Synaptic Transmitters Involved in LSD Administration :: Serotonin Psychology Essays

Synaptic Transmitters Involved in LSD Administration The nearly synchronic discovery of serotonin (5-HT) and LSD-25 in the 1950 s encouraged a lot of research to be done on the relationship between LSD and serotonin, which helped to develop a greater understanding of the role serotonin plays as a neurotransmitter in the brain (Nichols, 2004). Today it is believed that LSD (and other hallucinogens) stimulate 5-HT2A sense organs (Kalat, 2004). Activation of these receptors causes cortical glutamate levels to increase. This is presumed to be a result of a presynaptic receptor-mediated release from neurons in the thalumus (Nichols, 2004).Early studies proposed that LSD antagonized the effects of serotonin on peripheral tissues. It was later proposed that the psychoactive properties of LSD whitethorn be a result of the blocking of serotonin receptors in the central nervous system (Nichols, 2004). This theory was short-lived however when it was discovered that a brominated differential g ear of LSD (BOL),a potent serotonin antagonist in peripheral tissues, was instal to have essentially no LSD like effects. In 1961, Freedman prepare that systematic use of LSD elevated serotonin content in the brain (cited in Nichols, 2004). In a later study in 1967, Rosencrans, et al. describe that LSD also reduced brain levels of acetic acid (5-HIAA) (cited in Nichols, 2004). The combined findings of these two studies demonstrated that LSD decreased serotonin turnover in the brain.It is now widely accepted that hallucinogen action is primarily located on receptor 5-HT2A. In a study done in 1955, scientists found that daily administration of LSD resulted in an almost complete loss of sensitivity to the drug after 4 days. It is now believed that this is a result of 5-HT2A receptor down-regulation (cited in Nichols, 2004). In a later study published in 1985, it was found that daily LSD administration selectively decreased 5-HT2 receptor assiduity in rat brains (Nichols, 2004). Stu dies have shown that activation of 5-HT2A receptors increase inhibitory post-synaptic potentials. However, when compared to serotonin, the maximum effect produced by LSD is 30-50% of that of serotonin. LSD is therefore a partial agonist, quite an than an antagonist (Nichols, 2004). Antagonists block the action of a neurotransmitter, whereas agonists mimic or increase the effects of a neurotransmitter (Kalat, 2004). Conversely, LSD is a weak agonist when compared to less foolhardy compounds with stronger behavioral influences. Therefore it is thought that LSD must either activate another monoamine receptor that works with