After a neurotransmitter molecule has been recognized by a post-synaptic receptor, it is released back into the synaptic cleft. Once in the synapse, it must be quickly removed or chemically inactivated in order to prevent constant stimulation of the post-synaptic cell and an excessive firing of action potentials.
Some neurotransmitters are removed from the synaptic cleft by special transporter proteins on the pre-synaptic membrane. These transporter proteins carry the neurotransmitter back into the pre-synaptic cell, where it is either re-packaged into a vesicle and stored until it is once again needed to transmit a chemical message, or broken down by enzymes. Serotonin is one neurotransmitter that gets recycled in this way. Serotonin, a small-molecule neurotransmitter found in many areas throughout the brain, is involved in a wide range of behaviors, including sleep, appetite, memory, sexual behavior, neuroendocrine function, and mood.
Not all neurotransmitters are recycled by the presynaptic cell. Neuropeptide neurotransmitters merely quickly diffuse away from the receptors into the surrounding medium. One important neurotransmitter, acetylcholine, has a specialized enzyme for inactivation right in the synaptic cleft called acetylcholinesterase (AChE. AChE is an enzyme present at all cholinergic synapses which serves to inactivate acetylcholine by hydrolysis. Acetylcholine (ACh), an excitatory small-molecule neurotransmitter found at various locations throughout the central and peripheral nervous systems and at all neuromuscular junctions, is composed of acetate and choline. AChE breaks ACh into its component parts; acetate and choline. After hydrolysis, acetate quickly diffuses into the surrounding medium, while choline gets taken back into the presynaptic cell by a high affinity choline uptake (HACU) system. Choline is then recycled by the pre-synaptic cell for use in the synthesis of more ACh.
A. Enzymatic inactivation of neurotransmitters
B. Presynaptic transporters: inactivation of neurotransmitters by reuptake
© Williams College Neuroscience, 1998