Acetylcholine (ACh) serves as a neurotransmitter in the brain and at the junction between the motoneuron and skeletal muscle. Its action at this site has been thoroughly studied (l). On rapid release from the motor nerve ending at a 0.1-1 mM concentration (2), ACh diffuses through the synaptic cleft and causes the all-or-none opening of ionic channels selective for sodium, potassium, and other small cations. If the resulting depolarization is above threshold, it leads to an action potential and to muscle contraction (reviewed in 3). In the brain, ACh also acts as an excitatory transmitter (reviewed in 4).

The identification of the molecule that converts the ACh signal into an electrical response, the nicotinic acetylcholine receptor (AChR), has been greatly facilitated by using as highly specific ligands (5) a combination of a toxins from snake venoms (6, 7) on eel or Torpedo electric organs. These provide exceptionally rich sources of cholinergic synapses and possess a receptor closely resembling that from the neuromuscular junction (8, 9).