mGluRs modulate neuronal firing in the auditory midbrain.
mGluRs modulate neuronal firing in the auditory midbrain.
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mGluRs 调节听觉中脑的神经元放电。
DOI：
10.1016/j.neulet.2011.01.075
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发表时间：
2011
影响因子：
2.5
通讯作者：
Galazyuk,AV
中科院分区：
文献类型：
--
作者：
Voytenko,SV;Galazyuk,AV
在听觉系统中，声音诱发的神经元放电抑制的机制尚不清楚。为了探索下丘脑（IC）的作用机制，我们在清醒小鼠下丘脑神经元上应用了针对不同代谢型谷氨酸受体（mGluRs）的激动剂和拮抗剂。我们发现，I组特异性mGluR激动剂在52%的神经元中显著增加神经元放电，而I组拮抗剂在51%的神经元中具有相反的作用。II组特异性激动剂对神经元放电没有影响，但拮抗剂增加了48%神经元的放电率。iii组特异性mGluR激动剂和拮抗剂均未对IC中的神经元放电产生影响。我们还发现，声音刺激可抑制70%的IC神经元的自发放电。这种抑制被I组mGluR拮抗剂可逆阻断。这种抑制与两种感知现象之间可能存在联系：前向掩蔽和“残余抑制”，即在适当掩蔽声音后短暂减少/消除耳鸣。
The mechanisms underlying sound-evoked suppression of neuronal firing in the auditory system are poorly understood. To explore these mechanisms in the inferior colliculus (IC), agonists and antagonists targeting different groups of metabotropic glutamate receptors (mGluRs) were applied iontophoretically to IC neurons in awake mice. We found that a group I-specific mGluR agonist predominantly increased neuronal firing in 52% of neurons, whereas group I antagonist had the opposite effect in 51% of neurons. A group II specific agonist showed no effect on neuronal firing but an antagonist increased firing rate in 48% of neurons. Neither a group III-specific mGluR agonist nor an antagonist had an effect on neuronal firing in the IC. We also found that sound stimuli triggered suppression of spontaneous firing in 70% of IC neurons. This suppression was reversibly blocked by group I mGluR antagonists. There is a possible link between this suppression and two perceptual phenomena: forward masking and “residual inhibition,” the brief reduction/elimination of tinnitus following an appropriate masking sound.