Metabotropic glutamate receptors switch visual response mode of lateral geniculate nucleus cells from burst to tonic
Metabotropic glutamate receptors switch visual response mode of lateral geniculate nucleus cells from burst to tonic
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DOI：
10.1152/jn.1996.76.3.1800
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发表时间：
1996-09-01
影响因子：
2.5
通讯作者：
Sherman, SM
中科院分区：
文献类型：
--
作者：
Godwin, DW;Vaughan, JW;Sherman, SM
1.外膝状体中继细胞上的代谢型谷氨酸受体（mGluRs）似乎只由皮质输入激活。因此，我们试图操纵这些受体，以深入了解皮质膝状体途径的可能作用。我们在猫的体内使用记录和药理学技术来激活或抑制膝状体神经元上的这些受体，同时分析它们的反应特性.离子电渗应用mGluR激动剂1-氨基-环戊烷-1，3-二羧酸（ACPD）的X和Y细胞在膝状体A板减少或废除的低阈值Ca 2+尖峰的爆发活动特性。这伴随着视觉反应的显著变化，包括用接收器操作特性曲线测量的信号可检测性的降低。ACPD效应似乎特异于mGluRs，因为离子型谷氨酸受体（iGluRs）的特异性拮抗剂未能影响ACPD诱发的反应，ACPD的拮抗剂未能影响iGluRs介导的反应。我们发现，3，5-二羟基苯甘氨酸，一种激动剂，据报道是特异性的磷脂酰肌醇（PI）连接的mGluRs，具有类似的ACPD的效果，这意味着这些效果是由PI耦合mGluRs介导的。此外，据报道对PI连接的mGluR有效的拮抗剂可有效拮抗ACPD介导的作用，据报道与腺苷3 '，5'-环一磷酸级联偶联的mGluR激动剂物质本身不影响神经元反应。当将这些数据添加到我们的初步解剖数据中时，表明负责观察到的效应的受体可能是mGluR 1或功能等效的mGluR.4。mGluRs的激活产生膝状体中继细胞活性的变化，与体外研究中观察到的这些细胞的去极化一致。这种膜去极化已被证明可以控制电压依赖性Ca 2+电导的激活状态。并且这又确定中继单元是以紧张模式还是突发模式激发。我们的数据表明，ACPD的应用产生了反应模式从突发到强直的转变。由于反应模式是膝状体继电器的一个重要特征，因为某些mGluRs的激活状态，这有助于确定反应模式，可能是由皮质膝状体输入控制，我们得出结论，这种输入的一个重要功能是提供一个visuotopically离散的过渡，从突发到强直性反应模式。
1. Metabotropic glutamate receptors (mGluRs) on relay cells of the lateral geniculate nucleus appear to be activated exclusively by cortical inputs. We thus sought to manipulate these receptors in an effort to gain insight into the possible role of the corticogeniculate pathway. We used in vivo recording and pharmacological techniques in cats to activate or inactivate these receptors on geniculate neurons while analyzing their response properties.2. Iontophoretic application of the mGluR agonist 1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) to X and Y cells in the geniculate A laminae diminished or abolished burst activity characteristic of low-threshold Ca2+ spikes. This was accompanied by pronounced changes in the visual response, including a decrease in signal detectability as measured with receiver operating characteristic curves.3. ACPD effects appear specific to mGluRs, because a specific antagonist of ionotropic glutamate receptors (iGluRs) failed to affect the ACPD-evoked responses, and antagonists of ACPD failed to affect iGluR-mediated responses. We found that 3,5-dihydroxyphenylglycine, an agonist reported to be specific for phosphatidylinositol (PI)-linked mGluRs, had effects similar to those of ACPD, implying that these effects are mediated by PI-coupled mGluRs. Furthermore, antagonists reported to be effective against PI-linked mGluRs were effective in antagonizing the ACPD-mediated effects, and substances reported to be agonists to mGluRs coupled to the adenosine 3',5'-cyclic monophosphate cascade did not affect neuronal responses on their own. These data, when added to our preliminary anatomic data, indicate that the receptor responsible for the observed effects may be mGluR1, or a functionally equivalent mGluR.4. Activation of mGluRs produces changes in geniculate relay cell activity consistent with depolarization of these cells seen during in vitro studies. Such membrane depolarization has been shown to control the activation state of a voltage-dependent Ca2+ conductance. and this, in turn, determines whether the relay cell fires in tonic or burst mode. Our data show that application of ACPD produces a shift in response mode from burst to tonic. Because response mode is an important characteristic of the geniculate relay and because the activation state of certain mGluRs, which helps determine response mode, may be controlled by corticogeniculate input, we conclude that an important function of this input is to provide a visuotopically discrete transition from burst to tonic response mode.