Aug 10, · Addiction Center receives advertising payments from the treatment providers that respond to chat requests on the websites and is not associated with any specific treatment provider. Addiction Center is not a medical provider or treatment facility and does not provide medical advice GAMING ADDICTION RESEARCH PAPER. Download. In this regard, computer game addiction has more in common with gambling addiction than alcohol or drug addiction. Although somewhat similar to the symptoms of computer game addiction, the negative consequences of excessive gaming are often divided into five main categories: Social Consequences Nov 15, · Essay drug addiction with quotations Ap essay grading rubric. Essay about wheel of life short essay on sports and politics, write an expository essay on the topic population explosion in nigeria essay on old age home in hindi, natural selection essay topics essay about taman negara
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Try out PMC Labs and tell us what you think. Learn More, research paper about drug addiction. Neuroscientific approaches to drug addiction traditionally have been based on the premise that addiction is a process that results from brain changes that in turn result from chronic administration of drugs of abuse.
An alternative approach views drug addiction as a behavioral disorder in research paper about drug addiction drugs function as preeminent reinforcers. Although there is a fundamental discrepancy between these two approaches, the emerging neuroscience of reinforcement and choice behavior eventually may shed light on the brain mechanisms involved in excessive drug use.
Behavioral scientists could assist in this understanding by devoting more attention to the assessment of differences in the reinforcing strength of drugs and by attempting to develop and validate behavioral models of addiction. Drug addiction continues to take a massive toll in terms of economic loss and human misery, research paper about drug addiction. For the purpose of this article, we define drug addiction as the final outcome of a process that begins with occasional drug-taking, and ends with consumption of excessive amounts of drug to the detriment of society and the individual.
Drug addiction is a chronic, relapsing disorder that provides research and treatment challenges to scientists from widely ranging disciplines. Among these, geneticists and epidemiologists are particularly intrigued by the fact that drug-taking behavior exists on a continuum in humans: some people engage in it to excess, most in moderation, and many not at all. Clearly, genetic differences and specific societal-environmental conditions can play a role in the development of drug abuse. Psychiatrists and clinical psychologists attend more to the individual characteristics of the drug abuser, and consider how other cognitive co-morbidities, such as anxiety or depression, contribute to the development and maintenance of drug abuse and addiction.
Pharmacologists tend to focus on the drugs themselves, studying their mechanisms of action and attempting to develop potential drug antagonists that might be useful in the treatment of drug abuse.
And behavioral pharmacologists look for clues to the etiology and control of drug abuse in the effects of drugs on the behavior of humans or animals under controlled experimental conditions. Neuroscience, because it searches for relationships between brain function and behavior, is in an especially appropriate position to study the neural correlates of the behavior of drug abuse, and neuroscientists have contributed a tremendous amount to our understanding of the effects of drugs of abuse on the brain and nervous system.
This article will address some of the neuroscience research on the problem of drug abuse, research paper about drug addiction, but will touch only on limited aspects of what is a massive area of scientific inquiry. The first section on brain reward circuitry is included because this is the neuroanatomical basis for virtually all hypotheses and research on the neuroscience of drug abuse.
The next section describes some recent research from a few of the many neuroscientists who have concentrated their efforts on drug addiction. What is interesting and somewhat distressing for behavioral scientists is how little behavior is regarded in much of this research.
Because drug addiction generally is conceived as a process caused directly by chronic administration of drugs of abuse, the investigative effort is concentrated on a search for changes in the morphology or molecular biology in research paper about drug addiction parts of the brain as a function of chronic drug administration. The neuroscience skills and techniques used by these investigations are formidable, and interesting neuronal changes have been observed following chronic drug administration.
Even more technically fascinating is the possibility of recreating these localized neurobiological changes in the absence of drug administration—in effect producing an addicted brain without giving the addicting substance.
Animals so treated then can be evaluated behaviorally, to determine whether they are, in fact, addicted. Unfortunately, the behavioral measures used in these types of studies often are weak and not validated, bringing the conclusions of much of this work into question. Our generally negative critique of much of the most prominent work on the neuroscience of drug abuse is followed by a research paper about drug addiction of a strictly behavioral approach to drug abuse.
This behavioral approach is presented as an additional avenue to be explored by neuroscientists and others investigating drug abuse. We argue that drug addiction involves the excessive choice of a drug over other environmental stimuli, research paper about drug addiction, perhaps because the drug is a more potent reinforcer relative to competing reinforcers in the addict's life.
