EFFECTS OF ADDICTION ON THE BRAIN

REVIEW OF LITERATURE
BRAIN AND BEHAVIOUR

HARSHITHA S KUMAR
SRN: PES1UG25PY056
1ST SEMESTER A SECTION
[Link]

SUBMITTED TO
PROF. BHUMIKA BN
PROFESSOR
DEPARTMENT OF PSYCHOLOGY
PES UNIVERSITY
INTRODUCTION

Addiction is a chronic disorder that can be relapsing and is characterized by going on taking
drugs compulsively despite the harmful consequences, showcasing the persistent changes in
the brain’s motivational and control systems. It is a widely accepted view that addiction is not
only a matter of willpower but also a neurobehavioral disorder that involves the dysregulation
of the neural circuits that govern the aforementioned reward, learning, emotion, and self-
regulation (Volkow & Koob, 2015). The

mesolimbic dopamine pathway, which links the ventral tegmental area (VTA) to the nucleus
accumbens, is the key to these processes. The substances that are harmful to the body; in fact,
they overstimulate this system leading to the production of the exaggerated reward signals
and, consequently, drug-seeking behaviour gets reinforced. With the passage of time, the
chemical signalling in the pretty much overstimulated circuit changes to a point where
eventually the person cannot feel the same high as before (Robinson & Berridge, 2003).

At the same time, the long-term drug user suffers damage to the prefrontal cortex that is the
brain area responsible for executive control, decision-making, and impulse inhibition. This
neural degeneration in the person's brain makes it difficult for them to resist cravings or to
consider the long-term consequences of their actions (Goldstein & Volkow, 2011). The
environment through classical and operant conditioning contributes to making the burden of
substance being taken even harder to bear as it is infested with cues that trigger craving and
relapse. Furthermore, the continued use of drugs goes along with neuroadaptations in the
amygdala and the hypothalamic–pituitary–adrenal (HPA) axis, which together result in
heightened stress sensitivity and hence make negative emotional states the main drivers
behind the habit (Koob & Le Moal, 2008).

The contemporary psychological neuroscience considers addiction as a product of the

ongoing and variable interaction between the brain, behaviour, and the environment. It is a
process that involves both biological and psychological aspects: changes in the brain affect
the processes of thought and the degree of desire while cognitive, emotional and social
contexts also influencing the brain function (Gifford & Humphreys, 2007). It is of great
importance to comprehend these two-way mechanisms in order to construct very efficient
therapies that will not only attack the neurochemical factors of addiction but also the habits
and social conditions that keep it alive.
Addiction and the Brain’s Reward System

The reward system of the brain, which is the main factor in addiction, was developed to
support the survival of the species through reinforcement of behaviours like eating and
socializing. The normal situation is that the release of dopamine in the nucleus accumbens
indicates that the experience is rewarding or worth repeating. Drug addiction turns this
system upside down, as they release dopamine at a rate much greater than that of natural
rewards, thus changing the hierarchy of values (Wise & Jordan, 2021). The result of this, the
so-called incentive sensitization, is that the brain does not only become more and more
responsive to drug cues but also less and less responsive to natural rewards (Robinson &
Berridge, 2003).

Thus, the signalling of pleasure by the dopamine system gradually becomes weaker, while
craving grows stronger. This is the reason why drug-dependent people are often not getting
the same high from the drugs but at the same time feel a strong, unstoppable urge to acquire
them. The shift from “liking” to “wanting” is a characteristic change in the brain due to
addiction, and it shows the role of the dopaminergic system in the intertwined processes of
reward, motivation, and learning.

Learning, Memory, and Habit Formation

Conditioning processes explain why individuals experience strong cravings in response to

Conditioning processes can be regarded as the basis for the powerful cravings of some
individuals who react to the environmental cues or stressors even after a long period of
abstinence. This strong cue-reactivity is a very well-established behaviour that is maintained
by both neural and psychological mechanisms. It can, therefore, be concluded that addiction
is a form of learning that is improperly done as it gives priority to short-term reinforcement at
the cost of long-term wellbeing.

