The Neuro-pharmacological Basis of the Risks Associated with the Use of Cocaine, Cannabis, Ecstasy and Heroin - Coursework Example

The Neuro-pharmacological Basis of the Risks Associated with the use of Cocaine, Cannabis, Ecstasy and Heroin Student’s Name Institutional Affiliation Date Introduction There are several risks associated with the use of drugs and other substances such as cocaine, ecstasy, cannabis and heroin. The substances are agonists since they bind to receptors and activate them thereby leading to adverse biological responses that manifest through the abnormal behaviour of the drug abusers. Ecstasy and the associated drugs are derivatives of amphetamine that contain some of mescaline’s pharmacological properties. The effects of the drugs that the users intend to achieve encompass sexual arousal, enhanced energy, sociability and endurance. Teenagers and young adults suffice to be the greatest users of such drugs. The essay contrasts and compares the risks associated with the use of the drugs under a neuro-pharmacological basis. The paper also compares and contrasts the risks associated with the abuse of the drugs such as addiction, motivational effects, and toxicology among other aspects. Cocaine Cocaine drug users use nasal insufflation such as snorting in the administration of cocaine into their bodies (Ciccarone, 2011). The absorption of freebase cocaine occurs in the membranes of the alkaline environment of the body. Following the administration of cocaine into the body system, the drug reacts by elevating the mood of the individual as well enhancing the alertness and energy of the individual. This encompasses improved attention and concentration and decreased sense of fatigue. The individual also presents performance decrement resulting from the suppression of appetite, deprivation of sleep, and libido increase (Mirchevska et al., 2014). Moreover, there are several toxic effects associated with the intake of cocaine in high doses. Some of these effects encompass seizures, delirium, cardiac arrhythmias, stupor and coma. Sustained convulsions are potential effects of seizures that can have the effect of stopping the breathing process in an individual. The most substantial pharmacological effect of cocaine occurs in the event of acute administration. Under such a situation, cocaine impedes the reuptake of dopamine into the presynaptic terminal following its release from a neuron terminal. The result is an increase in the level of dopamine at their synapses. The brain’s mesocorticolimbic pathway (MCLP) presents increased levels of dopamine at the synapses between the neuron terminals that project from the ventral tegmental area and the neurons within the medial prefrontal cortex and the nucleus accumbens (Volkow et al., 2009). Rather than blocking the reuptake of dopamine via the synapses in the brain, cocaine also hampers the reuptake of serotonin and norepinephrine. The neurochemical reactions are responsible for the acute behavioural effects that manifest in individuals that intake cocaine. Cocaine’s reinforcing properties emanate from its ability to foster dopamine activity in the MCLP. The reinforcement properties are evident when dopamine activates at least two of the receptor subtypes contained in the different areas of the brain. The D1 and D2 dopamine receptor subtypes are examples of the receptors activated by dopamine thereby resulting in the manifested effects of the drug. The increase in dopamine activity through the receptors also bears paramount significance to the other behavioural effects of the drug presented by its users. The chronic administration of cocaine results in the activation of several neurochemical compensatory mechanisms of the brain. In the absence of cocaine, the autoreceptors operate by decreasing the level of dopamine at the synapses. In essence, it is proper to state that the intake of cocaine reduces the sensitivity of the autoreceptors thereby reducing their ability to control the release of dopamine into the synapse. The intake of cocaine also affects postsynaptic receptors. The chronic administration of cocaine also impacts on the intracellular mechanisms such as the second messenger systems that are responsible for the functionality of the dopamine neurons situated in the nucleus accumbens and the ventral tegmental area (Dasgupta, 2010). Cannabis The main composition of cannabis sativa is psychoactive cannabinoids particularly the cannabinoid delta-9-tetrahydrocannabinol (THC). The other cannabinoids are either weakly active or inactive. There are other several components that emanate from the smoking of marijuana. There is a particular receptor for THC in the brain connected to a second messenger and localised to particular regions of the brain such as the cerebral cortex, hippocampus, the axon fibre terminals and the cerebellum. The dopamine neurons in