Neuropharmacological Importance of Drugs - Essay Example

Comparison of Neuropharmacological Significance of Cocaine, Ecstasy, Heroin, and Cannabis Comparison of Neuropharmacological Importance for the Use of Cocaine, Ecstasy, Heroin, and Cannabis Many drugs act on and alter neurochemistry in the brain in various ways leading to changes in behaviour. The interactions relate to reinforcing drug properties or other drug-associated effects. The drug interaction with the brain varies with each type of drug, but sharing in how they refer to the brain’s reward system. The behavioural outcome of each drug depends on this ability (Copello et al., 2006). There is ongoing research on how various drugs interact with the brain in a broad subject referred to as neuropharmacology. Drugs such as cocaine and heroin alter neurochemical processes by either mimicking neurotransmitter action, changing the functioning of the receptors, or influencing intracellular processes et cetera. A drug effects these alterations if it diffuses into the brain from the blood circulation. Different drugs have different properties that affect how they penetrate the blood-brain barrier. Administration route for the drug also changes how fast a drug reaches the brain thus affecting drug efficacy and potency. Cocaine is a stimulant drug from the leaves of the coca plant. It is a white powder administered into the body through Snorting. In the form of ‘crack, it can be smoked or injected. Cocaine causes mood, energy, alertness and concentration elevation, reduced fatigue and appetite. Cocaine overdose causes seizures, delirium, coma, and convulsions. An individual may succumb to respiratory failure or cardiac arrest if no immediate care is administered. Cocaine acts on the presynaptic terminal of neurons. It blocks neurotransmitters dopamine, noradrenaline, and serotonin reuptake into the presynaptic terminal. The synaptic dopamine level increases in the brain’s Mesocorticolimbic pathway (MCLP) resulting in an elevated dopamine activity, believed to cause cocaine addiction. Cocaine’s ability to reinforce the action of dopamine is mediated through activation of dopamine receptor subtypes D1 and D2. The result is the acute behaviour associated with cocaine (Copello et al., 2006). Chronic administration of cocaine into the body triggers changes in brain neurochemical compensatory mechanisms. Dopamine receptors lose their sensitivity. The entire dopamine transmission and reception is interrupted due to alterations in genes that regulate intracellular mechanisms. Irregular cocaine administration may trigger the sensitization of specific motor activity such as stimulation in activity level. Tolerance to motor stimulation results from continuous administration of cocaine, leading to cocaine craving by the users. Dependency is evident due to withdraw syndrome observed in chronic cocaine users. Withdrawal symptoms include enhanced appetite, prolonged sleep, depression and craving. Cocaine may be eliminated in the urine or metabolized in the liver. Traces of cocaine are visible in the urine three days after administration. The brain becomes tolerant to acute effects of cocaine at a higher rate before plasma level of cocaine gets depleted. Cocaine is a social drug, and the risks of psychostimulant toxicity are higher in the case of binge snorting of cocaine. The individual snorts small intermittent doses in a short duration of time to compensate for the lower compensation and reward effects of the drug at lower doses (Rhodes & Lott, 2015). The risk is even higher because of consumption behaviours of the cocaine users. Most of these a poly-drug addicts and combines the cocaine with other drugs such as ecstasy, alcohols et cetera in order to medicate aversive recovery period following cocaine use. A problematic cocaine use of snorting large amounts is possible among users. Cocaine injectors are progressions from former heavy snorting or are injectors of other drugs that are starting on cocaine. Polydrug use of cocaine and alcohol leads to a development of a ‘symbiotic relationship" between the two drugs. Cocaine leads to alcohol tolerance and alcohol leads to bodys reaction to cocaine. These individuals have an increased risk of cardiac arrest. Ecstasy (MDMA/methylenedioxymethamphetamine) belongs