Neuroscience of Addictions

Addiction, tolerance and withdrawal

Addiction as the inability to continuously abstain from a specific behavior such as abusing drugs and this leads to reduced control over that behavior, dysfunctional emotional response and lack of recognition of consequent problems associated with the behavior and ones interpersonal relationships. Just like other chronic diseases addiction leads to a cycle of remission and relapse and if it never gets treated or the victim does not engage in recovery programs, the condition can worsen leading to disability or even death.

Tolerance, on the other hand, means an adaptation of a specific behavior such as substance abuse such that continuous consumption of the same amount of the substance has a lesser effect and if the amount is increased the same effect is produced. Tolerance can encourage a person to continue using a specific substance leading to dependency on it which eventually affects body organs preventing them from operating normally.

Finally, withdrawal can be defined as the symptoms that a substance addict experiences after abrupt reduction or cessation in consumption of a drug whether medical or recreational (Compton & Volkow, 2006). Any person who experiences withdrawal must have developed dependency on that drug whether psychologically, physically or both.Mechanisms by which tolerance occurs in abuse of marijuana, cocaine, and heroinDependence on cocaine has a great impact on neurotransmitters through inhibition of monoamine transporters in the brain especially dopamine.

Cocaine also has a minor impact on norepinephrine and serotonin transporters. Agonist in cocaine cannabinoids irritates relapse to cocaine seeking especially when someone withdraws from it for a long time. Antagonists of cannabinoids receptor then prevent relapse to the use of cocaine.

Cocaine leads to overproduction of dopamine which is a very important neurotransmitter that activates brain switches from one mood to another. The high amount of dopamine produced leads to high pleasurable feelings which leads to the victim to want more of the drug to produce more of the dopamine (Ben-Shahar, Moscarello, Jacob, Roarty & Ettenberg, 2005).

Marijuana, on the other hand, affects the cannabinoid receptors on the central part of the brain CB1 and the immune cells CB2. The CB1 receptors then enable restraining of calcium channels and adenylate cyclase, stimulation of mitogen-activated proteins and K+ channels (Jones, 2002). Some G protein cannabinoid receptors bring about tolerance to marijuana. However fewer amounts of dopamine neurotransmitters are produced after marijuana intake which explains why it easy to be dependent on drugs such as cocaine or heroin and not marijuana (Volkow, Fowler, Wang, Baler & Telang, 2009).

Tolerance to heroine begins to develop at cellular target levels. What happens is that when the heroine meets with opiate receptors, it prevents adenylate cyclase enzyme responsible for orchestrating some chemicals in the brain from maintaining impulse firing. When the heroin abuser continues to take the drug, the activation of the opiate receptor continues, and the enzymes get used to the heroin, and thus the drug will not be able to cause more changes firing of the cells. Tolerance to heroin begins at this level affecting areas involved in sending pain messages which are the thalamus and spinal cord (reward pathways) which in turn leads to the analgesic impact (Gonzez, Fernndez-Ruiz, Sparpaglione, Parolaro & Ramos, 2002).

Dependency or tolerance to heroin involves the thalamus and brainstem as well as reward pathways which eventually leads to addiction.Mechanisms by which withdrawal manifests after abuse of marijuana, cocaine, and heroinWhen an individual who has developed a dependency on cocaine withdraws from the drug, new neuroreceptor develops which motivates craving for the drug during the first week after abstinence from cocaine.

The main receptor involved is a subtype of ?±-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor and helps in regulating responses towards glutamate neurotransmitter in the brain. This regulation helps in linking feelings of satisfaction and reward to the victim motivating him to want more of the cocaine. Due to this craving, most of the abusers report the risk of relapse. Cocaine craving involves a very complicated neuronal circuit which includes the limbic and the cortical regions but the main.

Presence of glutamate inputs also plays a big role in cocaine seeking (Gonzlez, Fernndez-Ruiz, Sparpaglione, Parolaro & Ramos, 2002). Tetrahydrocannabinol (THC) is the main component of marijuana that causes the alteration in the brain through activation of cannabinoid receptors. These receptors are themselves activated by anandamide which is a neurotransmitter responsible for pain relieving. Since THC affects the normal functioning of the brain after meeting with anandamide, withdrawal from the drug will definitely lead to a craving for the same drug.

This means that without the activation of cannabinoid receptors by THC, the marijuana in the system will lose its rewarding properties. How first a marijuana abuser deals with the cravings for more will depend on the dosages taken and time frame (Budney, Hughes, Moore & Vandrey, 2004). Dependent on heroin develops when neurons get used to repeated drug intake and if the abuser withdraws from it withdrawal syndrome begins with severe impacts which might help the abuser to using the drug again. The opioid receptors having been adapted to the effect of heroin will require more of the drug to maintain the feeling (Buenaventura, Adlaka & Sehgal, 2008). Such a person seeking for more of the drug will require medicines such as naloxone which after meeting or binding with the opioid receptors blocks the effects of heroin or any other opioid drug.

References

Ben-Shahar, O., Moscarello, J. M., Jacob, B., Roarty, M. P., & Ettenberg, A. (2005). Prolonged daily exposure to iv cocaine results in tolerance to its stimulant effects.? Pharmacology Biochemistry and Behavior,? 82(2), 411-416.

Budney, A. J., Hughes, J. R., Moore, B. A., & Vandrey, R. (2004). Review of the validity and significance of cannabis withdrawal syndrome.? American journal of Psychiatry,? 161(11), 1967-1977.

Compton, W. M., & Volkow, N. D. (2006). Abuse of prescription drugs and the risk of addiction.? Drug and alcohol dependence,? 83, S4-S7.

Gonzlez, S., Fernndez-Ruiz, J., Sparpaglione, V., Parolaro, D., & Ramos, J. A. (2002). Chronic exposure to morphine, cocaine or ethanol in rats produced different effects in brain cannabinoid CB 1 receptor binding and mRNA levels.? Drug and alcohol dependence,? 66(1), 77-84.

Jones, R. T. (2002). Cardiovascular system effects of marijuana.? The Journal of Clinical Pharmacology,? 42(S1).

Ricardo Buenaventura, M., Rajive Adlaka, M., & Nalini Sehgal, M. (2008). Opioid complications and side effects.? A pain physician,? 11, S105-S120.

Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. (2009). Imaging dopamine's role in drug abuse and addiction.? Neuropharmacology,? 56, 3-8.

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