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首页> 外文期刊>Journal of Neurophysiology >Adenosine facilitates in vivo neurotransmission in the superior colliculus of the rat.
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Adenosine facilitates in vivo neurotransmission in the superior colliculus of the rat.

机译：腺苷促进大鼠上丘的体内神经传递。

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摘要

1. Electrical responses to volleys in afferent fibers in the optic tract were recorded in the superficial gray layer of anesthetized rat superior colliculus. A prominent negative wave with 4- to 6-ms peak latency in the upper part of the superficial gray layer and a sharp negative wave with 1.5- to 2-ms peak latency in the lower part of the superficial gray layer were elicited, corresponding to the C2 (upper part of the superficial gray layer) and the C1 (lower part of the superficial gray layer) postsynaptic potentials reported by Sefton. 2. These C1 and C2 waves were depressed by kynurenic acid or quinoxaline dione (DNQX) applied just beside the recording electrode, suggesting that neurotransmission in these pathways is mediated by glutamate. 3. Adenosine (10 microM) injected in the superficial gray layer enhanced both C1 and C2 potentials up to 170 and 140%, respectively. 4. Administration of a potent inhibitor of adenosine deaminase, erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA; 5 mg/kg sc) increased the amplitudes of both C1 and C2 potentials to 125 and 130% of the initial levels, respectively. 5. The extracellular application of adenosine uptake inhibitors, dipyridamole (100 microM) and nitrobenzylthioinosine (NBI; 10 microM) also enhanced postsynaptic potentials. 6. Prior application of L-homocysteine thiolactone (10 microM), a compound that facilitates the incorporation of adenosine into S-adenosylhomocystein and reduces the extracellular concentration of adenosine, attenuated the excitatory action of exogenously applied adenosine. 7. Excitatory effects were also observed upon application of a selective adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA) or a selective A2 receptor agonist, 2-[4-(2-carboxylethyl)- phenethylamino]-5'N-ethylcarboxamide adenosine hydrochloride (CGS21680). Selective A1 and A2 receptor antagonists, 8-cyclopentyl-1,3-dimethylxanthine (CPT) and 3,7-dimethyl-1-propargylxanthine (DMPX), respectively, failed to suppress the excitatory action by adenosine. However, combined application of these two agents blocked the facilitatory action by adenosine on the excitatory synapses. 8. The application of adenosine (10 microM) to the superficial gray layer via a microdialysis probe increased the glutamate release by approximately 230% of the basal level. Similarly, the administration of EHNA (5 mg/kg sc) enhanced the extracellular glutamate level up to approximately 170%. However, prior application of L-homocysteine thiolactone (10 microM) failed to potentiate the glutamate release by adenosine. 9. This is the first in vivo study to demonstrate an excitatory action of adenosine on synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)
机译：1.在麻醉的大鼠上丘的浅灰色层中记录视神经传入纤维上的截击的电响应。引起浅灰色层上部峰值潜伏期为4至6毫秒的显着负波和浅灰色层下部峰值潜伏期为1.5至2毫秒的尖锐负波，对应于Sefton报告的C2（浅灰色层的上部）和C1（浅灰色层的下部）的突触后电位。 2.这些C1和C2波被施加在记录电极旁边的犬尿酸或喹喔啉二酮（DNQX）抑制，表明这些途径的神经传递是由谷氨酸介导的。 3.注入浅表灰色层的腺苷（10 microM）将C1和C2电位分别提高了170％和140％。 4.给予有效的腺苷脱氨酶抑制剂erythro-9-（2-羟基-3-壬基）腺嘌呤盐酸盐（EHNA; 5 mg / kg sc），可使C1和C2电位的幅度增加至125％和130％初始水平。 5.腺苷摄取抑制剂，双嘧达莫（100 microM）和硝基苄基硫代肌氨酸（NBI; 10 microM）在细胞外应用也增强了突触后电位。 6.预先应用L-高半胱氨酸硫内酯（10 microM），该化合物可促进将腺苷掺入S-腺苷高半胱氨酸并降低腺苷的细胞外浓度，减弱外源应用腺苷的兴奋作用。 7.应用选择性腺苷A1受体激动剂N6-环己基腺苷（CHA）或选择性A2受体激动剂2- [4-（2-羧乙基）-苯乙基氨基] -5'N-乙基羧酰胺腺苷后，还观察到兴奋作用盐酸盐（CGS21680）。选择性的A1和A2受体拮抗剂8-环戊基-1,3-二甲基黄嘌呤（CPT）和3,7-二甲基-1-炔丙基黄嘌呤（DMPX）不能抑制腺苷的兴奋作用。但是，这两种药物的联合应用阻断了腺苷对兴奋性突触的促进作用。 8.通过微透析探针将腺苷（10 microM）应用于浅层灰色层，可使谷氨酸释放量增加约230％的基础水平。同样，EHNA（5 mg / kg sc）的给药将细胞外谷氨酸水平提高到大约170％。但是，L-高半胱氨酸硫代内酯（10 microM）的先前应用未能增强腺苷释放谷氨酸。 9.这是第一个证明腺苷对突触传递有兴奋作用的体内研究。（摘要截短为250字）

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