Neural Plasticty

The long term effects of cocaine are very extreme. Once having tried cocaine, an individual may have difficulty controlling the urge to use the drug and the perspective might change leaving the consumption of the drug as primordial. Cocaine’s stimulant and addictive effects are due primarily as a result of its ability to stop the reabsorption of dopamine by nerve

According to the biological perspective, drug use may start off as casual, but through continued use, it produces changes in the brain that influences the onset and maintenance of drug addiction. (Horvath et al., 2013). Drugs have their most prominent effects on the function of neurotransmitters. Almost all major drugs of abuse activate the reward system and cause a flood in the levels of dopamine which is a neurotransmitter that is involved in pleasure. As a result, not only do people learn to associate drug use with pleasure, but the brain also starts to reduce its own natural dopamine production in adjustment to the levels of dopamine produced by the drugs. This is called tolerance, and the consequences of tolerance are highly influential

Cocaine influences dopamine, norepinephrine and serotonin neurotransmission by inhibiting their reuptake. Pimozide, alpha-flupenthixol, perphenazine and chlorpromazine, all dopamine antagonists, were used to pre-treat rats in an attempt to demonstrate the reinforcing effects of dopamine.

The addictive properties of cocaine are a dopamine D2-receptor researchers “indicate that these dopaminergic neural systems play an important part in rewarding effects” (Miller, Gold, Smith, 1997, p.64).

“There are changes in the brain caused by drug use that occur and persist, but are only unmasked after withdrawal from a drug — in this case, cocaine," senior author David Dietz explained in the press release. "Cocaine use alters the connections between certain neurons through changes in the shape of the cells."

drawn from this finding. One is that no shift from one hemisphere to the other has occurred

Drug addiction is a brain disease because drugs change the brain’s structure and how they work. Over a period of time drugs start to affect the brain by challenging an addicted person’s self-control and interfere with their ability to resist intense urges to take drugs. “Most drugs affect the brain's reward circuit by flooding it with the chemical messenger dopamine. This overstimulation of the reward circuit causes the intensely pleasurable "high" that leads people to take a drug again and again. Over time, the brain adjusts to the excess dopamine, which reduces the high that the person feels compared to the high they felt when first taking the drug—an effect known as tolerance. They might take more of the drug, trying to achieve the same dopamine high.”, States National Institute on Drug Abuse. After long term use of drugs it affects functions such as learning, judgment, decision-making, stress, memory, and behavior. Even though an addict knows this, they still use

The [C]raclopride plays a role in determining the extracellular dopamine in the synapse. The theory of addiction is the idea that addictive drugs have a particular nature of releasing dopamine, while psychoactive non-addictive drugs do not. Alcohol and Cannabis have been demonstrated to lack certain qualities associated with inducing the release of dopamine in comparison to [C]cocaine. Figure 2 demonstrates an increase of dopamine levels in the ventral striatum which is produced by amphetamine and alcohol administration. In regards to [C]cocaine, there is a reduction in the radiotracer as a result of decreased expression of postsynaptic dopamine receptors. Alcohol dependent individuals demonstrated to have a decreased number of radiotracers, and cannabis detected almost no changes in the dopamine receptor availability. The article itself suggested that addiction is a complex mechanism that involves external factors such as environment, along with variation in drug reaction from person to person. It was suggested he it was unlikely that a single neurotransmitter could explain every aspect associated with addiction. The role of dopamine is concluded to have a central role in addiction to ‘stimulant drugs; which directly affect the dopamine system, but less so, in reference to mediating the addiction of other drugs – such as

Dopaminergic system: One of the main neurobilógicos systems involved in addiction to cocaine is the brain reward system (brain reward pathway), and dopamine its most important neurotransmitter (Koob, Le Moal, 1997). The dopaminégicos brain neurons that circuit are preferably located in the ventral tegmental area, projecting above for the nucleus accumbens and the prefrontal cortex (Tzschentke, 2001). The liberation of dopamine in these areas is involved with reward and positive reinforcement for certain type of behavior is well known that the action of cocaine causes such effect. Physiologically, these brain regions are activated when the individual performs a behavior closely related to their survival or their species, for example, to feed, quench thirst, have sex, take care of younger individuals. When cocaine increases dopamine release in these brain regions of reward, the body misinterprets the drug is related to their survival mechanisms, going to seek it incessantly (Koob, Le Moal, 2001). As mentioned, substance dependence relates also to the psychological profile of the consumer and to the environment where it is inserted. Adolescence is a difficult time for a large

