Review Spontaneous electrical activity in the prostate gland Betty Exintaris a, * , Dan-Thanh T. Nguyen a , Anupa Dey a , Richard J. Lang b a Prostate Research Co-operative, Victorian College of Pharmacy, Monash University, Parkville 3052, Melbourne, Australia b Department of Physiology, Monash University, Clayton 3800, Melbourne, Australia Received 7 November 2005; received in revised form 17 February 2006; accepted 27 February 2006 Abstract The cellular mechanisms that underlie the initiation, maintenance and propagation of electrical activity in the prostate gland remain little understood. Intracellular microelectrode recordings have identified at least two distinct electrical waveforms: pacemaker potentials and slow wave activity. By analogy with the intestine, we have proposed that pacemaker activity arises from a morphologically distinct group of c-Kit positive interstitial cells that lie mainly between the glandular epithelium and smooth muscle layers. We speculate that pacemaker activity arising from the prostatic interstitial cells (PICs) is likely to propagate and initiate slow wave activity in the smooth muscle cells resulting in contraction of the stromal smooth muscle wall. While spontaneous electrical activity in the prostate gland is myogenic in origin, it is clear that nerve-mediated agents are able to modulate this activity. Excitatory agents such as histamine, phenylephrine and a raised potassium saline all increase slow wave discharge. In contrast, nitric oxide donors reduce or abolish the spontaneous electrical events. However, the cellular mechanisms underlying the action of various endogenously released agents remain to be elucidated. D 2006 Elsevier B.V. All rights reserved. Keywords: Smooth muscle; Prostate; Slow waves; Pacemaker activity; Spike potentials; Spontaneous transient depolarisations Contents 1. Introduction ........................................................... 371 2. Innervation ........................................................... 372 3. Electrical activity ........................................................ 373 3.1. Neurobiotin ....................................................... 374 3.2. Slow wave activity ................................................... 374 3.3. Extracellular and intracellular Ca 2+ ........................................... 374 3.4. Pacemaker potentials................................................... 375 3.5. Interstitial cells of Cajal (ICCs) ............................................. 375 3.6. Spikes .......................................................... 377 4. Summary ............................................................ 377 References .............................................................. 378 1. Introduction There has been a renewed interest in the pathophysiology and pharmacology of the prostate gland as it is the only accessory genital organ that commonly enlarges in aging males, a condition known as benign prostatic hyperplasia (BPH). Because of its anatomical location, the increase in prostatic size leads to occlusion of the urethra with a resultant constellation of lower urinary tract symptoms. The lack of correlation between prostate size and severity of symptoms has reinforced the concept that there is a dual component to BPH: a static component, which is caused by the anatomical obstruction of the urethra by the enlarged prostate, and a 1566-0702/$ - see front matter D 2006 Elsevier B.V. All rights reserved. doi:10.1016/j.autneu.2006.02.019 * Corresponding author. Tel.: +61399039071; fax: +61399039638. E-mail address: betty.exintaris@vcp.monash.edu.au (B. Exintaris). Autonomic Neuroscience: Basic and Clinical 126 – 127 (2006) 371 – 379 www.elsevier.com/locate/autneu