One of the ways in which a NEURON can save energy is by re-accumulating the NEUROTRANSMITTERS (or parts of transmitters) it releases. The neurotransmitter DOPAMINE for example is recaptured whole; ACETYLCHOLINE is broken down in the SYNAPTIC CLEFT, but one of the products of this breakdown, CHOLINE, is taken back up by neuronal terminals. This process—known as REUPTAKE, or more simply as UPTAKE—requires energy and the presence of SODIUM but is nevertheless not as costly as synthesizing molecules de novo. There are four points of interest about reuptake processes. (1) Reuptake is often described as being HIGH or LOW AFFINITY.
High affinity reuptake processes will collect molecules when they are in a relatively low concentration; low affinity uptake requires molecules to be in higher concentrations to be effective. (2) Reuptake sites can exist at many different sites on neurons, at terminals as well as on axons and at other places, and are found on GLIAL CELLS as well as on neurons. (3) Reuptake is achieved by specialized transporter mechanisms in neuronal membranes (and within neurons, specialized transporters—VESICULAR TRANSPORTERS—exist to capture molecules from the CYTOPLASM and package them into VESICLES). (4) Reuptake mechanisms have functional importance. Experimental and therapeutic drugs can act by blocking reuptake, thereby increasing the concentrations of neurotransmitter within the synaptic cleft. The neurotoxins 6-HYDROXYDO PAMINE, 5,7-DIHYDROXYTRYPTAMINE and AF-64A all act through reuptake processes, using these transport mechanisms to gain entry to specific types of neurons. Once inside a cell they produce toxic metabolites.
This is the complete article, containing 247 words
(approx. 1 page at 300 words per page).