The Role of Stress and Emotional Regulation

Chronic substance use hinders the proper function of the brain’s stress and emotional
regulation systems. It causes the extended amygdala and HPA axis to become overactive,
thus, contributing to anxiety, irritability, and dysphoria during withdrawal (Koob & Le Moal,
2008). Negative emotional states that result from withdrawal cause relapse as the person tries
to cope with the distress by reverting to drug use. Thus, addiction has both positive (seeking
pleasure) and negative (avoiding distress) reinforcement. With time, negative reinforcement
takes over, and the use of drugs is no longer about attaining pleasure but rather about the
relief of discomfort.

Cognitive Control and Self-Regulation

At the onset of addiction, the activity and connectivity of the prefrontal cortex—the area in
charge of decision-making, planning, and inhibitory control—start to decrease. Functional
imaging studies conducted in this respect have shown that there is hypoactivity in regions
such as the orbitofrontal cortex and anterior cingulate cortex, which are involved in self-
monitoring and consequence evaluation (Goldstein & Volkow, 2011). These deficits lead to
the compulsivity and lack of judgment that characterize addiction, whereby the individual is
aware of the harm being caused but still finds it difficult to control the impulses.

Later, behaviour becomes automatic and stimulus-driven—a neural shift from the prefrontal
cortex to striatal circuits that parallels psychological loss of control.

Integrating Brain and Behaviour

Taking into account addiction from the biological and psychological dimensions' perspective
provides a complete explanation for the compulsive use of substances. The changes
happening in the brain due to addiction, dysfunction of dopamine system, reduction of
efficiency in the cortex, and increased activity of the stress system, keep on having
interactions with such behavioural patterns, environmental cues, and cognitive processes like
expectation and self-efficacy (Gifford & Humphreys, 2007).

Psychological science helps by associating these brain processes with visible behaviours and
by creating treatments that use the principles of learning and motivation—contingency
management, motivational interviewing, and cognitive-behavioural therapy being some of
them—so as to facilitate recovery. Addiction is therefore not a fixed brain disease but rather a
dynamic phenomenon of neural plasticity and behavioural adaptation that is influenced by
personal and environmental factors, thus it is best understood this way.
PAPER 1: “THE BRAIN ON DRUGS: FROM REWARD TO
ADDICTION” Nora D. Volkow and Marisela Morales (2015)

Abstract

Volkow and Morales (2015) dive deep into how drugs hijack the brain’s reward and
motivation systems, showing how casual use slips into compulsive addiction. They lay out
addiction as a chronic, relapsing brain disease, rooted in changes to key dopamine
pathways—especially between the ventral tegmental area (VTA) and the nucleus accumbens
(NAc). Early drug use floods the brain with intense bursts of dopamine, making those first
experiences powerfully rewarding. But as drug use continues, these waves of dopamine start
to reshape the brain. Natural rewards lose their appeal, and the prefrontal cortex—the region
that keeps self-control and decision-making in check—starts to falter.

The authors show that addiction sticks not just because of the drugs themselves, but through
conditioned learning, stress, and changes in how the brain manages emotion, with the
amygdala and extended amygdala playing big roles. They make it clear: addiction isn’t about
moral failure. It’s about brain circuits gone haywire. With time, people lose their ability to
fight cravings and get pulled back by drug-related cues, slipping into compulsive patterns
even when the drugs no longer feel good.
Drawing from neuroimaging and molecular studies, this review pins addiction down as a
disorder built on both a broken reward system and shaky self-control. This view opens the
door for medical and behavioural treatments that go after the brain’s altered wiring, rather
than blaming the person.
PAPER 2: “ADDICTION AND ITS BRAIN SCIENCE” Rainer Spanagel
and Markus Heilig (2005)

