Sergeant G P, Thornbury K D, McHale N G, Hollywood M A
Smooth Muscle Research Centre, Dundalk Institute of Technology, Co. Louth, Ireland.
J Cell Mol Med. 2006 Apr-Jun;10(2):280-91. doi: 10.1111/j.1582-4934.2006.tb00399.x.
The smooth muscle layer of the urethra generates spontaneous myogenic tone that is thought to make a major contribution to urinary continence. The mechanisms underlying generation of tone remain unclear, however recent studies from our laboratory highlighted a role for a specialised population of pacemaker cells which we originally referred to as interstitial cells (IC) and now term ICC. Urethra ICC possess an electrical pacemaker mechanism characterised by rhythmic activation of Ca(2+)-activated Cl(-) channels leading to spontaneous transient inward currents (STICs) under voltage clamp and spontaneous transient depolarisations (STDs) under current clamp conditions. Both STICS and STDs are now known to be associated with spontaneous Ca(2+) oscillations that result from a complex interplay between release of Ca(2+) from intracellular stores and Ca(2+) influx across the plasma membrane. In this review we will consider some of the precise mechanisms involved in the generation of pacemaker activity and discuss how these are modulated by excitatory and inhibitory neurotransmitters.
尿道的平滑肌层会产生自发性肌源性张力，这种张力被认为对尿失禁起着主要作用。然而，产生这种张力的机制尚不清楚，不过我们实验室最近的研究突出了一类特殊起搏细胞的作用，我们最初将其称为间质细胞（IC），现在称为尿道内间质细胞（ICC）。尿道ICC具有一种电起搏机制，其特征是钙激活氯通道有节律地激活，在电压钳制下导致自发性瞬时内向电流（STICs），在电流钳制条件下导致自发性瞬时去极化（STDs）。现在已知STICs和STDs都与自发性钙振荡有关，这种振荡是由细胞内钙库释放的钙与跨质膜的钙内流之间复杂的相互作用引起的。在这篇综述中，我们将探讨起搏活动产生所涉及的一些精确机制，并讨论这些机制是如何被兴奋性和抑制性神经递质调节的。
