Comparison of the Mechanisms of Dopamine Release Stimulation - Essay Example

An analytical Comparison of the mechanisms employed by Cocaine, Ecstasy, Heroin, and Cannabis to stimulate Dopamine release in the Brain and how thisrelates to their Abuse potential Name University Date Introduction The basic function of the brain in relation to the actions and signals received as a result of an administered drug, and the neurobiological basis for addiction form the general grounding on which this research essay paper is founded.  Dopamine is involve in a number of functions which are very essential for an organism’s survival, such as attentiveness, learning, motricity and memorization (Bardo, 2011: 86-88). Most importantly, dopamine is a key element in the identification of natural rewards for organisms. These natural stimuli for instance water and food make individuals to engage in approach behaviours. Also, dopamine is involved in unconscious memorization of signs accompanying these rewards (Kaminery & Winter, 2011). It is of note that all substances that trigger dependencies in human beings raise the release of a neuromediator, dopamine in a particular area of the brain called the nucleus accumbens. Ecstasy Ecstasy (MDMA) is a synthetic drug (American society for Clinical Investigation, 2007: 1061). It’s considered both as a hallucinogen and a stimulant due to its molecular structure, which is similar to that of both LSD and amphetamines. Ecstasy lumps the reuptake pumps of some neurotransmitters, thereby increasing their levels of content in the synaptic gap and consequently their effect on the post-synaptic neurons’ receptors.  Ecstasy potentiates the effects of dopamine and norepinephrine, it is differentiated from other psychostimulants due to its sturdy affinity for serotonin transporters. Ecstasy’s initial effect is an increased release of serotonin by the serotonergic neurons. The person may then experience euphoria, increased energy, and the suppression of particular inhibitions in relation to other people. As time passes by, the serotonin levels decrease, accompanied by low activity levels of tryptophane hydroxylase, which is the enzyme that synthesizes serotonin (Schiffer et al., 2003: 81). This decrease may last much lengthier than the initial increase. Once again, an artificial rise in the level of a neurotransmitter exercises negative response on the enzyme manufacturing it. Consequently, when intake of the drug is stopped, the excess turns into a shortage. Like most psychoactive drugs that results to a sensation of pleasure, ecstasy too increases the dopamine release into the reward circuit. The extra serotonin created by ecstasy results indirectly to anticipation of the dopaminergic neurons by the serotonergic neurons connecting to them.  It’s not established clearly effects of toxicity of ecstasy for humans, but studies on animals have shown that chronic high doses of MDMA results to selective damage of the terminal buttons of the serotonergic neurons (Carter et al., 2012: 10-13). Opiates (heroin, morphine, etc.) Self & Stanley debated that human body naturally produces its own opiate-like substances and then uses them as neurotransmitters. These opiate-like substances comprise the dynorphin, endorphins, and enkephalins, which are collectively called endogenous opioids (2010: 32). The endogenous opioids control our reactions to painful stimuli. Again they regulate essential functions such as thirst and hunger and are engaged in immune response, mood control, among other processes.  Opiates such as morphine and heroin affect people so powerfully because the exogenous substances fix to the same receptors just like our endogenous opioids. The three kinds of receptors generally distributed all over the brain: mu, delta, and kappa receptors; though are second messengers, effect the possibility that ion channels will be open, which in some cases decreases the excitability of neurons (Nahes & Burks, 1997). This decreased excitability is the likely cause of the euphoric effect of opiates and seems to be mediated by the delta and mu receptors.  The euphoric effect again appears to involve another process in which the GABA-inhibitory interneurons of the ventral tegmental contribute to (Winger et al, 2-004). Exogenous opioids decrease the quantity of GABA released by being attached to their mu receptors. Usually, GABA reduces the quantity of dopamine secreted in the nucleus accumbens. By way of inhibiting this inhibitor, the opiates resultantly increase the amount of dopamine produced and thus the amount of pleasure felt.  