to a family of stimulant drugs known as amphetamines. When administered orally in tablet form, ecstasy is well absorbed in the gut. The effects of ecstasy are felt within half an hour of administration and lasting more than eight hours after administration (Hartley et al., 2015). Ecstasy use manifests in euphoria elevated socialization and consciousness, excess energy, extraversion, appetite loss and increased pulse. Other effects include a positive mood, heightened sensory perception, peacefulness and tranquillity, wakefulness and hallucinations. Ecstasy enhances the extracellular level of serotonin eventually depleting the serotonin. Just like cocaine, ecstasy also elevates the dopamine level in the synapses (Hanson et al., 2008). The role of serotonin in regulating mood, sexual activity sleep, body temperature et cetera are adversely affected by ecstasy. Dopamine is known to regulate cognition, motivation and reward thus the stimulating action of MDMA (Hanson et al., 2008). Ecstasy overdose may lead to toxicity since the small increases in blood level may lead to disproportionate increases in the blood (Hartley et al., 2015). Some contents of ecstasy are known to be bioactive and is a possible cause of the toxicity. Ecstasy metabolism in the liver varies with different people. Toxicity depends on how fast the ecstasy clears from the body with people who have low metabolisms of ecstasy being more at risk of toxicity (Parrott, 2000). Other factors affecting toxicity includes drug interactions that influence ecstasy elimination from the system thus slowing down the elimination process. Contamination of ecstasy preparation also taken causes toxicity. Both cocaine and ecstasy have similar overall effect in the body. Heroin is an opioid drug administered by either intravenous injection, orally or smoking. When orally administered, heroin is rapidly metabolized in the liver and its potency is adversely decreased (Darke et al., 2002). Smoked or injected heroine is absorbed rapidly into the bloodstream with the rapid onset of effects that last up to seven hours. Carlson (2015) observes that the effects are depressants in nature and have a numbing effect on the body parts where administered. The body develops tolerance with repeated heroin use thus higher doses in the next administration of heroin. Withdrawal signs and symptoms are not as adverse for heroin as are those of cocaine or alcohol. Since heroin is short acting, addicts end up injecting or smoking three to four increasing doses of heroin to sustain the dependency. Rhodes and Lott (2015) note that most users are unable to support the addiction due to the many doses needed in a day. A single dose goes for about 50 dollars. Cheaper heroin is usually adulterated and potentially may lead to heroin toxicities. As a result, the addict is driven to seek comfort from other drugs such as alcohol and cannabis. Heroin overdose is common with most mortality resulting from combining heroin use with alcohol. Apart from being so different in their mode of action, both heroin and cocaine pose a great physical harm because they are injected into the body. The addicts are regularly prone to infection of injection sites, and may suffer scarring, wounds and thrombosis. Bacteria and other pathogens may gain access to the body through the needle wounds leading to systemic infections such as pneumonia, and septicaemia. Thamotharan and Fields (2015) observe that sharing needle sticks lead to transmission and spread of blood-borne viruses such as HIV or HBV. Cannabis is the most readily available illicit drug in most countries. Marijuana users do not usually develop complications from its use. Cannabis sativa is known to have over 400 bioactive chemicals with the most psychoactive ingredient being delta-9-tetrahydrocabaminol (THC) (Pereti-Watel and Lorente, 2004). As Hall (2000) notes, THC can dissolve in lipids, enhancing it to directly infiltrating the brains fatty tissues. It is also one of the reasons cannabis metabolites are very hard to eliminate from the system. Cannabis is administered through smoking and sometimes through eating. Cannabis is not associated with fatal overdose. However, sustained use of cannabis leads to a dependency syndrome characterized by withdrawal and tolerance (Illicit drugs, 