Generalized cortex activation by the auditory midbrain: mediation by acetylcholine and subcortical relays
Generalized cortex activation by the auditory midbrain: mediation by acetylcholine and subcortical relays
复制标题
DOI：
10.1007/s00221-006-0427-5
复制
发表时间：
2006-09-01
影响因子：
2
通讯作者：
Murdoch, Jennifer
中科院分区：
文献类型：
--
作者：
Dringenberg, Hans C.;Sparling, Joseph S.;Murdoch, Jennifer
下丘是将听觉信息从脑干传递到前脑的上行投射系统的重要组成部分。最近的证据表明，除了在听觉处理中发挥作用外，IC还可以通过激活新皮质脑电(ECoG)对前脑产生广泛的调制作用。由于IC向皮质的直接投射稀疏，似乎IC产生ECoG激活的作用是间接的，由一个或几个神经调节系统介导，这些神经调节系统可以弥漫地进入整个皮质地幔。然而，IC影响大脑皮质活动的解剖学机制尚未阐明。在目前的实验中，电刺激IC抑制了乌拉坦麻醉大鼠大脑皮质中缓慢的、大幅度的振荡，取而代之的是更高频率的皮质激活。这种作用可被M受体拮抗剂东莨菪碱(0.5-1.0 mg/kg，i.p)阻断，提示乙酰胆碱(ACh)的释放起关键作用。与这一假说一致的是，向胆碱能基底前脑复合体局部注入利多卡因(2%，1亩L)可显著降低由IC刺激引起的皮层脑电活动。为了确定IC和基底前脑之间的额外传递，还研究了利多卡因注入上丘、内侧前额叶皮质、中线丘脑和中缝背侧的影响。上丘和中缝背侧的失活降低了IC诱导的激活，而前额叶皮质和丘脑灌流无效。同时发生的基底前脑和中缝灭活产生的效应类似于单独的基底前脑失活，这表明这两个区域是串联排列的，而不是作为独立的、平行的通路。这些结果表明，IC诱导ECoG激活的能力在很大程度上是由基底前脑胆碱能系统介导的。与解剖学证据一致的是，上丘和中缝背侧似乎提供了重要的连接，使IC在功能上连接到基底前脑，使IC间接接触整个皮质外套膜，并加强新皮质网络的处理。
The inferior colliculus (IC) is a critical component of the ascending projection system carrying auditory information from the brainstem to the forebrain. Recent evidence indicates that, in addition to its role in auditory processing, the IC can exert a generalized, modulatory effect on the forebrain by activating the neocortical electrocorticogram (ECoG). Given the sparse direct projections from the IC to the cortex, it appears that the effect of the IC to produce ECoG activation is indirect, mediated by one or several neuromodulatory systems that have diffuse access to the entire cortical mantle. However, the anatomical relays that permit the IC to influence cortical activity have not been elucidated. In the present experiments, electrical stimulation of the IC suppressed slow, large amplitude oscillations in the ECoG of urethane anesthetized rats, replacing them with higher-frequency cortical activation. This effect was blocked by the muscarinic receptor antagonist scopolamine (0.5-1.0 mg/kg, i.p.), suggestive of a critical role of acetylcholine (ACh) release. Consistent with this hypothesis, localized lidocaine infusions (2%, 1 mu l) into the cholinergic basal forebrain complex strongly reduced ECoG activation elicited by IC stimulation. To identify additional relays between the IC and basal forebrain, the effects of lidocaine infusions into the superior colliculus, medial prefrontal cortex, midline thalamus, and dorsal raphe were also studied. Inactivation of the superior colliculus and dorsal raphe reduced IC-induced activation, while prefrontal cortex and thalamic infusions were ineffective. Concurrent basal forebrain and raphe inactivation produced effects similar to that of inactivation of the basal forebrain alone, suggesting that these two areas are arranged in series, rather than acting as independent, parallel pathways. These results suggest that the ability of the IC to induce ECoG activation is mediated, in large parts, by the basal forebrain cholinergic system. Consistent with anatomical evidence, the superior colliculus and dorsal raphe appear to provide important links to functionally connect the IC to the basal forebrain, allowing the IC to indirectly access the entire cortical mantle and enhance processing in neocortical networks.