Continuous consumption of opiates hinders the production of cAMP, but this hindrance is offset in the long run by other cAMP producing mechanisms (Barceloux, 2012: 10). At a time when no opiates are available, the raised cAMP production capacity arises highly and effects in neural hyperactivity and consequently the sensation of craving the drug. Rats self-administer heroin Wang (2003) argues that the experiment set-up is such that, the rat is self-administering heroin by a small needle positioned directly into the nucleus accumbens. The drug induces the rat to feel good and thus keeps on pressing the bar to receive more heroin. The heroin is positively reinforcing and it’s serving as a reward. When the injection needle is positioned in an area nearby the nucleus accumbens, the rat doesnt self-administer the heroin. It has been found by scientists that dopamine release is increased inside the reward pathway of the rats self-administering heroin. Therefore, since more dopamine is in the synaptic space, the dopamine-dependent neurotransmission is normally augmented, resulting to the activation of the reward pathway. Cannabis Sensations of relaxation, slight euphoria, and amplified visual and auditory perceptions produced by marijuana come as a result of its impact on the cannabinoid receptors in the brain (Bukoski & Sloboda, 2003: 139-140). The cannabinoid receptors are present almost in all parts of the brain, and they are naturally bound to an endogenous molecule called the anandamide. The endogenous molecule; anandamide is involved in regulating appetite, pain, mood, memory, cognition, and emotions (Nave, 2010: 291-292). Any time cannabis is present in the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), which interferes with all of the functions of anandamide. This process is begun by THC binding to the CB1 receptors for anandamide. The receptors then adjust the activity of various intracellular enzymes, such as reducing the activity of cAMP. Less cAMP results to less protein kinase A. The less activity of the enzyme protein kinase A, affects the calcium and potassium channels thus reducing the amount of neurotransmitters produced. Generally the excitability of the brain’s neural networks is consequently reduced.  Conversely, in the reward circuit, as in the situation of other drugs, additional dopamine is released. As per to opiates, this paradoxical rise is explained by the point that the dopaminergic neurons in the particular circuit do not have CB1 receptors, though they are normally inhibited by GABAergic neurons which do have them. The cannabis get rid of this inhibition by the GABA neurons thereby activating the dopamine neurons (Castle & Murray, 2004: 135). Prolonged consumption of cannabis causes loss of CB1 receptors in the brain’s arteries and thus reducing the flow of blood, and subsequently the flow of oxygen and glucose, to the brain. The major effects of this are impaired learning ability, attention deficits, and memory loss. Cocaine Cocaine blocks the reuptake of some neurotransmitters such as serotonin, dopamine and norepinephrine. Cocaine binds to the transporters which usually remove the excess of the neurotransmitters off the synaptic gap, thus preventing them from reabsorption by the neurons that released them and hence raises their concentration in the synapses (Miller, 2013: 213). This amplifies the natural influence of dopamine on the post-synaptic neurons. The modified group of neurons results to moods of confidence (from serotonin), increased sense of dependency (from dopamine), and energy (from norepinephrine) as normally experienced by individuals who take cocaine.  To add on, since the norepinephrine neurons project their axons, found in locus coeruleus, into wholly the central structures of the forebrain, the authoritative overall effect of cocaine is easily understood.  