This section serves two purposes: one is to present an option to the neuroscience approach and to suggest how addiction can be described more appropriately; the other is to prepare for the next section which returns to neuroscience, but in a more behavioral context. In this next section, we describe some experiments that indicate that neuroscience embedded in a more behavioral context potentially can identify the neurological correlates of behavioral constructs, such as reinforcer strength.
For example, investigations of the brain correlates of choice eventually may clarify the regions in the brain and the patterns of brain activity that are correlated with preference for higher magnitude reinforcers. Although the work described in this section does not involve studies of drugs as reinforcers per se, it easily could be extended to complement a behavioral model of addiction. The behavioral approach to drug addiction presupposes that drugs are not qualitatively different from non-drug reinforcers.
The last section of this article describes recent neuroscientific studies that assess the validity of this assumption. For example, do the brain changes that accompany reinforcement differ if the stimulus is cocaine compared with other non-drug stimuli? Finally, the perspectives offered in this paper are limited by both space and our time. It would add useful knowledge to review what is known about the neuroanatomy and neurophysiology of Pavlovian conditioning e.
Also useful would be a discussion of several psychological theories that have been posited to research paper about drug addiction drug addiction, many of which were put forward by neuroscientists and based on hypothesized or observed drug-induced brain changes e. However, our interest in data rather than theories led us to exclude this conjunction of drug addiction and neuroscience.
In a simplified view, the brain can be thought of as the locus for the retrieval, processing, and storage of information transmitted from the environment via neurons.
Quite a bit is known about the location of the specific sensory input and motor output areas of the brain, but less is understood about the brain structures and processes involved in the formation of constructs such as values, emotions, research paper about drug addiction, and memories see review by Glimcher, The current general concept of input and output anatomy within the brain involves parallel sensory and motor circuits that can be described as cortical-striatal-pallidal-thalamic-cortical Heimer, These circuits carry information from either research paper about drug addiction somatosensory cortex or the motor cortex to related areas in the putamen.
Circuits run medially from the putamen to the globus pallidus or to the substantia nigra, and the globus pallidus sends projections to specific areas of the thalamus.
The thalamus closes the loop by returning information to local areas of the cortex. The key concept in these circuits is topographical organization. Different parts of each of these anatomical areas are activated depending on the nature e. The association areas of the brain also may be connected in several circuits that run somewhat parallel to the input and output circuits.
A locus of particular importance in this pathway is the ventral striatum which includes the nucleus accumbens. Dopamine is released into the ventral striatum via dopaminergic neurons that project from the ventral tegmentum Figure 1, research paper about drug addiction. The ventral tegmentum also sends dopaminergic neurons to dorsal striatal and cortical areas. The ventral striatum has non-dopaminergic, primarily glutamatergic, research paper about drug addiction from the amygdala and hippocampus, which are involved in memory and emotional processing.
Many of these pathways are reciprocal, with information passing back to the structure that originated the stimulation. Dark lines indicate dopamine pathways.
Bottom Relation of thalamus with lateral thalamic nuclei to the more lateral caudate nucleus and globus pallidus. The cortical areas involved in reward circuitry are thought to include the entorhinal and perirhinal cortices, the anterior cingulate cortex, the temporal lobe and the posterior area of the medial orbital frontal cortex, research paper about drug addiction.
Projections from these cortical areas travel to the ventral striatum as well. In the ventral striatum there is close interdigitation with pallidal structures, and there are neuronal connections from the striatum to the ventral pallidum, the internal globus pallidus, and down to the substantia nigra pars reticulata.
The medial dorsal thalamus is innervated by fibers from research paper about drug addiction pallidal areas, and thalamic projections complete the circuit by traveling to the anterior cingulate cortex. Thus, a cortical-striatal-pallidal-thalamic-cortical circuit can be described in the emotional areas of the brain.
The cortical areas are different from those involved in motor control and sensory input; the striatal and pallidal areas typically are located more ventrally, have considerable non-cortical input, and a distinct thalamic nucleus is involved.
Nevertheless, research paper about drug addiction, this circuit has parallels with other primary circuits in the brain Alexander et al. What clearly is missing is how the various circuits are interconnected to integrate the sensory input with the motor output. This question stimulates much of the research on the neurocircuitry of reward. Although the parallel circuitry suggests that integration is possible at many cortical and subcortical levels, the precise pathways whereby sensory input is evaluated, modified by processes associated with memorial, emotional, and motivational factors, and converted into motor output have not been delineated clearly, research paper about drug addiction.
It has been thought that the nucleus accumbens, with its shell and core components, as well as its strong connection to various amygdaloid nuclei, is critical to emotional coordination of behavioral output. The extended amygdala is a fairly recently described structure that is an important part of this system; it consists of two components. One includes the central amygdaloid nucleus and the lateral bed nucleus of the stria terminalis, and carves a sweeping circuit beneath the main body of the striatum and the globus pallidus.