2011). Cannabis is known to impair cognitive functions of the user, For instance, loss of memory, inability to maintain attention. Uncertainty about whether these changes though not debilitating are reversible. Cannabis smokers suffer respiratory complications such as chronic bronchitis and carcinogenic histopathological changes of epithelial cells in the respiratory system. Dependence syndrome in cannabis is less pronounced as in alcohol and cocaine (Giesbrecht and Haydon, 2006). Cannabis is different from cocaine, heroin and ecstasy in that it produces a hallucinogenic effect (Illicit Drugs, 2011). In conclusion, the Neuropharmacology focuses on drugs relationship with behaviour and drug dependence affects the human brain. The mode of drug administration has been shown to affect drugs potency and efficacy. Orally taken drugs have a lower potency than either the snorted or injected ones. Cocaine and ecstasy share interaction characteristics with the central nervous system as well as the sympathetic nervous system (Jansen, 1999). They have a reward compensation mechanism that keeps the person craving for more. Addiction and dependency are as a result of alterations of the brain structure that may or may not be reversed depending on the kind of drug. Drug addicts may suffer overdose toxicity, and they may need emergency resuscitation to restore respiratory and cardiac functions. On the other hand, heroin and cannabis withdrawal do not exhibit significant debilitating effects as do cocaine ecstasy. Heroin requires more doses per day because it is a short-acting drug. They are treatable diseases because of the physiological alterations they all produce in the brain. References Carlson, R., Wang, J., Falck, R., & Siegal, H. (2005). Drug use practices among MDMA/Ecstasy users in Ohio: a latent class analysis. Drug And Alcohol Dependence, 79(2), 167-179. doi:10.1016/j.drugalcdep.2005.01.011 Copello, A., Templeton, L., & Velleman, R. (2006). Family interventions for drug and alcohol misuse: is there a best practice? Current Opinion In Psychiatry, 19(3), 271-276. doi:10.1097/01.yco.0000218597.31184.41 Darke, S., Topp, I., Kaye, H., & Hall, W. (2002). Heroin use in New South Wales, Australia, 1996-2000: 5 year monitoring of trends in price, purity, availability and use from the Illicit Drug Reporting System (IDRS). Addiction, 97(2), 179-186. doi:10.1046/j.1360-0443.2002.00032.x Giesbrecht, N., & Haydon, E. (2006). Community-based interventions and alcohol, tobacco and other drugs: foci, outcomes and implications. Drug And Alcohol Review, 25(6), 633-646. Doi:10.1080/09595230600944594 Hall, W., & Degenhardt, L. (2000). Cannabis use and psychosis: a review of clinical and epidemiological evidence*. Aust NZ J Psychiatry, 34(1), 26-34. doi:10.1046/j.1440-1614.2000.00685.x Hanson, K., Luciana, M., & Sullwold, K. (2008). Reward-related decision-making deficits and elevated impulsivity among MDMA and other drug users. Drug And Alcohol Dependence, 96(1-2), 99-110. doi:10.1016/j.drugalcdep.2008.02.003 Hartley, R., Zhang, G., Moncrief, J., Ding, C., Anastasio, N., & Fox, R. et al. (2015). Positive allosteric modulators of the serotonin 2C receptor as novel therapeutics for the cocaine use disorder. Drug And Alcohol Dependence, 146, e137. doi:10.1016/j.drugalcdep.2014.09.290 Illicit Drugs. (2011). Choice Reviews Online, 49(01), 49-0016-49-0016. Doi:10.5860/choice.49-0016 Jansen, K. (1999). Ecstasy (MDMA) dependence. Drug And Alcohol Dependence, 53(2), 121-124. doi:10.1016/s0376-8716(98)00111-2 Parrott, A. (2000). Psychobiological problems in heavy ecstasy (MDMA) polydrug users. Drug And Alcohol Dependence, 60(1), 105-110. doi:10.1016/s0376-8716(99)00146-5 Peretti-Watel, P., & Lorente, F. (2004). Cannabis use, sports practice and other leisure activities at the end of adolescence. Drug And Alcohol Dependence, 73(3), 251-257. doi:10.1016/j.drugalcdep.2003.10.016 Rhodes, J., & Lott, D. (2015). Combining strategies: Using evidence-based interventions to build a more effective treatment program. Drug And Alcohol Dependence, 146, e80. doi:10.1016/j.drugalcdep.2014.09.586 Thamotharan, S., & Fields, S. (2015). Emerging adult gender differences in sexual discounting and HIV risk behavior. Drug And Alcohol Dependence, 146, e2-e3. doi:10.1016/j.drugalcdep.2014.09.689 Read More