It has been found that the increased use of a prosthetic limb can reduce phantom limb pain (PLP) in amputees suffering from strong pain. How that occurs is still up for research and debate, but some ideas have been formulated as to how the brain can adapt to the trauma of losing a limb. In their article, Preißler et al. (2013), detail the relationships between cortical plasticity, the use of prosthesis, and reduction in PLP linked with prosthesis use. Furthermore, by understanding the effects of cortical plasticity and reorganization that occurs in the aftermath of limb amputation, we are better able to comprehend how prosthetic use can mitigate pain in severe PLP sufferers.

According to Rabipour & Raz (2012) our ability to learn is a function called neuroplasticity or brain plasticity. What this means is that the brain has the ability to change throughout life. In essence, we are remarkable in this respect, our brains “plasticity”, gives it the amazing ability to reorganize itself by forming new connections between brain cells. Thus we are capable of acquiring a wide range of skills given the appropriate training (Rabipour & Raz, 2012).

Robinson and Berridge postulate that repeated exposure to drugs of abuse, persistently changes the brain circuits involved in attributing incentive salience. In accordance with that theory are several studies that have demonstrated that exposure to certain drugs such as cocaine enhances the motivation to seek or self-administer these drugs in the future (Horger, Shelton & Schenk, 1990; Deroche, LeMoal & Piazza, 1999). For a detailed discussion of this theory please refer to Robinson and Berridge (1993;

Cocaine, on the other hand, has been found to have a profound effect on increased dopamine activity. Kennedy & Hanbauer (1983; cited in Karch, 2007) found a strong correlation between cocaine binding and the inhibition of dopamine uptake, and therefore proposed that dopamine transporters are binding sites for cocaine. Such research, which correlates strong reinforcing properties of cocaine with inhibition of dopamine transporters, suggests that cocaine has a more significant affect upon dopamine, than than it has upon serotonin and noradrenaline. The excessive role of dopamine can explain the high degree of pleasure that users of cocaine experience, as well as depression and cravings, which follow.

The complexity of the human brain creates mystery when determining the influence of neurophysiological factors and their role in the process of addiction. There is a proposed relationship between drug addiction and the mesolimbic dopamine system, with the mesolimbic pathway from the ventral tegmental area to the nucleus accumbens considered the ‘reward centre’ of the human brain (Alcohol Rehab, 2011). A release of dopamine is necessary for ‘reward’ which is hypothesised to initiate the addiction cycle by providing positive reinforcement for drug self-administration (Feltenstein & See, 2009). Methamphetamine triggers the release of dopamine from synaptic vesicles which flood the synaptic cleft activating feelings of euphoria, well-being

“The overstimulation of this reward system, which normally responds to natural behaviors linked to survival (eating, spending time with loved ones, etc.), produces euphoric effects in response to psychoactive drugs. This reaction sets in motion a reinforcing pattern that “teaches” people to repeat the rewarding behavior of abusing drugs ”(“Understanding Drug Abuse). Using addictive drugs floods the limbic brain with dopamine, taking it up to as much as five or ten times the normal level. A person with elevated dopamine levels now has a brain that begins to associate the substance with an outside neurochemical reward (“Your Brain on Drugs”). As a person continues to abuse drugs, the brain adapts to the overwhelming surges in dopamine by producing less dopamine or by reducing the number of dopamine receptors in the reward circuit. The result is a lessening of dopamine’s impact on the reward circuit, which reduces the abuser’s ability to enjoy the drugs, as well as the events in life that previously brought pleasure. The decrease in normal dopamine levels encourages the addict to keep abusing drugs in an attempt to bring the dopamine function back to normal, except now larger amounts of the drug are required to achieve the same dopamine high, an effect known as tolerance (“Understanding Drug Abuse ). That is what leads to the state of addiction, which leaves the person in a cycle of craving, using, withdrawal, and relapse.