Alcohol and Cocaine Addiction (Essay Sample)

Alcohol and cocaine addiction
Name
Institution
Alcohol and cocaine addiction
Introduction
Drug addiction is one of the public health issues in the society. The addiction has been associated with different cognitive deficits in the abuser that include emotional regulation, working memory, motivation, attention, flexibility, decision-making and learning (Banerjee 2014). Various neurophysiological studies indicate that drugs that are abused have the reinforcing and addictive properties that affect the mesolimbic and mesocortical dopamine-mediated reward system through transmitters. This essay examines the brain’s involvement in the addiction of alcohol and cocaine; anxiety and schizophrenia disorders. The author will also evaluate how the changes in the brain are addressed using medication as one of the biologically-based intervention measures to counter addiction.
Brains involvement in the addiction
Alcohol is considered to be one of the powerful drugs that affect the brain’s normal activities through addiction behavior. It induces changes in the neurological pathways of the brain such as the dopaminergic, γ‑amino butyric acid (GABA), serotoninergic and glutamate pathways (Banerjee 2014). The ethanol, contained in the alcohol affects the central nervous system (CNS) by depressing the activities of the brain (Banerjee 2014). The person who is addicted to ethanol exhibit the feelings of relaxation and good mood. Alcohol interacts with the brain neurotransmitters of the reward and stress circuits. In this case, the alcohol acute reinforcing effects are produced; that later affects the neuronal function that is primary in alcohol addiction (Vengeliene, et al. 2008).
The dopamine pathway is a neurotransmitter that controls the circuit of the mesolimbic system (Banerjee 2014). The course is significant in controlling how the organisms react to the incentive changes of the environment. Dopamine, therefore, influences the incentive motivation that is linked to the ethanol intoxication. Alcohol affects the serotonin neurotransmitters of the brain by increasing the level of the serotonin in the nucleus accumbens of the brain (Vengeliene, et al. 2008; Banerjee 2014). The GABA, being one of the major inhibitory neurotransmitters in the brain is influenced by ethanol that enables high production of GABA that is felt around the central nucleus of the amygdala region. GABA functions through the assistance of subtype receptors called GABAA and GABAB. The Glutamate is an important excitatory neurotransmitter in the brain that operates through the N‑methyl‑D‑aspartate (NMDA) receptors (Banerjee 2014; Vengeliene, et al. 2008). Glutamate reinforces the acute effects of ethanol on the organism. Alcohol hinders the functions of the glutamate in the brain by reducing their levels in the striatum part of the brain that has nucleus accumbens (Banerjee 2014). The chronic alcohol exposure suppresses the glutamate-mediated signal in the amygdala.
According to Wakabashi and Kiyatkin (2014), the abuse of cocaine induces transient nucleus accumbens shells glutamate release that has distinct peripheral and central sources. The cocaine-initiated glutamate becomes acute and produces a dependency sensitization to the user. However, according to Gabach and others (2013), the behavioral sensitization is contributed by Nitric oxide. In Gabach and others perspective, nitric oxide contained in cocaine, acquires and maintains the effects of the drug in the brain of the user. The nitric oxide is involved in the activation of the neuronal nitric oxide synthase (nNOS)/NO/soluble guanylyl cyclase (sGC)/ cyclic guanosine monophosphate (cGMP) signaling pathway in the brain (Gabach 2013). The stimulation of nNOS/NO/sGC/cGMP pathway by continuous intake of cocaine activates the glutamate pathways and nucleus accumbens shells (Wakabashi & Kiyatkin 2014; Gabach, et al. 2013). The cocaine intake enhances the hippocampal LTP by stimulating the hippocampal ventral subiculum that increase the cocaine-seeking behavior (Gabach, et al. 2013).
Anxiety and Schizophrenia disorders
According to Smith and Randall (2012), the effects alcohol has on biopsychosocial can result in anxiety. Alcohol use involves the episodes of intermittent consumption and frequent utilization and withdrawal that destabilize the nervous system hence producing or worsening the state of anxiety. The acute alcohol use increases the anxiolytic effect by increasing the activity of the GABA neurotransmitters. The withdrawal period contributes to hyperexcitability of some of the brain components such as the limbic system, and the norepinephrine involved in the production of panic attacks (Smith & Randall 2012). The repeated withdrawal episodes are known to cause neural adaptation (kindling) exposing the drinker to anxiety and stress-induced effects of alcohol consumption. Symptoms such as increased heart rate, shallow and faster breathing are common to people who have abstained from alcohol (Smith & Randall 2012).
According to Buckner and others (2011), the use of cocaine, produces similar anxiolytic properties to those of alcohol. However, the abuser is susceptible to using other chemicals despite being an addict of cocaine. The patients that are withdrawing from cocaine experience higher levels of anxiety sensitivity that force them to abuse more cocaine to avoid the effects of anxious arousal (Buckner, et al. 2011). In this case, anxiety is used to maintain the substance use, and in some instances, the substance use is meant to avoid the effects of anxiety.
The schizophrenia is one of the mental disorders that have psychological symptoms such as hallucinations and delusions (Harvey & Yee 2013). The negative and cognitive effects of schizophrenia emerge when the levels of glutamate that are signaled through N-methyl-d-aspartate (NMDA) channel, are little. According to Harvey and Yee (2013), the addictive properties of alcohol and cocaine are governed by the rewarding property induced by the drugs that facilitate the consumption and the drug-seeking behavior. A person under the influence of alcohol or cocaine, therefore, is likely to experience frequent effects of schizophrenia due to the lower levels of glutamate in the brain (Harvey & Yee 2013). Alcohol and cocaine have been noted to reduce the levels of glutamate in the striatum; in this case the higher rate of depreciation of glutamate in the brain will subject the abuser to the frequent episodes of hallucinations and delusions (Harvey & Yee 2013).
Biological-based intervention measure of alcoholism and cocaine addiction
This section of the essay provides an evaluation of the use of medication as a biological-based intervention measure to interfere with the effects produced by alcohol and cocaine addiction in the brain. According to Banerjee (2014), the injection of small doses of a compound that interferes with the normal activities of the dopamine can block the consumption of alcohol. Although the reduction or absence of dopamine in the mesolimbic dopamine system does not guarantee the absolute abstinence from alcohol consumption, it is one of the measures that can be taken in reducing the levels of addiction. Serotonin pathways can also be targeted in alleviating addiction; introducing chemical compound that target the reuptake of serotonin in the system has been discovered to have the suppressive ability in alcohol-reinforced behavior. For instance, when the levels of serotonin are down, the urge to take alcohol is decreased (Banerjee 2014).
The working principle of GABAA and GABAB receptor in the brain of an addict is interfered in the presence of chemical drugs (Banerjee 2014). Since acute alcohol use increases the transmission of GABA in the amygdala region, the medication that targets the α1‑subunit in the GABAA receptor component will reduce the rate of consumption of alcohol (Banerjee 2014). The administration of the drug is done to the ventral pallidum; the region of the brain that receives signals from the neurons located in the amygdala extension (Banerjee 2014). According to Harvey and Yee (2013) the sarcosine-based non-competitive GlyT1-selective inhibitors such as Org 25935 and Org 24598 can be administered to reduce alcohol preference and the relapse of drinking. However, the competitive GlyT1 inhibitors in humans are yet to be evaluated in models of alcoholism (Harvey & Yee 2013). Acamprosate is used to control the activities of glutamate by acting on the NMDA receptor and metabotropic glutamate receptors (Banerjee 2014). Acamprosate reduces the workloa...