The ultimate generation of a nerve impulse in a postsynaptic neuron (firing) depends on the summation of excitatory and inhibitory impulses reaching that neuron. This allows precise regulation of the reaction of a postsynaptic neuron (or muscle fiber or gland cell). The function of synapses is not simply to transmit impulses in an unchanged manner from one neuron to another. Rather, synapses allow for the processing of neuronal input. Typically, the impulse passing from the presynaptic to the postsynaptic neuron is modified at the synapse by other neurons that, although not in the direct pathway, nevertheless have access to the synapse (see Fig. 12.5). These other neurons may influence the membrane of the presynaptic neuron or the postsynaptic neuron and facilitate or inhibit the transmission of impulses. The firing of impulses in the postsynaptic neuron is caused by the summation of the actions of hundreds of synapses.
A number of molecules that serve as neurotransmitters have been identified in various parts of the nervous system. The most common neurotransmitters are the following.
 Acetylcholine (ACh). ACh is the neurotransmitter between axons and striated muscle at the neuromuscular junction (see page 322) and serves as a neurotransmitter in the ANS. ACh is released by the presynaptic sympathetic and parasympathetic neurons and their effectors. ACh is also secreted by postsynaptic parasympathetic neurons, as well as by a specific type of postsynaptic sympathetic neuron that innervates sweat glands. Neurons that use ACh as their neurotransmitter are called cholinergic neurons. The receptors for ACh in the postsynaptic membrane are known as cholinergic receptors and are divided into two classes on the basis of their interactions with muscarine, a substance isolated from poisonous mushrooms (muscarinic ACh receptor), and nicotine, isolated from tobacco plants (nicotinic ACh receptor). The muscarinic ACh receptor in the heart is an example of a G-protein–coupled receptor that is linked to K channels. ACh release stimulated by parasympathetic stimulation of the heart opens K channels, causing hyperpolarization of cardiac muscle fibers. This hyperpolarization slows rhythmic contraction of the heart. In contrast, the nicotinic ACh receptor in skeletal muscles is a transmitter-gated Na channel. Opening of this channel causes rapid depolarization of skeletal muscle fibers and initiation of contraction. Various drugs affect the release of ACh into the synaptic cleft as well as its binding to its receptors. For instance, curare, the South American arrow-tip poison—binds to Na channels and blocks the action of nicotinic ACh receptors, causing muscle paralysis. Atropin, an alkaloid extracted from the belladonna plant, blocks the action of muscarinic ACh receptors. The botulinum toxin produced by Clostridium botulinum that grows in improperly canned meat and vegetable products inhibits ACh release. Inhibition of ACh release decreases receptor stimulation and leads to paralysis of skeletal muscles, including respiratory muscles.