Functional characterization of membrane channels by patch clamp techniques has revealed great diversity of transmitter or Voltage gated channels in native membranes. Concomitantly recombinant DNA techniques revealed a plethora of genes encoding channel subunits. Thus functional diversity within a particular class of channels may be generated by families of genes encoding homologous channel subunits that assemble in various combinations into functionally distinct channel subtypes. For most channels the subunit composition and stoichiometry of a particular functional subtype is not yet established except for the nicotinic acetylcholine receptor of Torpedo. One way to identify the subunit composition of channels in native membranes is to compare their functional properties with those of channels expressed in a host membrane, following introduction of subunit coding nucleic acids (cRNA or eDNA) into a host cell. In the case of ligand-gated channels, such as channels gated by acetylcholine (AChR channels) or ?-amino butyric acid (GABAR channels) and voltage gated K+ channels mediating delayed or transient outward currents (RCK channels) it has been shown that particular functions of the channel can be attributed to particular channel subunits. Examples are the %,and e-subunits of skeletal muscle AChR channels or the I~and ?.subunits of GABAR channels, which specify channel subtypes with different pharmacological, kinetic and conductance properties. In the case of voltage gated K + channels single RCK subunits specify functionally diverse homomultimeric K+ channels, which mediate transient and delayed K+ currents. However, heteromultimeric channels with novel properties can also assemble from different RCK subunits. The constituent RCK subunits specify sensitivity to K+ channel blockers, gating and conductance properties. A clear correlation between particular channel phenotypes in the native membrane, their subunit composition and gene regulation of the respective mRNAs has been established for the nicotinic AChR channel in skeletal muscle. Here a developmental switch in the expression of the ?. and e-subunit genes causes a change in end-plate channel properties from the fetal type, composed of ctl3~tS-subunits to the adult type subtype composed of al3&-subunits. Northern blot and in situ hybridisation analysis of AChR subunit specific mRNAs in fetal, adult and denervated skeletal muscle indicate that the expression of subunit specific mRNAs is regulated by multiple transcriptional mechanisms. First, in a mechanism which is restricted to the end-plate, subsynaptic nuclei become "imprinted" early during synaptogenesis to express subunit specific mRNAs. The expression then remains independent of nervous or muscular signals. Second, a more generalized mechanism operates on extrasynaptic nuclei and is dependent on the electrical activity of muscle fibres. Each AChR subunit gene is under multiple transcriptional controls each having different importance for each subunit. The functional diversity of channels may allow control of gene expression by multiple transcription mechanisms. A switch in the expression of genes encoding particular subunits can occur in response to external stimuli causing a change in the channel phenotypes. This may be required for longterm adaptive changes in synaptic efficacy and in electrical excitability of neurones during development or differentiation.