Universities have been attempting to control the use of performance enhancing drugs on their campuses in an attempt to promote fairness and equality. In the past, universities have been focused on halting the widening use of steroids by college athletes, specifically football players, who were looking to gain a competitive advantage by rapidly gaining muscle mass (Apuzzo, Gillum, & Goldman, 2012). However, as our society has become more technologically oriented and the academic environment has become more competitive, universities have been witnessing a shift from the abuse of physical enhancement drugs to mental enhancement drugs. Abuse is defined as the use of a drug outside of its intended purpose.
Students have turned to drugs to help …show more content…
The Federal Drug Administration approved Obetrol in 1960 as a weight-loss medication to treat obesity. Obetrol, however, never caught traction and eventually reached a point where it was no longer profitable enough to stay on the market (Phelan, 2006). Rexar Pharmaceuticals, manufacturer of Obetrol, sold the drug’s formula rights to Shire-Richwood in 1994. The company rebranded the drug as Adderall and got the Food and Drug Administration’s approval in 1996 to market the product as a treatment for Attention-deficit/hyperactivity disorder (ADHD) and narcolepsy (Pelham et al., …show more content…
Amphetamines are characterized as dopamine releasers that elevate levels of dopamine in the synaptic cleft, the space between neurons at a nerve synapse, by four distinct mechanisms. The primary mechanism involves amphetamine acting as a substrate for dopamine transporters. The transporters are responsible for pumping dopamine out of the synaptic cleft back into the cytoplasm of presynaptic neurons. The binding of amphetamines to dopamine transporters, inhibit dopamine uptake resulting in a larger concentration of dopamine remaining in the cleft (Calipari & Ferris, 2013). The other mechanisms by which amphetamine increases the concentration of dopamine in the synaptic cleft are: binding of amphetamines to the presynaptic membrane of dopaminergic neurons to induce the release of dopamine from the nerve terminal; binding to monoamine oxidase to inhibit the enzymatic breakdown of cytosolic dopamine; and binding of amphetamines to dopamine re-uptake proteins in order to force the protein to act in reverse and transport dopamine out of the nerve terminal into the synaptic cleft (Ellinwood et al.,
Students have turned to drugs to help …show more content…
The Federal Drug Administration approved Obetrol in 1960 as a weight-loss medication to treat obesity. Obetrol, however, never caught traction and eventually reached a point where it was no longer profitable enough to stay on the market (Phelan, 2006). Rexar Pharmaceuticals, manufacturer of Obetrol, sold the drug’s formula rights to Shire-Richwood in 1994. The company rebranded the drug as Adderall and got the Food and Drug Administration’s approval in 1996 to market the product as a treatment for Attention-deficit/hyperactivity disorder (ADHD) and narcolepsy (Pelham et al., …show more content…
Amphetamines are characterized as dopamine releasers that elevate levels of dopamine in the synaptic cleft, the space between neurons at a nerve synapse, by four distinct mechanisms. The primary mechanism involves amphetamine acting as a substrate for dopamine transporters. The transporters are responsible for pumping dopamine out of the synaptic cleft back into the cytoplasm of presynaptic neurons. The binding of amphetamines to dopamine transporters, inhibit dopamine uptake resulting in a larger concentration of dopamine remaining in the cleft (Calipari & Ferris, 2013). The other mechanisms by which amphetamine increases the concentration of dopamine in the synaptic cleft are: binding of amphetamines to the presynaptic membrane of dopaminergic neurons to induce the release of dopamine from the nerve terminal; binding to monoamine oxidase to inhibit the enzymatic breakdown of cytosolic dopamine; and binding of amphetamines to dopamine re-uptake proteins in order to force the protein to act in reverse and transport dopamine out of the nerve terminal into the synaptic cleft (Ellinwood et al.,