the receptor cells send fibres to the basal ganglia (Ashton, 2001). THC impacts negatively on both the cognitive and motor aspects of the brain. The cognitive aspect of the brain has an association with memory impairment whereas the motor effect entails decreased motor coordination. The effects are evident when THC acts on the receptors (Iversen, 2003). There exists an endogenous neurotransmitter that interacts with the receptor prior to the presentation of the effects. Anandamide suffices to be one of the suspected neurotransmitters that interact with the receptors in the brain to yield the effects. Apart from THC, there are several other compounds that an individual inhales into the body upon smoking marijuana. However, different individuals present different reactions to marijuana. Some of the factors that influence the variability of the reactions encompass the experience, user expectation, setting, dose, the compounds produced when smoking marijuana and the sample’s cannabinoid content. An initial phase of euphoria suffices to be one of the adverse behavioural effects of smoking marijuana. The individual also undergoes periods of sedation and drowsiness after smoking marijuana (Oliver et al., 2007). The other negative effects of marijuana compounds encompass altered time perceptions, dissociation of ideas and distortion of vision and hearing (Johns, 2001). Chronic intoxication results in several adverse effects that include apathy, impairment of memory, concentration and judgment, dullness, and reduced interest of pursuing life goals. Ecstasy Pharmacodynamics MDMA increases the secretion of monoamine neurotransmitters such as dopamine, serotonin and noradrenaline from their axon terminals. There exists a transporter that is responsible for the reuptake of serotonin. The action of MDMA is to bind to the transporter thereby disabling the transportation of serotonin that leads to its uptake. By so doing, MDMA also hinders the reuptake of dopamine to a comparatively less extent (Liechti & Vollenweider, 2000). It is proper to state that the physiological effects of MDMA and MDA are similar to those of amphetamine that acts as a releaser of noradrenaline and dopamine. The distinctive mental effects associated with MDMA emanate from its action of increasing the secretion of serotonin and dopamine in the brain (Kalant, 2001). On the other hand, the physical effects of the drug that are similar to the effects of amphetamine emanate from its action of increasing the release of noradrenaline. Some of the undesired effects of MDMA include insomnia, flight of ideas, hyperactivity and increased arousal (Kalant, 2001). The other effects include depersonalisation, mild hallucinations, agitation, anxiety, and bizarre behaviour (Fisk et al., 2011). On certain occasions, the symptoms may lead to delirium, panic attacks and psychotic episodes. Complaints associated with the mind or mood of the individual include depression, anxiety, fatigue and difficulty in concentration (Degenhardt et al., 2009). The adverse effects of the drug on the physical functions of the drug include increase alertness and arousal and increased tension manifested through tooth grinding, constant movements of restlessness, jaw clenching and muscular tension. Heroin The drug has a diminishing and negative effect on the brain that leads to addiction. The opiates bind to the receptors produced by the body naturally to perform the role of neurotransmission (van Dorp et al., 2007). It is evident that the action of heroin is similar to the action of other endogenous opioids. The receptors are responsible for influencing the opening of the ion channels that determines the excitability of neurons thereby resulting in euphoric effects. Heroin binds to these receptors. The action also includes the GABA-inhibitory interneurons located in the ventral tegmental area. The action of heroin of binding to the receptors entails the reduction in the rate of secretion of GABA-inhibitory interneurons. Following its secretion, GABA lowers the level of dopamine secretion in the nucleus accumbens. On the other hand, heroin acts by increasing the secretion of dopamine thereby resulting in an increase in the pleasure feeling (Volkow, 2014). The continuous consumption of heroin has an inhibiting effect on the secretion of cAMP. In the event that the user does not intake heroin, the concentration of cAMP increases thereby resulting in a craving for heroin and neural hypersensitivity (Zovco & Criscuolo, 2009). The adverse effects of heroin comprises of both short-term and long-term effects. Some of the short-term effects encompass mitotic pupils of the user that emanate from the stimulating effect of heroin on the central nervous system that excites the oculomotorius nuclei thereby having an effect on the sphincter muscles of the iris. Users of the drug also encounter issues in the