Presynaptic adenosine A₁ receptors modulate excitatory transmission in the rat basolateral amygdala.
Presynaptic adenosine A₁ receptors modulate excitatory transmission in the rat basolateral amygdala.
复制标题
突触前腺苷A₁受体调节大鼠基底外侧杏仁核的兴奋性传播。
DOI：
10.1016/j.neuropharm.2013.10.029
复制
发表时间：
2014-02
影响因子：
4.7
通讯作者：
Weiner JL
中科院分区：
文献类型：
--
作者：
Rau AR;Ariwodola OJ;Weiner JL
基底外侧杏仁核（BLA）在焦虑症和酒精中毒的病因学中起着不可或缺的作用。虽然我们对支配BLA兴奋性的内在回路有很多了解，但我们对控制BLA兴奋的神经调质的理解是不完整的。在许多脑区，腺苷（ADO）调节神经元的兴奋性，主要是通过A1受体抑制谷氨酸释放，和基础的腺苷能张力是足够高的张力抑制神经元的兴奋。虽然ADO信号调节许多焦虑和酒精相关的行为，很少有人知道ADO调节BLA神经传递。为此，我们使用膜片钳方法在啮齿类动物脑切片的特点腺苷兴奋性神经传递到BLA锥体细胞的调制。ADO显着抑制EPSC引起的刺激无论是内侧或外侧的多巴胺能输入到BLA。这种作用被A1，但不是由A2a，激动剂模仿。配对脉冲比和微型EPSC实验表明，A1受体位于BLA神经元能突触的突触前位点。此外，浴应用A1受体拮抗剂显着增强EPSC，提供的证据，紧张性腺苷能紧张的BLA突触。此外，强直性ADO受腺苷激酶调节，但不受腺苷脱氨酶调节。最后，激活A1受体对BLA锥体细胞的内在兴奋性没有直接影响。总的来说，这些数据表明，紧张A1受体信号可能在调节BLA兴奋性中发挥重要作用，并建议一个可能的神经生物学底物，通过ADO可能有助于焦虑症和酒精成瘾的病理生理学。
The basolateral amygdala (BLA) plays an integral role in the etiology of anxiety disorders and alcoholism. Although much is known about the intrinsic circuitry that governs BLA excitability, our understanding of the neuromodulators that control BLA excitation is incomplete. In many brain regions, adenosine (ADO) regulates neuronal excitability, primarily via A1 receptor inhibition of glutamate release, and basal adenosinergic tone is high enough to tonically inhibit neuronal excitation. Although ADO signaling modulates many anxiety- and alcohol-related behaviors, little is known about ADO regulation of BLA neurotransmission. To that end, we used patch clamp methods in rodent brain slices to characterize adenosinergic modulation of excitatory neurotransmission onto BLA pyramidal cells. ADO significantly inhibited EPSCs evoked by stimulation of either medial or external glutamatergic inputs into the BLA. This effect was mimicked by an A1, but not by an A2a, agonist. Paired-pulse ratio and miniature EPSC experiments revealed that A1 receptors reside at a presynaptic locus on BLA glutamatergic synapses. Moreover, bath application of an A1 receptor antagonist significantly enhanced EPSCs, providing evidence of tonic adenosinergic tone at BLA glutamatergic synapses. In addition, tonic ADO was regulated by adenosine kinase, but not adenosine deaminase. Finally, activation of A1 receptors had no direct effects on the intrinsic excitability of BLA pyramidal cells. Collectively, these data suggest that tonic A1 receptor signaling may play an important role in regulating BLA excitability and suggest a possible neurobiological substrate through which ADO may contribute to the pathophysiology of anxiety disorders and alcohol addiction.
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影响因子：
5.5
作者：
KATZ, B;MILEDI, R
通讯作者：
MILEDI, R
影响因子：
2.5
作者：
Hawryluk, J. M.;Ferrari, L. L.;Arrigoni, E.
通讯作者：
Arrigoni, E.
影响因子：
--
作者：
Etkin, Amit;Prater, Katherine E.;Greicius, Michael D.
通讯作者：
Greicius, Michael D.
影响因子：
2.9
作者：
FREDHOLM, BB;DUNWIDDIE, TV;LINDSTROM, K
通讯作者：
LINDSTROM, K
影响因子：
6.2
作者：
Boison, Detlev
通讯作者：
Boison, Detlev