Pape Hans-Christian, Munsch Thomas, Budde Thomas
Institut für Physiologie, Medizinische Fakultät, Otto-von-Guericke-Universität Magdeburg, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Pflugers Arch. 2004 May;448(2):131-8. doi: 10.1007/s00424-003-1234-5. Epub 2004 Feb 10.
Traditionally, the role of calcium ions (Ca(2+)) in thalamic neurons has been viewed as that of electrical charge carriers. Recent experimental findings in thalamic cells have only begun to unravel a highly complex Ca(2+) signalling network that exploits extra- and intracellular Ca(2+) sources. In thalamocortical relay neurons, interactions between T-type Ca(2+) channel activation, Ca(2+)-dependent regulation of adenylyl cyclase activity and the hyperpolarization-activated cation current ( I(h)) regulate oscillatory burst firing during periods of sleep and generalized epilepsy, while a functional triad between Ca(2+) influx through high-voltage-activated (most likely L-type) Ca(2+) channels, Ca(2+)-induced Ca(2+) release via ryanodine receptors (RyRs) and a repolarizing mechanism (possibly via K(+) channels of the BK(Ca) type) supports tonic spike firing as required during wakefulness. The mechanisms seem to be located mostly at dendritic and somatic sites, respectively. One functional compartment involving local GABAergic interneurons in certain thalamic relay nuclei is the glomerulus, in which the dendritic release of GABA is regulated by Ca(2+) influx via canonical transient receptor potential channels (TRPC), thereby presumably enabling transmitters of extrathalamic input systems that are coupled to phospholipase C (PLC)-activating receptors to control feed-forward inhibition in the thalamus. Functional interplay between T-type Ca(2+) channels in dendrites and the A-type K(+) current controls burst firing, contributing to the range of oscillatory activity observed in these interneurons. GABAergic neurons in the reticular thalamic (RT) nucleus recruit a specific set of Ca(2+)-dependent mechanisms for the generation of rhythmic burst firing, of which a particular T-type Ca(2+) channel in the dendritic membrane, the Ca(2+)-dependent activation of non-specific cation channels ( I(CAN)) and of K(+) channels (SK(Ca) type) are key players. Glial Ca(2+) signalling in the thalamus appears to be a basic mechanism of the dynamic and integrated exchange of information between glial cells and neurons. The conclusion from these observations is that a localized calcium signalling network exists in all neuronal and probably also glial cell types in the thalamus and that this network is dedicated to the precise regulation of the functional mode of the thalamus during various behavioural states.
传统上，钙离子（Ca(2+)）在丘脑神经元中的作用被视为电荷载体。丘脑细胞最近的实验发现才刚刚开始揭示一个高度复杂的Ca(2+)信号网络，该网络利用细胞外和细胞内的Ca(2+)来源。在丘脑皮质中继神经元中，T型Ca(2+)通道激活、Ca(2+)依赖性腺苷酸环化酶活性调节与超极化激活阳离子电流（I(h)）之间的相互作用，在睡眠和全身性癫痫发作期间调节振荡性爆发放电，而通过高压激活（很可能是L型）Ca(2+)通道的Ca(2+)内流、通过兰尼碱受体（RyRs）的Ca(2+)诱导Ca(2+)释放与复极化机制（可能通过BK(Ca)型K(+)通道）之间的功能性三联体，在清醒时支持所需的强直性峰电位放电。这些机制似乎分别主要位于树突和胞体部位。在某些丘脑中继核中，涉及局部GABA能中间神经元的一个功能区是小球，其中GABA的树突释放由通过典型瞬时受体电位通道（TRPC）的Ca(2+)内流调节，从而大概使与磷脂酶C（PLC）激活受体偶联的丘脑外输入系统的递质能够控制丘脑中的前馈抑制。树突中的T型Ca(2+)通道与A 型K(+)电流之间的功能相互作用控制爆发放电，这有助于在这些中间神经元中观察到的振荡活动范围。丘脑网状（RT）核中的GABA能神经元募集一组特定的Ca(2+)依赖性机制来产生节律性爆发放电，其中树突膜中的一种特定T型Ca(2+)通道、非特异性阳离子通道（I(CAN)）和K(+)通道（SK(Ca)型）的Ca(2+)依赖性激活是关键因素。丘脑中的胶质细胞Ca(2+)信号似乎是胶质细胞与神经元之间动态和综合信息交换的基本机制。这些观察结果得出的结论是，丘脑中所有神经元类型以及可能的胶质细胞类型中都存在局部钙信号网络，并且该网络致力于在各种行为状态下精确调节丘脑的功能模式。
