Dringenberg H C, Olmstead M C
Department of Psychology and Center for Neuroscience Studies, Queen's University, Kingston, Ontario, K7L 3N6, Canada.
Neuroscience. 2003;119(3):839-53. doi: 10.1016/s0306-4522(03)00197-0.
Efferents from the pedunculopontine tegmentum (PPTg) exert widespread control over neocortical electrocorticographic (ECoG) activity and aid in maintaining high-frequency ECoG activation during waking and rapid eye movement sleep. The mechanisms and subcortical routes that allow the PPTg to influence cortical activity remain controversial. We examined the relative contributions of the thalamus and basal forebrain in ECoG activation elicited by PPTg stimulation in urethane-anesthetized rats. Stimulation (100 Hz, 2 s) of the PPTg suppressed large-amplitude, low-frequency oscillations, replacing them with high-frequency beta-gamma activity. Systemic administration of the anti-muscarinic drug scopolamine (1 mg/kg, i.p.) abolished activation elicited by PPTg stimulation, suggestive of an essential role of acetylcholine in this effect. Local infusions of lidocaine (1 microl, 1%) into the region of the cholinergic basal forebrain complex produced a strong reduction in activation elicited by PPTg stimulation. Lidocaine infusions into the reticular thalamic nucleus had no effect, but infusions into central thalamus produced a small attenuation of PPTg-evoked cortical activation. Combined basal forebrain-central thalamic infusions (1 microl/site) produced roughly additive effects, leading to a greater loss of activation than single-site infusions. These results indicate that, under the present experimental conditions, high-frequency cortical ECoG activation elicited by the PPTg involves relays in both the basal forebrain and central thalamus, with a predominant role of the basal forebrain. After concurrent central thalamic-basal forebrain inactivation, the forebrain can maintain only limited, short-lasting activation in response to PPTg stimulation. The additivity of infusion effects suggests that, rather than participating in one serial system, basal forebrain and central thalamus constitute parallel activating pathways. These findings aid in resolving previous controversies regarding the role of thalamus and basal forebrain in activation by emphasizing the importance of multiple, large-scale networks between brainstem and cortex in regulating the activation state of the mammalian neocortex.
来自脚桥被盖区（PPTg）的传出神经对新皮质脑电图（ECoG）活动施加广泛控制，并有助于在清醒和快速眼动睡眠期间维持高频ECoG激活。使PPTg影响皮质活动的机制和皮质下途径仍存在争议。我们研究了在乌拉坦麻醉的大鼠中，丘脑和基底前脑在PPTg刺激引起的ECoG激活中的相对作用。刺激（100Hz，2秒）PPTg可抑制大幅度低频振荡，代之以高频β-γ活动。全身性给予抗毒蕈碱药物东莨菪碱（1mg/kg，腹腔注射）可消除PPTg刺激引起的激活，提示乙酰胆碱在此效应中起重要作用。向胆碱能基底前脑复合体区域局部注入利多卡因（1微升，1%）可使PPTg刺激引起的激活显著降低。向丘脑网状核注入利多卡因无效，但向丘脑中央核注入可使PPTg诱发的皮质激活稍有减弱。联合向基底前脑-丘脑中央核注入（1微升/部位）产生大致相加效应，导致激活丧失比单部位注入更大。这些结果表明，在当前实验条件下，PPTg引起的高频皮质ECoG激活涉及基底前脑和丘脑中央核的中继，其中基底前脑起主要作用。在丘脑中央核-基底前脑同时失活后，前脑对PPTg刺激仅能维持有限的、短暂的激活。注入效应的相加性表明，基底前脑和丘脑中央核并非参与一个串联系统，而是构成平行激活途径。这些发现有助于解决先前关于丘脑和基底前脑在激活中的作用的争议，强调了脑干和皮质之间多个大规模网络在调节哺乳动物新皮质激活状态中的重要性。