gastrointestinal region thereby presenting constipation, vomiting and nausea (Volkow, 2010). Heroin also impacts negatively on other sphincter muscles of the body such as sphincter pylori, sphincter ani externus and sphincter urethrae. The drug also depresses the respiratory system leading to slow breathing that turns out to be the major cause of death for the drug users. The long-term effects of the drug include liver disease, collapsed veins, kidney disease, respiratory problems and pulmonary complications. Comparison Being a stimulant, the primary target of cocaine is the dopamine transporter. The targets of Cannabis, Heroin and Ecstasy are CB1 receptors, opioid receptors and NMDA respectively. The pharmacological effect of cocaine entails inhibiting the reuptake of dopamine into the presynaptic terminal following its release from a neuron terminal that results in an increase in its concentration at the synapses. Cocaine also impedes the reuptake of serotonin and norepinephrine. On the other hand, marijuana activates CB1 and CB2 receptors. Just like injected THC, the distribution of CB1 receptors includes in the limbic areas, basal ganglia, thalamus, cerebellum and cerebral cortex. As mentioned before, heroin targets the opioid receptors of the brain. On the other hand, ecstasy targets NMDA. Heroin acts by binding to the opioid receptors that are responsible for neurotransmission in the brain. The result is a reduction in the secretion of GABA-inhibitory neurons thereby reducing the secretion of dopamine. Ecstasy acts by increasing the secretion of monoamine neurotransmitters such as dopamine, serotonin and noradrenaline from their axon terminals. Conclusion All the drugs present several risks to the user. Addiction is a common characteristic risk for all the drugs. Drug-related deaths suffice to be a major concern that arises when users get addicted to the drugs. The common action of the drugs entails preventing the reuptake of serotonin and dopamine by binding to the receptors. The result is an increase in the concentration of serotonin and dopamine at the synapses that is responsible for the mental effects of the drugs. The physical effects of the drugs emanate from their action of increasing the concentration of noradrenaline at the synapses as opposed to the normal situations where receptors transport the substances. The major risks associated with the use of the drugs include bizarre behaviour, hypersensitivity, increased arousal, addiction and death resulting from comas and depressed respiratory systems. References Ashton, C. H. (2001). Pharmacology and effects of cannabis: a brief review. The British Journal of Psychiatry, 178(2), 101-106. Ciccarone, D. (2011). Stimulant abuse: pharmacology, cocaine, methamphetamine, treatment, attempts at pharmacotherapy. Primary Care: Clinics in Office Practice, 38(1), 41-58. Dasgupta, A. (2010). Pharmacology of commonly abused drugs. In Beating Drug Tests and Defending Positive Results (pp. 11-28). Humana Press. Degenhardt, L., Roxburgh, A., Dunn, M., Campbell, G., Bruno, R., Kinner, S. A., ... & Topp, L. (2009). The epidemiology of ecstasy use and harms in Australia. Neuropsychobiology, 60(3-4), 176-187. Fisk, J. E., Murphy, P. N., Montgomery, C., & Hadjiefthyvoulou, F. (2011). Modelling the adverse effects associated with ecstasy use. Addiction, 106(4), 798-805. Iversen, L. (2003). Cannabis and the brain. Brain, 126(6), 1252-1270. Johns, A. (2001). Psychiatric effects of cannabis. The British Journal of Psychiatry, 178(2), 116-122. Kalant, H. (2001). The pharmacology and toxicology of “ecstasy”(MDMA) and related drugs. Canadian Medical Association Journal, 165(7), 917-928. Liechti, M.E, Vollenweider, F. X. (2000). Acute psychological and physiological effects of MDMA (“ecstasy”) after haloperidol pretreatment in healthy humans. Eur Neuropsychopharmacol, 10, 289-95. Mirchevska, L., Mojsoska, S., Tanevski, V., & Jakasanovski, O. A. (2014). Prospective Study to use and Misuse of Benzodiazepines to Different Examined Groups by Education in R. Macedonia. International Journal of Sciences: Basic and Applied Research (IJSBAR) Volume, 14, 67-74. Oliver, P., Forrest, R., & Keen, J. (2007). Benzodiazepines and cocaine as risk factors in fatal opioid overdoses. Research briefing, 31. van Dorp, E. L., Yassen, A., & Dahan, A. (2007). Naloxone treatment in opioid addiction: the risks and benefits. Expert opinion on drug safety, 6(2), 125-132. Volkow, N. D, Fowler, J. S, Wang, G. J, Baler, R., & Telang F. (2009). Imaging dopamine's role in drug abuse and addiction. Neuropharmacology. 1, 3–8. Volkow, N. D. (2010). Prescription drug abuse. National Institute of Drug Abuse. Volkow, N. D. (2014). Heroin. Research Report Series. Zovko, A., & Criscuolo, C. L. (2009). The pharmacological effects of diacetylmorphine (heroin) after diffusion through the blood-brain barrier. Read More