Abstract
Spanagel and Heilig (2005) dig into how far we've come in understanding addiction, pulling
insights from neuroscience, genetics, and behavioural research. They don’t just call addiction
a matter of physical dependence or withdrawal. Instead, they describe it as a chronic
condition—something marked by compulsive drug-seeking, losing control, and a tendency to
relapse over and over.
Sure, dopamine plays a big role, especially in making drugs feel rewarding. But Spanagel and
Heilig push back against the idea that dopamine tells the whole story. Addiction runs deeper,
tangled in the workings of several brain systems—the mesolimbic, mesocortical, and
nigrostriatal pathways all get involved. Addictive behaviour doesn’t just pop up for one
reason. It grows out of the complicated mix of reinforcement, motivation, habit-building, and
stress. One thing the authors bring to the table is a three-step neurobiological framework for
studying addiction. First, they map out which brain regions matter, using animal studies and
neuroimaging. Next, they dig into genetics—using quantitative trait locus (QTL) analysis and
gene expression profiling to see which genes get involved. Finally, they test these candidate
genes with both molecular and behavioural methods. This approach helps connect changes in
the brain’s biology to actual behaviour, bridging the gap between lab research and real-world
addiction.
Spanagel and Heilig don’t agree with the idea of a single “molecular switch” for addiction.
Instead, they see it as a disorder shaped by a web of genetic, molecular, and environmental
factors, all shifting brain function over time. They argue for an interdisciplinary approach—
neuroscience, psychology, and genetics need to work together if we want to develop better
treatments and prevention strategies. Addiction, in their view, is complex, and that
complexity demands teamwork across fields.
PAPER 3: “THE ADDICTED HUMAN BRAIN: INSIGHTS FROM
IMAGING STUDIES” Nora D. Volkow, Joanna S. Fowler, Gene-Jack
Wang (2003)

Abstract

Volkow, Fowler, and Wang (2003) took brain imaging—PET and fMRI—and showed, in
vivid detail, how addiction rewires the brain. They mapped out four main circuits that drugs
hijack: reward, motivation, memory, and control. When someone uses drugs, dopamine
floods the nucleus accumbens, lighting up that reward pathway and creating an intense rush
of pleasure. But as drug use continues, the brain adapts. Dopamine receptors dwindle.
Suddenly, everyday rewards—food, relationships, the small joys—don’t register the same
way. The prefrontal cortex and orbitofrontal cortex, which normally handle judgment and
self-control, start to falter. Their scans captured another striking pattern: when people crave
drugs or see drug cues, the amygdala and hippocampus go into overdrive, while the brain’s
control centres lag behind. That imbalance drives the compulsive pull to use, even when
someone desperately wants to stop. The authors outline a model where the brain, through
repeated exposure, learns to overvalue drugs and undervalue everything else. They go further,
arguing that individual differences in dopamine D2 receptors could explain why some people
are more vulnerable to addiction than others.

What stands out in this work is its clear message: addiction changes the brain. It’s not just a
matter of weak willpower—it’s a disorder rooted in measurable, structural, and functional
brain shifts. Their model points toward practical strategies: restore dopamine balance, rebuild
cognitive control, and help people reconnect with natural rewards. This study weaves
together biology, behaviour, and imaging to deliver one of the most thorough neurobiological
accounts of addiction to date.
PAPER 4: “ADDICTION AS A BRAIN DISEASE REVISED: WHY IT
STILL MATTERS, AND THE NEED FOR CONSILIENCE” Markus
Heilig, James Mackillop, Diana Martinez (2021)

Abstract

Heilig and his team (2021) jump back into the debate over whether addiction counts as a
brain disease, especially in light of new critics who push back against seeing addiction only
through a biological lens. They admit the brain disease model has helped fight stigma and
push for treatments grounded in evidence, but critics say it’s too narrow—too focused on
biology, and not enough on the social and environmental pieces. So, the authors dig into the
research. They argue that, despite its flaws, the neurobiology behind addiction holds up, both
scientifically and clinically. They point to specific, measurable changes in brain circuits—
especially in the fronto-striatal and limbic systems—areas that handle motivation, rewards,
self-control, and decision-making. But they don’t stop there. Heilig and colleagues make it
clear: calling addiction a brain disorder doesn’t mean we can ignore the psychological, social,
or cultural forces at play. These factors shape and reshape the brain’s own wiring. They also
address a few common misunderstandings. Just because some people recover on their own,
that doesn’t mean addiction isn’t a disease. And showing that people with addiction can still
make some choices doesn’t mean their brains aren’t affected.

