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Biochemical Addiction
Among the numerous definitions for addiction, there lies yet another to define it from a biochemical perspective. Milkman (1983) defines it as " self-induced changes in neurotransmission that result in social problem behaviors." This definition encompasses the psychological, biochemical and social aspects of addictive processes. It is not limited to substance abuse and can be applied to any activity characterized by compulsion, loss of control and continuation of the substance despite harm. This has helped investigators gain a better understanding of the nature of addiction. It has been shown that individuals turn to drugs that elicit a mood or level of arousal consistent with their mode of dealing with stress. Those who deal with stress by confrontation choose drug stimulants. Those who withdrawal from stress choose opiate drugs. Others who deal with stress through activities related to imagery or fantasy turn to hallucinogens. These differences between behavior and drug preference are thought to be biochemically driven.
The basis for biochemical activity is neurotransmission, the mechanism by which signals or impulses are sent from one nerve cell to another. The more rapid the transmission through certain central nervous system (CNS) pathways, the more intense the feeling or state of arousal. Thus, the arousal-type person will seek activities or substances that will increase the rate of neurotransmission in the part of the brain responsible for that mood. Those individuals that indulge in thrill-seeking behavior, such as gambling or skydiving, will choose stimulants such as amphetamines. In contrast, those individuals who seek activities that decrease the rate of neurotransmission, such as meditation, overeating or watching excessive television, will choose depressants such as barbiturates.
Once a change in neurotransmission is brought about, whether from an activity or from a substance, the brain attempts to reestablish the rate of neurotransmission that was present before the activity or substance intake. Once the rate is reestablished, the individual becomes tolerant to the original level of the substance or activity. To achieve the desired state of arousal brought about by a change in the rate of neurotransmission the individual must increase the level of the activity. After this point, there is an altered response of the individual to the drug. Any removal of the activity or drug would then result in withdrawal symptoms. This would compensate for the altered brain chemistry and stress placed on the CNS that was established during the period of abuse.
The Mechanics of Neurotransmission
To understand the relationship between neurotransmission and addiction, one needs to have an understanding of neurotransmission itself. The Central Nervous System (CNS) is composed of the brain and spinal cord. Nerve cells or neurons connect all aspects of the nervous system. The neuron is composed of a body, axon, and dendrites. The Dendrites receive and transmitthe nerve impulse, the body integrates the signal, and the axon propagates it. The body will make the decision as to whether or not to transmit the signal or inhibit the signal from continuing on to the next neuron. The CNS is malleable, rather than hard-wired, and must be able to rapidly adapt to varying signals.
Between nerve cells there are spaces called synaptic junctions.
Disruptions that increase neurotransmission (Stimulants)
There are several points at which the transmission of an electrical impulse can be disrupted. Within the pre-synaptic terminal, there are enzymes that will degrade the neurotransmitters before they are released into the synaptic junction. If degraded, these neurotransmitters will never reach the post- synaptic nerve terminal, and the impulse will cease to be transmitted. Degradation can also occur within the synaptic junction itself. Enzymes that remain in the junction can be present in over or under abundance. Hence, transmission can either be enhanced or subdued. Drugs that occupy the receptor but may or may not exhibit the same effect as the neurotransmitter can saturate receptors at the post-synaptic terminal. Lastly, the cAMP pathway can be interrupted which will result in delayed or diminished transmission of the impulse. Each of these points can be altered by exogenous drug administration.
