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From this, he concluded that nerves send messages by releasing chemicals. These chemicals are the neurotransmitters that are synthesized by neurons, which are derived from the foods we eat. The neuron then transports them to axon terminals. From there, an action potential causes their release from the terminals. Once released, they attach to receptors and alter the activity of the postsynaptic neuron. When the molecules are separated form the receptors, they may become inactive chemicals. They may be taken back into the presynaptic terminal to be used again, also known as reuptake. Some empty vesicles return to the cell body to pick up a neurotransmitter (54-55). There are five different types of neurotransmitters: amino acids, peptides, acetylcholine, monoamines, purines, and gases. Serotonin falls into the monoamines, which are defined as “non-acidic neurotransmitters containing an amine group (NH2), formed by a metabolic change of certain amino acids” (56). Serotonin plays a part in some drug effects, attack behaviors, depression, eating regulation, learning, sleep, and PMS. Some hallucinogens, including LSD, DMT, psilocin, and psilocybin, inhibit the release of serotonin. They act as false transmitters, by attaching to the postsynaptic receptor sites and not allowing serotonergic activity. No one really understands how these drugs produce such profound changes in mental functioning. “One speculation of how they manifest their alterations of mood, perception, and thought is that the pontine raphe, a major center of 5-HT activity, serves as a filtering station for incoming sensory stimuli” (66). It screens the sensations and throws out the unimportant or irrelevant. These drugs may disrupt this process and allow a surge of data and an overload of brain circuits (66). Methylenedioxymethamphetamine, or MDMA, is better known as Ecstasy and is growing in use as a psychedelic drug. MDMA, at low doses, stimulates the dopamine receptors. At high doses, they produce greater effects on serotonin synapses, creating effects similar to LSD. These effects can last for up to two weeks after initial intake. Unlike LSD, it not only stimulates the serotonin synapses; it destroys them. This is why regular users say the effects seem to get weaker; because they have actually destroyed the serotonin synapses (72). An experiment was done with monkeys to find if the receptors would regenerate. They seemed to grow in some parts of the brain and not others. Where they did grow, it was a gradual process and took more than a year. However, it is not known whether this regeneration occurs in humans. Since the discovery of serotonin in the 1950’s, researchers have found evidence that it plays a role in emotions and judgment. Accumulating evidence has shown that depression results from a deficiency on serotonin or inefficient serotonin receptors. For example, the picture on page __ shows a severely depressed person (left) and a healthy person (right). They were both given fenfluramine, which is a drug known to increase serotonin activity. These pictures show that the health person’s serotonin activity increased, but the depressed patient showed little response or low serotonin activity. Studies have shown that low serotonin levels can lead to impulsive behavior, such as suicide, overeating, and other aggressive behaviors. Depression is commonly treated with antidepressants, which fall into three categories: tricyclics, MAOI’s, and “second generation” or selective serotonin reuptake inhibitors (421). The tricyclics act by preventing the reabsorbing of catecholamines or serotonin by the presynaptic neuron. Therefore the transmitter will stay in the synaptic cleft longer and stimulate the postsynaptic cell longer. The monoamine oxidase inhibitors (MAOI’s) block the monoamine oxidase enzyme, which metabolizes catecholamines and serotonin into inactive forms. The “second generation” or selective serotonin reuptake inhibitors (SSRI) are similar to the tricyclics. SSRI’s block the reuptake of serotonin, which leads to increased serotonergic activity. For some, the drug may not have had a great effect, if any at all, for this reason psychotherapy has been helpful for these patients and may produce long lasting relief. Before antidepressants and psychotherapy, depression was treated with electro convulsive therapy (ECT). It started out as treatment for schizophrenia and epilepsy. After being tested on other disorders, it seemed to be helpful in many depressed patients and became a common treatment. It became overused and developed a bad reputation, so its use declined. When it seemed that new antidepressants could not help, it made a small come back. It is now used with informed consent, for those in which no antidepressants work and for those with strong suicidal tendencies because it works faster than drugs. Bibliography: Word Count: 813
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