In their view, addiction isn’t set in stone. It’s not strictly determined, but shaped by a mix of
neural and behavioural systems working together, sometimes unpredictably. To really move
the field forward, the authors call for a big-picture approach—one that brings together
neuroscience, psychology, genetics, clinical work, and the social sciences. Their updated
model doesn’t box addiction into one corner. Instead, it connects the biology to the lived
experience, showing addiction as a complicated brain-based condition, always shaped by
human context and experience.
PAPER 5: “ADDICTION FROM A PSYCHOLOGICAL
PERSPECTIVE.” American Journal of Psychology and Brain Studies
Manseur, N. (2025).

Abstract

Manseur (2025) doesn’t just see addiction as a string of bad habits or simple substance
misuse. He digs deeper, treating it like a complex psychological disorder that shapes how
people think, feel, and act. His paper zeroes in on the mental, cognitive, and social forces
behind addiction, showing how these interact with both biology and the environment. He
draws a clear line between chemical addictions—think alcohol, nicotine, opioids—and
behavioural addictions like gambling or compulsive internet use. Both types share the same
psychological hallmarks: compulsion, loss of control, and a stubborn persistence even when
people know it’s hurting them. Manseur identifies several big psychological risk factors.
Impulsivity stands out, along with low self-esteem, weak coping skills, emotional instability,
and a history of stress or trauma. To make sense of addiction, he weaves together a range of
psychological theories. Behavioural theory frames addiction as something learned through
reinforcement and reward. Cognitive theory focuses on warped thinking and twisted beliefs.
Psychoanalytic theory looks at old, unresolved conflicts and emotional deprivation at a
deeper, unconscious level. Neurological theory brings the brain into the picture, pointing to
dopamine-fuelled changes in the reward system.

The paper doesn’t stop there. Manseur explores what addiction actually does to people: mood
swings, slipping cognitive abilities, pulling away from friends and family, and even losing a
sense of self. When it comes to treatment, he highlights what works—evidence-based
approaches like Cognitive Behavioural Therapy (CBT), motivational interviewing, family
and group therapy, plus medication when needed. Prevention matters just as much: early
intervention, teaching kids in schools, and building up community resilience all help lower
the risk. In the end, Manseur paints addiction as a tangled psychological and social problem.
Tackling it takes a full-spectrum approach—neuroscience, psychology, and community
support all working together. That’s the path to real recovery and lasting prevention.
PAPER 6: “ADDICTION, ATTACHMENT, AND THE BRAIN: A
FOCUSED REVIEW OF EMPIRICAL FINDINGS AND FUTURE
DIRECTIONS HUMAN” Friedrich Unterrainer (2025)

Abstract

In this focused review, Unterrainer (2025) combines a variety of perspectives from

developmental neuroscience, attachment theory, and psychodynamic psychotherapy to depict
substance abuse disorder as a problem that comes from the trauma of early relationships and
broken attachments. The author brings together empirical data indicating that insecure and
disorganized attachment styles are closely related to emotional regulation problems, lack of
self-awareness, and changes in neural functioning within important brain networks—such as
the insular cortex, default mode network (DMN), and salience network—author's drawing
upon the neuro-evolutionary framework. The author's main point here is that the biological
and emotional systems which support attachment—like the SEEKING and CARE circuits—
overlap with the neural substrates of reward and addiction. Neuroimaging as well as
behavioural research on individuals suffering from poly-drug use disorder (PUD) detect the
presence of unusual structural changes in the brains, the absence of oxytocin's action on
attachment cues, and the disintegration of communication among the brain areas that control
emotional and social cognition. A clinical case study demonstrates that the synergistic effect
of EEG neurofeedback and psychodynamic psychotherapy is promising with regard to the
treatment of depression and psychophysiological regulation. The review portrays addiction as
a breakdown of emotional and relational processing, an attempt to make up for the lack of
early attachment experiences. One of the proposed research directions is to conduct long-term
studies with neuroimaging to look at the neuroplasticity of attachment-based interventions
and the creation of integrative neuropsychodynamic treatment models that will tackle the
relational and neural aspects of addiction recovery
PAPER 7: “ADDICTION AND ITS EFFECT ON THE BRAIN: A
REVIEW OF STRUCTURAL AND FUNCTIONAL ALTERATIONS IN
THE HUMAN BRAIN” Dabosmita Parial (2025)

