Drug Effects on the Nervous System
The business of the nervous system is to transmit information from one cell to another. Although this happens in different locations and with different neurotransmitters, the basic process is common to all cell-to-cell transmission. First, neurotransmitter molecules must be synthesized. Then, they must be packaged in synaptic vesicles. At the appropriate time, they must exit the cell by exocytosis, cross the synaptic cleft and bind and activate receptors on the post-synaptic neuron. The neurotransmitter molecules must then be either degraded or taken back into the presynaptic neuron, a process known as reuptake. Psychoactive drugs exert their effects by interfering with one or more of these steps.
Some of these drugs, known as stimulants, increase synaptic activity. Amphetamines, for example, increase the release from presynaptic cells of the group of neurotransmitters known as catecholamines. These include epinephrine, norepinephrine, and dopamine. The presence of amphetamines can intensify the effect of nerve impulses that occur, and can actually cause the release of catecholamines in the absence of a nerve impulse. Amphetamines also block the reuptake of norepinephrine and dopamine.
Caffeine is a competitive inhibitor of the neuromodulator adenosine, whose function is to inhibit the release of excitatory catecholamine transmitters. Caffeine competes with adenosine for presynaptic receptors, making it unable to perform its inhibitory function.
Nicotine activates certain acetylcholine receptors at neuromuscular junctions and in the central nervous system. It also activates receptors in the autonomic ganglia of the sympathetic nervous system, resulting in an increase in heart rate and a release of epinephrine from the adrenal medulla.
Cocaine blocks the reuptake of catecholamines from synapses. Used short term, this causes heightened alertness and euphoria, as would be expected from increased synaptic activity. Prolonged use, however, produces tolerance, increased use, sleeplessness, and behavior that can resemble schizophrenia.
The hallucinogens LSD and psilocybin are agonists of the serotonin receptors, meaning that they mimic the effects of serotonin. How they produce heightened awareness of sensory stimuli and a dreamlike state is not fully understood.
The cannabinoids, including marijuana and hashish, mimic endogenous molecules named anandamides. Receptors for these molecules are found in the substantia nigra, hippocampus, cerebellar cortex, and cerebral cortex. Cannabinoids produce hallucinations and relaxation.
The so-called depressants decrease activity in the nervous system. Alcohol, for example, increases the number of GABA receptors on post-synaptic membranes. Because GABA is an inhibitory neurotransmitter, more GABA receptors allow more GABA molecules to affect post-synaptic neurons, decreasing their rate of firing.
Opioids, including heroin and morphine, resemble endogenous molecules called endorphins that are involved in the control of pain. The binding of these molecules to presynaptic receptors decreases the release of acetylcholine, norepinephrine and dopamine. Opioid receptors are present throughout the brain, but are especially concentrated in parts of the brain that transmit and modulate information about pain, including the periaquaductal gray region and raphe nuclei of the brain stem and the dorsal horn of the spinal cord.
In certain cases, two drugs interact so that one intensifies or negates the effect of the other. Alcohol and barbiturates are both depressant drugs. Taken together, they have a synergistic effect. Doses of these two drugs that would be tolerated if taken separately become lethal if taken together. The drug nalaxone, on the other hand, is an antagonist of the opioids, and prevents the opioids from exerting their full effect. For this reason, it can be used as an antidote for overdoses of morphine.
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