Tamea Sisco
They would even endure tremendous pain and hardship for an opportunity to press the lever. Olds had clearly found an area in the limbic system that provided a powerful reward for these animals.
Research on human subjects revealed that the electrical stimulation of some areas of the brain (the medial hypothalamus) produced a feeling of quasi-orgasmic sexual arousal (Olds and Olds 1969). If certain other areas of the brain were stimulated, an individual experienced a type of light-headedness that banished negative thoughts. These discoveries demonstrated that pleasure is a distinct neurological function that is linked to a complex reward and reinforcement system (Hall, Bloom and Olds 1977).
During the past several decades research on the biological basis of chemical dependency has been able to establish some of the brain regions and neurotransmitters involved in reward. In particular it appears that the dependence on alcohol, opiates and cocaine relies on a common set of biochemical mechanisms (Cloninger 1983, Blum et al. 1989). A neuronal circuit deep in the brain involving the limbic system and two regions called the nucleus accumbens and the globus pallidus appears to be critical in the expression of reward for people taking these drugs (Wise and Bozarth 1984). Although each substance of abuse appears to act on different parts of this circuit, the end result is the same: Dopamine is released in the nucleus accumbens and the hippocampus (Koob and Bloom 1988). Dopamine appears to be the primary neurotransmitter of reward at these reinforcement sites.
Although the system of neurotransmitters involved in the biology of reward is complex, at least three other neurotransmitters are known to be involved at several sites in the brain: serotonin in the hypothalamus, the enkephalins (opioid peptides) in the ventral tegmental area and the nucleus accumbens, and the inhibitory neurotransmitter GABA in the ventral tegmental area and the nucleus accumbens (Stein and Belluzi 1986, Blum 1989). Interestingly, the glucose receptor is an important link between the serotonergic system and the opioid peptides in the hypothalamus. An alternative reward pathway involves the release of norepinephrine in the hippocampus from neuronal fibers that originate in the locus coeruleus.
In a normal person, these neurotransmitters work together in a cascade of excitation or inhibition-between complex stimuli and complex responses-leading to a feeling of well being, the ultimate reward (Cloninger 1983, Stein and Belluzi 1986, Blum and Koslowski 1990). In the cascade theory of reward, a disruption of these intercellular interactions results in anxiety, anger and other “bad feelings” or in a craving for a substance that alleviates these negative emotions. Alcohol, for example, is known to activate the norepinephrine system in the limbic circuitry through an intercellular cascade that includes serotonin, opioid peptides and dopamine. Alcohol may also act directly through the production of neuroamines that interact with opioid receptors or with dopaminergic systems (Alvaksinen et al. 1984; Blum and Kozlowski 1990). In the cascade theory of reward, genetic anomalies, prolonged stress or long-term abuse of alcohol can lead to a self-sustaining pattern of abnormal cravings in both animals and human beings.
Support for the cascade theory can be derived from a series of experiments on strains of rats that prefer alcohol to water. Compared to normal rats, the alcohol-preferring rats have fewer serotonin neurons in the hypothalamus, higher levels of enkephalin in the hypothalamus (because less is released), more GABA neurons in the nucleus accumbens (which inhibit the release of dopamine), a reduced supply of dopamine in the nucleus accumbens and a lower density of dopamine D2 receptors in certain areas of the limbic system (Russell, Lanin and Taljaard 1988; McBride et al. 1990; Zhou et al. 1990; McBride et al. 1993).
These studies suggest a four-part cascade in which there is a reduction in the amount of dopamine released in a key reward area in the alcohol-preferring rats. The administration of substances that increase the supply of serotonin at the synapse or that directly stimulate dopamine D2 receptors reduce craving for alcohol (McBride et al. 1993). For example, D2 receptor agonists reduce the intake of alcohol among rats that prefer alcohol, whereas D2 dopamine-receptor antagonist increase the drinking of alcohol in these inbred animals (Dyr et al. 1993).
Support for the cascade theory of alcoholism in human beings is found in a series of clinical trials. When amino-acid precursors of certain neurotransmitters (serotonin and dopamine) and a drug that promotes enkephalin activity were given to alcoholic subjects, the individuals experienced fewer cravings for alcohol, a reduced incidence of stress, an increased likelihood of recovery and a reduction in relapse rates