Rather than blocking the reuptake of dopamine via the synapses in the brain, cocaine also hampers the reuptake of serotonin and norepinephrine. The neurochemical reactions are responsible for the acute behavioural effects that manifest in individuals that intake cocaine. Cocaine’s reinforcing properties emanate from its ability to foster dopamine activity in the MCLP. The reinforcement properties are evident when dopamine activates at least two of the receptor subtypes contained in the different areas of the brain.

The D1 and D2 dopamine receptor subtypes are examples of the receptors activated by dopamine thereby resulting in the manifested effects of the drug. The increase in dopamine activity through the receptors also bears paramount significance to the other behavioural effects of the drug presented by its users. The chronic administration of cocaine results in the activation of several neurochemical compensatory mechanisms of the brain. In the absence of cocaine, the autoreceptors operate by decreasing the level of dopamine at the synapses.

In essence, it is proper to state that the intake of cocaine reduces the sensitivity of the autoreceptors thereby reducing their ability to control the release of dopamine into the synapse. The intake of cocaine also affects postsynaptic receptors. The chronic administration of cocaine also impacts on the intracellular mechanisms such as the second messenger systems that are responsible for the functionality of the dopamine neurons situated in the nucleus accumbens and the ventral tegmental area (Dasgupta, 2010).

Cannabis The main composition of cannabis sativa is psychoactive cannabinoids particularly the cannabinoid delta-9-tetrahydrocannabinol (THC). The other cannabinoids are either weakly active or inactive. There are other several components that emanate from the smoking of marijuana. There is a particular receptor for THC in the brain connected to a second messenger and localised to particular regions of the brain such as the cerebral cortex, hippocampus, the axon fibre terminals and the cerebellum.

The dopamine neurons in the receptor cells send fibres to the basal ganglia (Ashton, 2001). THC impacts negatively on both the cognitive and motor aspects of the brain. The cognitive aspect of the brain has an association with memory impairment whereas the motor effect entails decreased motor coordination. The effects are evident when THC acts on the receptors (Iversen, 2003). There exists an endogenous neurotransmitter that interacts with the receptor prior to the presentation of the effects.

Anandamide suffices to be one of the suspected neurotransmitters that interact with the receptors in the brain to yield the effects. Apart from THC, there are several other compounds that an individual inhales into the body upon smoking marijuana. However, different individuals present different reactions to marijuana. Some of the factors that influence the variability of the reactions encompass the experience, user expectation, setting, dose, the compounds produced when smoking marijuana and the sample’s cannabinoid content.

An initial phase of euphoria suffices to be one of the adverse behavioural effects of smoking marijuana. The individual also undergoes periods of sedation and drowsiness after smoking marijuana (Oliver et al., 2007). The other negative effects of marijuana compounds encompass altered time perceptions, dissociation of ideas and distortion of vision and hearing (Johns, 2001). Chronic intoxication results in several adverse effects that include apathy, impairment of memory, concentration and judgment, dullness, and reduced interest of pursuing life goals.

Ecstasy Pharmacodynamics MDMA increases the secretion of monoamine neurotransmitters such as dopamine, serotonin and noradrenaline from their axon terminals. There exists a transporter that is responsible for the reuptake of serotonin. The action of MDMA is to bind to the transporter thereby disabling the transportation of serotonin that leads to its uptake.

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