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

机译:兔脑中的特定牛磺酸识别位点负责牛磺酸对体温调节的影响。

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摘要

(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 (+/-)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 x 10(-6)-4.8 x 10(-5) mol) induced a dose-related hypothermia, vasodilation at ear vascular bed and inhibition of GMB. CAHS, at the highest dose tested (4.8 x 10(-5) 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 x 10(-7) mol caused death within 24 h after treatment. (4) CAHS (4.8 x 10(-5) mol) antagonized the hyperthermic effect induced by TAG (1.2 x 10(-6) mol), AEA (1.2 x 10(-8) mol) or ISE (4.8 x 10(-5) mol). (5) In conclusion, these findings may indicate the existence of a recognition site specific for taurine, responsible for its effects on thermoregulation.
机译:(1)牛磺酸和GABA被认为是内源性冷冻剂。在先前的研究中,牛磺酸的一些结构类似物,即6-氨基甲基-3-甲基-4H-1,2,4-苯并噻二嗪1,1-二氧化物(TAG),2-氨基乙基ar(AEA),2-羟基乙磺酸(ISE )和(+/-)顺式-2-氨基环己烷磺酸(CAHS)已显示出取代了兔脑突触膜制剂中的[(3)H]牛磺酸结合,而没有与GABA能系统或牛磺酸摄取发生相互作用。机理,因此表现得像直接的牛磺酸能药物。 (2)为了回答牛磺酸作为内源性致冷剂的作用是取决于GABA受体的激活还是特定的牛磺酸受体的激活,将牛磺酸或以上结构类似物分别经脑室内注射到有意识的,受约束的兔子中,或单独注射。监测其联合使用及其对直肠(RT)和耳朵皮肤温度以及总体运动行为(GMB)的影响。 (3)牛磺酸(1.2 x 10(-6)-4.8 x 10(-5)mol)引起剂量相关的体温过低,耳血管床的血管舒张和GMB抑制。 CAHS在最高测试剂量下(4.8 x 10(-5)mol)对RT或GMB诱导牛磺酸样作用。相反,以相同剂量的牛磺酸注射的ISE引起了与剂量相关的体温过高,血管收缩和GMB兴奋。 AEA和TAG引起剂量相关的体温过高,但在治疗后24小时内,高于1.2 x 10(-7)mol的剂量引起死亡。 (4)CAHS(4.8 x 10(-5)mol)拮抗TAG(1.2 x 10(-6)mol),AEA(1.2 x 10(-8)mol)或ISE(4.8 x 10( -5)mol)。 (5)总之,这些发现可能表明存在一个专门针对牛磺酸的识别位点,该位点负责其对温度调节的作用。

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