Drugs and Neurotransmitters
Research on neurotransmitters has been crucial for neuroscience and has allowed enor-mous progress in our understanding of how the nervous system functions. In addition, this research has produced another benefit: Discoveries about neurotransmission have taught us a lot about how various drugs—legal and illegal—exert their effects.
In general, there are various ways either to enhance or impede the actions of a neurotransmitter. Chemicals that enhance a transmitter’s activity are called agonists— a term borrowed from Greek drama, in which the agonist is the name for the hero. Drugs that impede such actions are antagonists, a term that refers to the hero’s opponent (so to speak, the villain; Figure 3.17).
Agonists and antagonists exert their influence in many ways. Some agonists actually mimic the transmitter; so, on their own, they can activate the receptors. Other agonists block the reuptake of the transmitter into the presynaptic cell, and still others work by counteracting the cleanup enzyme that breaks down the transmitter after it has triggered a response. Both of these mechanisms have the effect of leaving more transmitter within the synaptic gap; this increases the transmitter’s opportunity to influence the postsynaptic membrane and so ends up increasing both the strength and duration of the transmitter’s effect. Still other agonists work by promoting the production of the transmit-ter, usually by increasing the availability of some “ingredient” needed for the transmitter’s chemical manufacture. This increased availability allows the body to produce more of the transmitter, so that more can be released upon stimulation.
Antagonists work through similar mechanisms, but with the opposite effect. Thus, some antagonists prevent the transmitter from working by binding themselves to the synaptic receptor and blocking off the transmitter—essentially serving as a kind of putty in the synaptic lock. Other antagonists operate by speeding up reuptake, and others by augmenting cleanup enzymes.
Many of the agonists and antagonists identified by neuroscience depend on endogenous substances. These substances are produced naturally within the body, and they provide a way for the nervous system to modify and control its own functioning. One example is the endorphins—a family of chemicals, produced inside the brain, that powerfully influence howwe perceive and cope with pain (Hughes et al., 1975). These naturally produced painkillers influence the brain in much the same way that morphine does. In fact, much of what we know about endorphins comes from parallels with our understanding of how drugs like morphine or heroin influence the body.
In other cases, neurotransmission can be modified by exogenous agonists or antagonists—chemicals introduced from outside the body. Getting these agents into the brain can be difficult: The cells that make up the nervous system are extremely sensitive to toxins, and so they’re protected by the blood-brain barrier—a layer of tightly joined cells that surrounds the blood vessels in the brain and literally acts as a filter to prevent toxins from reaching the central nervous system (Mayhan, 2001). This barrier obviously evolved to keep out toxic substances, but it’s also an obstacle to medications. As a result, investiga-tors trying to develop medicines aimed at brain cells need to design an effective medication as well as ensure that it will pass through the barrier and reach the target cells.
Once in the brain, these medications have their influence by altering neurotransmission— some working as agonists, others as antagonists. Cocaine, for example, is an agonist; it works by blocking the reuptake of dopamine, norepinephrine, and epinephrine into the presynaptic molecules. The effect is arousal throughout the body, restlessness, and in some cases euphoria. Many antidepression medications—including Prozac, Zoloft, and Paxil— work in roughly the same way but specifically block the reuptake of serotonin. Still other drugs are antagonists. Some of the medications used for schizophrenia, for example, block postsynaptic receptors and seem effective in helping patients control psychotic thinking and restore normal functioning in their lives.
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