的行动是终端。

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皮特曼QJ

的行动是终端。

杂志。1999年11月1日,Pt 3:629 520。

PubMed ID

10545129 (在PubMed

]

文摘

视上核的神经元magnocellular已经深入研究了因为他们独特的破裂和相位的活动模式。虽然这些可以部分解释为固有膜电导,现在还明显,传入输入是重要的雕刻和发起的活动模式。调制这些输入,因此,提供了一种强大的方法来调节magnocellular神经元活动。摘要Oliet &生理学杂志》上的这一问题也提供了证据表明,腺苷酸可能是这样一个调制器在它徒presynaptically视上核(儿子)抑制兴奋性和抑制性突触电流到magnocellular神经元。此外,作者能够证明一个动作的内源性腺苷片通过阻断,A1-type拮抗剂,累进突触抑郁症所带来的持续传入刺激在1赫兹/ 2分钟或更多。本文因此增加了令人信服的证据表明,腺苷发射机的行动在中枢神经系统(Dunwiddie, 1985)。本研究的几个方面值得评论和提问服从实验。在抑制腺苷是均等的万能和EPSCs,从而引起了外界关于腺苷行动的后果细胞核的输出。虽然可以认为,强烈的兴奋性输入会衰减,同样也适用于抑制,使净效应相当小。一个可能的影响是稳定的活动水平突触后细胞水平有助于内在压敏电阻器的生成活动模式。 Another possibility is that adenosine is simply acting to reduce overall metabolic activity; since the metabolic consequences of activity in the presynaptic terminal would be similar in excitatory and inhibitory terminals, it may be irrelevant as to the nature of the transmitter. It is also interesting that the maximum inhibition attained in response to adenosine is only 60 % for either excitatory or inhibitory inputs. This is in contrast to such presynaptic modulators as baclofen, acting at GABAB receptors, where there is 100 % attenuation of afferent evoked potentials (Pittman et al. 1998). Whether this is due to a distribution of adenosine receptors on only a limited number of afferent terminals, or whether it reflects a mechanism of action that is only partially effective in reducing the transmitter release is not known. For example, if adenosine receptors were coupled to only a subset of the calcium channels engaged in transmitter release, one might predict that only part of the transmitter release would be inhibited. However, data from the Oliet & Poulain paper indicate that miniature EPSCs and miniature IPSCs are inhibited by adenosine; as most evidence indicates that TTX-resistant spontaneous currents in magnocellular neurons are calcium insensitive, this suggests that adenosine acts downstream of the calcium influx, perhaps by interfering with the transmitter release machinery (reviewed in Wu & Saggau, 1997). It would also be interesting to determine whether the presynaptic A1 receptors identified here display a sensitivity to pertussis toxin pretreatment. While such receptors are known to be G-protein coupled, presynaptic receptors are often insensitive to inhibition by pertussis toxin. The identification of an action of endogenous adenosine required repetitive stimulation, perhaps because reuptake mechanisms at lower frequencies efficiently removed adenosine. The source of this endogenous adenosine is still unknown. While it could be released by a nucleoside transporter from either glial cells or neurons, another possibility is that it may be produced by metabolic breakdown of ATP (Cunha et al. 1998). ATP is known to be released in the SON from noradrenergic afferents (Buller et al. 1996) and there is also some evidence that it may be released from the magnocellu

DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
Arbaclofen	γ-氨基丁酸B型受体亚基1	蛋白质	人类	是的	受体激动剂	细节
Arbaclofen	γ-氨基丁酸B型受体亚基2	蛋白质	人类	是的	受体激动剂	细节
Arbaclofen Placarbil	γ-氨基丁酸B型受体亚基1	蛋白质	人类	是的	受体激动剂	细节
Arbaclofen Placarbil	γ-氨基丁酸B型受体亚基2	蛋白质	人类	是的	受体激动剂	细节
巴氯芬	γ-氨基丁酸B型受体亚基1	蛋白质	人类	未知的	受体激动剂	细节
巴氯芬	γ-氨基丁酸B型受体亚基2	蛋白质	人类	是的	受体激动剂	细节