The brain of chronic cocaine consumers comes to rely on the exogenous drug to uphold the high degree of pleasure connected to the artificially elevated levels of certain neurotransmitters in its reward circuits (Vester, 2012: 89-90). The postsynaptic membrane has a possibility to even adapt to these high dopamine levels such that it essentially manufactures new receptors. The resulting amplified sensitivity yields cravings and depression if cocaine consumption ceases and the levels of dopamine return to normal. Addiction on cocaine is thus closely associated to its effect on the neurons of the particular reward circuit. Rats self-administer cocaine According to Bevins, scientists have investigated increased dopamine quantities in the synapses of the reward pathway in an experiment of rats self-administering cocaine (2004: 264-270). Rats press a bar to take injections of cocaine straight into the areas of the reward pathway such as the VTA and the nucleus accumbens. Again, when the injection needle is positioned next to these regions, but not inside them, the rat will never press the bar to administer the cocaine. The capability of rats to self-administer cocaine is a clear indicator of the addictive nature of this drug. Summary When an individual repeatedly uses a drug like heroin, dependence also occurs. One develops dependence when the neurons adapt to the repeated exposure of the drug and only function in a normally way in the presence of the drug. Withdrawal of the drug causes several physiologic reactions such as mild, fatigue or even life threatening and thus resulting to a phenomenon called withdrawal syndrome (Barbaro, 2007: 51-52). Various parts of the brain are responsible for the dependence and addiction to drugs. Hence, one can be dependent on a drug but not addicted to it. References List AMERICAN SOCIETY FOR CLINICAL INVESTIGATION. (2007). Science in medicine. Sudbury, Mass, Jones and Bartlett Publishers. BARBARO, G. (2007). Management of medical disorders associated with drug abuse and addiction. New York, Nova Science Publishers. BARCELOUX, D. G. (2012). Medical toxicology of drug abuse: synthesized chemicals and psychoactive plants. Hoboken,N.J., John Wiley & Sons. BARDO, M. T., FISHBEIN, D. H., & MILICH, R. (2011). Inhibitory control and drug abuse prevention: from research to translation. New York, Springer. BERNTSON, G. G., & CACIOPPO, J. T. (2009). Handbook of neuroscience for the behavioral sciences. Hoboken, N.J.,Wiley. Top of Form BEVINS, R. A. (2004). Motivational factors in the etiology of drug abuse: volume 50 of the Nebraska Symposium on Motivation, [March 28 and 29 of 2002]. Lincoln, Neb. [u.a.], Univ. of Nebraska Press. Bottom of Form Top of Form BUKOSKI, W. J., & SLOBODA, Z. (2003). Handbook of drug abuse prevention: theory, science, and practice. New York, NY [u.a.], Kluwer Acad./Plenum Publ. CARTER, A., HALL, W., & ILLES, J. (2012). Addiction neuroethics: the ethics of addiction neuroscience research and treatment. London, Academic Press. CASTLE, D. J., & MURRAY, R. (2004). Marijuana and madness psychiatry and neurobiology. Cambridge, UK, Cambridge University Press. http://site.ebrary.com/id/10130358. GALIZIO, M., & MAISTO, S. A. (1985). Determinants of substance abuse: biological, psychological, and environmental factors. New York, Plenum Press. DIENER, E., KAHNEMAN, D., & SCHWARZ, N. (2003). Well-being: the foundations of hedonic psychology. New York, NY, Russell Sage Foundation. GUY, G. W. (2004). The medicinal uses of cannabis and cannabinoids. London [u.a.], Pharmaceutical Press. ḲAMINER, Y., & WINTERS, K. C. (2011). Clinical manual of adolescent substance abuse treatment. Washington, DC, American Psychiatric Pub. http://search.ebscohost.com/login.aspx?direct=true&scope=site&db=nlebk&db=nlabk& N=342721. MILLER, P. M. (2013). Biological research on addiction. Amsterdam, Elsevier. http://public.eblib.com/EBLPublic/PublicView.do?ptiID=1125288.Bottom of Form Top of Form NAHAS, G. G., & BURKS, T. F. (1997). Drug abuse in the decade of the brain. Amsterdam, IOS Press. SCHIFFER, R. B., RAO, S. M., & FOGEL, B. S. (2003). Neuropsychiatry. Philadelphia, PA, Lippincott Williams & Wilkins. http://ovidsp.ovid.com/ovidweb.cgi?T=JS&MODE=ovid&NEWS=n&PAGE=booktext&D=books&AN=00149810$&XPATH. NEVE, K. A. (2010). The dopamine receptors. New York, Humana Press. http://public.eblib.com/EBLPublic/PublicView.do?ptiID=511122. SELF, D. W., & STALEY, J. K. (2010). Behavioral neuroscience of drug addiction. Heidelberg [etc.], Springer. Bottom of Form VERSTER, J. C. (2012). Drug abuse and addiction in medical illness causes, consequences and treatment. New York, NY, Springer. http://dx.doi.org/10.1007/978-1-4614-3375-0. WANG, J. Q. (2003). Drugs of abuse neurological reviews and protocols. Totowa, N.J., Humana Press. http://site.ebrary.com/id/10181287. WINGER, G., WOODS, J. H., & HOFMANN, F. G. (2004). A handbook on drug and alcohol abuse the biomedical aspects. New York, Oxford University Press. http://catalog.hathitrust.org/api/volumes/oclc/53356664.html. Read More