The degradation or recapture of neurotransmitters is necessary to limit the duration of stimulation or inhibition of the post-synaptic membrane. The most common process of neurotransmitter removal after its release into the synaptic cleft is called high-affnity reuptake. About 80% of released neurotransmitters are removed by this mechanism, in which they are bound into specifc neurotransmitter transport proteins located in the presynaptic membrane. Neurotransmitters that were transported into the cytoplasm of the presynaptic bouton are either enzymatically destroyed or reloaded into empty synaptic vesicles. For example, the action of catecholamines on postsynaptic receptors is terminated by the reuptake of neurotransmitters into the presynaptic bouton utilizing Nadependent transporters. The efficiency of this uptake can be regulated by several pharmacologic agents such as amphetamine and cocaine, which block catecholamine reuptake and prolong the actions of neurotransmitters on the postsynaptic neurons. Once inside the presynaptic bouton, catecholamines are reloaded into synaptic vesicles for future use. The excess of catecholamines is inactivated by the enzyme catechol O-methyltransferase (COMT) or is destroyed by another enzyme found on the outer mitochondrial membrane, monoamine oxidase (MAO). Therapeutic substances that inhibit the action of MAO are frequently used in the treatment of clinical depression; selective COMT inhibitors have been also developed.
Enzymes associated with the postsynaptic membrane degrade the remaining 20% of neurotransmitters. For example, acetylcholinesterase (AChE), which is secreted by the muscle cell into the synaptic cleft, rapidly degrades ACh into acetic acid and choline. Choline is then taken up by the cholinergic presynaptic bouton and reused for ACh synthesis. The AChE action at the neuromuscular junction can be inhibited by various pharmacological compounds, nerve agents, and pesticides resulting in prolonged muscle contraction. Clinically, AChE inhibitors have been used clinically in the treatment of myasthenia gravis (see Folder 11.4 in Chapter 11), a degenerative neuromuscular disorder, glaucoma, and more recently Alzheimer’s disease.
Substances needed in the axon and dendrites are synthesized in the cell body and require transport to those sites.
Most neurons possess elaborate axonal and dendritic processes. Because the synthetic activity of the neuron is concentrated in the nerve cell body, axonal transport is required to convey newly synthesized material to the processes. Axonal transport is a bidirectional mechanism. It serves as a mode of intracellular communication, carrying molecules and information along the microtubules and intermediate filaments from the axon terminal to the nerve cell body and from the nerve cell body to the axon terminal. Axonal transport is  described as the following:  Anterograde transport carries material from the nerve cell body to the periphery. Kinesin, a microtubule-associated motor protein that uses ATP, is involved in anterograde transport (see page 59).
 Retrograde transport carries material from the axon terminal and the dendrites to the nerve cell body. This transport is mediated by another microtubule-associated motor protein, dynein (see page 59).
The transport systems may also be distinguished by the rate at which substances are transported:  A slow transport system conveys substances from the cell body to the terminal bouton at the speed of 0.2 to 4 mm/day. It is only an anterograde transport system. Structural elements such as tubulin molecules (microtubule precursors), actin molecules, and the proteins that form neurofilaments are carried from the nerve cell body by the slow transport system. So, too, are cytoplasmic matrix proteins such as actin, calmodulin, and various metabolic enzymes.