Dringenberg Hans C, Kuo Min-Ching
Department of Psychology and The Center for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada, K7L 3N6.
Eur J Neurosci. 2003 Oct;18(8):2285-91. doi: 10.1046/j.1460-9568.2003.02975.x.
The neuromodulator histamine plays an important role in the regulation of behavioural state and the neocortical electrocorticogram (ECoG). With the present experiments, we characterized the anatomical targets that mediate the cortical-activating effects of histamine. Urethane-anaesthetized rats displayed continuous large-amplitude, low-frequency oscillations with a maximal spectral power in the delta (0.5-3.9 Hz) frequency band. Electrical (100 Hz) stimulation of the pontine-tegmentum suppressed slow, large-amplitude oscillations and induced ECoG activation. Application of histamine (1 mm) into the basal forebrain cholinergic complex by reverse microdialysis enhanced ECoG activation elicited by tegmental stimulation without changing resting ECoG activity. Ventrolateral or central thalamic application of histamine had no effect on resting ECoG activity, and ventrolateral thalamic application produced only a slight enhancement of brainstem-induced activation. Neocortical application of histamine in close proximity (< 500 micro m) to the recording electrode reduced low-frequency delta power in the resting ECoG without affecting stimulation-induced ECoG activation. These data suggest that, under the present experimental conditions, histamine facilitates ECoG activation primarily by potentiating the excitatory influence of brainstem fibers at the level of the basal forebrain. Histamine release in some parts of the thalamus results in a minor enhancement of ECoG activation, and cortical histamine release produces a small but consistent suppression of slow delta oscillations in the resting ECoG. These concurrent subcortical and cortical actions probably permit histamine to effectively modulate cortical activation and excitability across different behavioural states.
神经调质组胺在行为状态调节和新皮质脑电图（ECoG）中发挥着重要作用。通过本实验，我们确定了介导组胺皮质激活作用的解剖学靶点。用乌拉坦麻醉的大鼠表现出持续的大幅度低频振荡，在δ（0.5 - 3.9赫兹）频段具有最大频谱功率。对脑桥被盖进行电刺激（100赫兹）可抑制缓慢的大幅度振荡并诱导ECoG激活。通过反向微透析将组胺（1毫米）注入基底前脑胆碱能复合体可增强被盖刺激引起的ECoG激活，而不改变静息ECoG活动。在腹外侧或中央丘脑应用组胺对静息ECoG活动没有影响，在腹外侧丘脑应用仅轻微增强了脑干诱导的激活。在靠近记录电极（<500微米）处向新皮质应用组胺可降低静息ECoG中的低频δ功率，而不影响刺激诱导的ECoG激活。这些数据表明，在本实验条件下，组胺主要通过增强脑干纤维在基底前脑水平的兴奋性影响来促进ECoG激活。丘脑某些部位的组胺释放导致ECoG激活略有增强，而皮质组胺释放会使静息ECoG中的缓慢δ振荡产生小但持续的抑制。这些同时发生的皮质下和皮质作用可能使组胺能够有效地调节不同行为状态下的皮质激活和兴奋性。
