Pharmacology and Regulation of the Ion Channels of the Brown Adipocyte Plasma Membrane

Abstract

Brown adipose tissue is responsible for regulatory nonshivering thermogenesis in most mammals of smaU body size. Sympathetic nerve endings throughout the tissue aUow neuronal control. After stimulation by their transmitter noradrenaline, the adipocyte shows a biphasic response of its membrane potential. An early brief depolarisation and a late long-lasting depolarisation are separated by a hyperpolarisation about 1 min after the stimulus (1,2). The underlying ion channels have at least partly been identified by single channel analysis. A nonselective channel for monovalent cations probably accounts for the tetrodotoxin(TTX)-insensitive sodium influx (3, 4, for review see 5). Part of the potassium efflux is mediated by a voltage-dependent K-channel (6, 7). Another major contribution to the potassium efflux derives from a Ca²⁺-activated K-channel first demonstrated by flux measurements (8) and later shown by whole-cell patch clamp experiments (9). Recently a further K-channel was shown that is voltage-insensitive (7). There are indications that further ion channels contribute to the response. In this paper we will focus on pharmacological mechanisms which can modify the nonselective cation channel as weU as some of the K-channels.