Taurine and GABA are recognized as endogenous cryogens. In a previo'/> A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation
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A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation

机译:兔脑中特定的牛磺酸识别位点负责牛磺酸对温度调节的作用

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摘要

class="enumerated" style="list-style-type:decimal">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 [3H]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.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.Taurine (1.2 × 10−6–4.8 × 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 × 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 × 10−7 mol caused death within 24 h after treatment.CAHS (4.8 × 10−5 mol) antagonized the hyperthermic effect induced by TAG (1.2 × 10−6 mol), AEA (1.2 × 10−8 mol) or ISE (4.8 × 10−5 mol).In conclusion, these findings may indicate the existence of a recognition site specific for taurine, responsible for its effects on thermoregulation.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 牛磺酸和GABA被认为是内源性致冷剂。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)已证明可取代兔脑突触膜制剂中的[ 3 H]牛磺酸结合,而不会与GABA能系统相互作用,也不会与具有牛磺酸吸收机制,因此表现得像直接的牛磺酸能药物。 回答以下问题:牛磺酸作为内源性致冷剂的作用取决于GABA受体的活化还是特定的牛磺酸受体(牛磺酸)的活化或将上述结构类似物单独或联合注射入有意识的,受约束的兔子的脑室内,并监测其对直肠(RT)和耳皮肤温度以及总运动行为(GMB)的影响。 牛磺酸( 1.2×10 −6 –4.8×10 −5 mol)引起剂量相关假设rmia,耳部血管床血管舒张和GMB抑制。在最高测试剂量(4.8×10 −5 mol)下,CAHS诱导了牛磺酸对RT或GMB的影响。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1.2×10 −7 mol的剂量会导致死亡。 CAHS(4.8×10 −5 mol)拮抗TAG(1.2×10 −6 mol),AEA(1.2×10 −8 mol)或ISE诱导的高温效应(4.8×10 −5 mol)。 总而言之,这些发现可能表明存在专门针对牛磺酸的识别位点,该位点对牛磺酸的温度调节具有影响。

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