisaki et al, , 1993Namima et al, 1983). In the auditory brainstem, GABA B Rs are shown to be expressed in presynaptic terminals of rat ICC neurons (Ma et al, 2002;Zhang and Wu, 2000).…”

Section: How Does Taurine Reduce the Neuronal Excitability And Depresmentioning

confidence: 97%

Taurine acts as a glycine receptor agonist in slices of rat inferior colliculus

et al. 2006

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Effects of taurine on depolarization-evoked release of amino acids from rat cortical synaptosomes

Cited by 41 publications

References 24 publications

Manganese exposure inhibits the clearance of extracellular GABA and influences taurine homeostasis in the striatum of developing rats

Manganese exposure inhibits the clearance of extracellular GABA and influences taurine homeostasis in the striatum of developing rats

A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation

Taurine acts as a glycine receptor agonist in slices of rat inferior colliculus

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