The other consists of the medial amygdaloid nucleus and the medial bed nucleus of the stria terminalis, and travels along with the central component under the lenticular nuclei Alheid, The central and medial nuclei of the amygdala have substantial input from the basal lateral nucleus of the amygdala and many projections to the cortex and to autonomic and endocrine areas in the hypothalamus and brain stem.
It is in the various parts of this reward circuit anatomy and its connection with motor circuitry where neuroscientists look for brain changes that reflect reinforced behavior.
Neuroscientists primarily interested in drug abuse typically search for changes in some aspect of the reward circuitry that accompany the development of drug addiction. This presupposes a consensus on what addiction is, and most neuroscientists agree that drug addiction is a behavioral disorder. Measures of the reinforcing effects of drugs drug self-administration are used by several neuroscientists as indicators of the development of addiction. Even more popular are measures of sensitization an increase over time in the locomotor stimulating effects of a drug as a consequence of repeated administration of the drugconditioned place preference a selection by the animal of an environment where it previously experienced the effect of a drugand reinstatement an increase in extinguished, drug-maintained responding as a consequence of non-contingent drug administration, stress, or other intervention.
However, as indices of addiction, these measures leave much to be desired. Sensitization has only the fact that it is produced by repeated administration of a drug, and is maintained for several weeks or months following drug withdrawal, to recommend it as a model of addiction. This drug-induced increase in locomotion lacks even face validity as an indicator of compulsive drug taking or loss of control of drug-taking behavior.
It can be argued that the lack of a validated behavioral measure of addiction is the biggest impediment for neuroscientists who focus on brain changes associated research paper about drug addiction chronic drug administration. Despite these challenges, the actual neuroscience is typically innovative and productive. One of the research paper about drug addiction provocative neural changes that occurs as a consequence of drug administration involves drug-induced alterations in gene expression.
Learning and memory may have neural mechanisms in common with drug research paper about drug addiction because both reflect changes in reinforced behavior over extended time periods. Neuroscientists, research paper about drug addiction, stating that drug addiction is a relatively stable condition, are especially interested in gene expression changes that have an extended duration, research paper about drug addiction. There are many places where gene expression can be modified.
The group headed by Eric Nestler has emphasized long-term, drug-induced changes in transcription factors as a potentially critical aspect of gene expression that might be related to drug addiction. Transcription factors are proteins that attach to the part of DNA that is responsible for the rate at which this DNA is transferred to RNA and subsequently to the rate of synthesis of specific proteins. A number of neurotransmitters act through their membrane receptors to alter levels of transcription factors.
Because drugs of abuse can directly affect the action of some neurotransmitters on their receptors, this is a logical place to begin to look for the effects of drugs on protein synthesis. A recent review Nestler, research paper about drug addiction, describes two transcription factors that his laboratory has evaluated that meet some of their criteria as important factors in drug addiction.
Both of these, CREB cAMP response element binding protein and deltaFos B, are increased in the nucleus accumbens following chronic administration of cocaine. Elevated levels of CREB are fairly short lasting, declining within several days after cocaine administration has been stopped. They also are associated with decreased sensitivity to a wide variety of stimuli, including drugs of abuse Barrot et al.
It is therefore a more interesting candidate as a correlate of drug addiction. Levels of deltaFos B can be modified in the nucleus accumbens and the dorsal striatum of mice the same areas in which they are increased by cocaine administration using technically sophisticated procedures that do not involve cocaine administration. If elevated striatal deltaFos B levels play a role in drug addiction, mice with enhanced striatal deltaFos B levels in the absence of cocaine exposure should respond differently to cocaine than mice with normal striatal deltaFos B levels.
A variety of behavioral indices support this hypothesis. Interestingly, these effects appear to be somewhat specific to cocaine; the two groups did not differ in research paper about drug addiction of food-maintained responding. These results suggest that higher striatal levels of deltaFos B may be correlated with enhanced sensitivity to the incentive properties of cocaine.
However, research paper about drug addiction, an important comparison that was not made was to determine whether mice with histories of chronic cocaine self-administration, and presumably cocaine-induced increases in deltaFos B, also showed similar patterns of responding as those mice with artificially increased deltaFos B expression. A driving concern of neuroscientists is identification of the proteins that are synthesized in increased amounts as a result of deltaFos B and CREB overexpression.
The Value of Drug Addiction Research: Michael Nader at TEDxWakeForestU
, time: 21:38Drug And Alcohol Slang Terms - Addiction Center
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