Abstract

The paper by Parial (2025) presents a comprehensive review of literature that discusses the
human brain's structural and functional changes, which are consequences of both substance
and behavioural addictions. The writer elucidates the concept of chronic addictive behaviours
resulting in long-lasting impairments in brain areas responsible for impulse control,
emotional regulation, attention, and decision-making, based on the evidence from
neuroimaging and neuropsychological studies. A comparison of the results of various studies
shows that a significant decline in gray matter (GMD) and white matter density (WMD)
occurs in the prefrontal cortex and the blood flow to the dorsolateral prefrontal cortex
(DLPFC) gets decreased. Heavy alcohol or marijuana intake among adolescents was found to
be associated with the smaller size of the hippocampus and prefrontal regions, which in turn
relate to the memory and executive functioning deficits. The use of functional MRI brings to
light the reduced activation of crucial cortical areas such as the orbitofrontal cortex (OFC)
and anterior cingulate cortex (ACC), which co-relates to the disrupted inhibitory and
emotional control. The same type of changes was noted in behavioural addictions, including
gambling, pornography, and Internet Gaming Disorder (IGD) with one study noting
decreased gray matter associated with decision-making and another one reporting increased
activation of the caudate nucleus—both indicating neural overactivity as a response. The
review indicated that the evidence from different researchers strengthens the argument that
addiction, whether it is connected to a drug or a behaviour, creates measurable and sometimes
very long-lasting alterations in the connections made by the brain in self-regulation and
reward. The author suggests that the current use of neuroimaging techniques in addiction
studies is a significant step towards providing therapies that will target the neurocognitive
effects of addiction and hence mitigate their impact on the cognitive functioning of
individuals.
PAPER 8: “THE EFFECTS OF DIGITAL ADDICTION ON BRAIN
FUNCTION AND STRUCTURE OF CHILDREN AND ADOLESCENTS:
A SCOPING REVIEW” Keya Ding, Yining Shen [Link] (2023)

Abstract
This scoping review investigates the impact of digital addiction, which refers to the excessive
use of smartphones, the internet, and gaming, on the structure and function of the developing
brain in children and adolescents. By combining data from neuroimaging,
neuropsychological, and behavioral studies, the review points out the existence of alterations
in the brain regions that are responsible for processing rewards, controlling one's actions and
emotions, and so forth. The application of functional MRI and diffusion tensor imaging (DTI)
has shown that there is a decline in the integrity of the white matter tracts that are linking the
prefrontal cortex, the anterior cingulate cortex, and the striatal areas, which means there is a
connectivity impairment in the circuits that are controlling attention and impulse as well.
Besides that, structural changes consist of a reduction in the volume of the gray matter in the
dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC), which is
accompanied by the abnormal activation in the insula and limbic system, the latter being the
case of substance use disorders as well. Adding to this, the neurofunctional findings further
illustrate the situation through increased activity in the nucleus accumbens and amygdala
when digital stimuli are presented, which in turn reinforces the compulsive engagement and
seeking of reward behavior. These changes in neurobiology, taken together, are associated
with cognitive impairments, less effective emotional regulation, and higher impulsivity. One
major point being made by the review is that the developing brain is particularly susceptible
to the consequences of digital overuse, and the authors advocate longitudinal studies to
uncover the nature of the relationship and whether it is reversible. Moreover, in addition to
that, those researchers recommend having prevention programs in place that will involve
neuroeducation and family-centered strategies, along with behavioral therapy, to lessen the
impact of digital addiction on the neurocognitive development of the young population.
PAPER 9: “EFFECTS OF INTERNET AND SMARTPHONE
ADDICTION ON COGNITIVE CONTROL IN ADOLESCENTS AND
YOUNG ADULTS: A SYSTEMATIC REVIEW OF FMRI STUDIES” M.
Leon Mendezai. Padron (2024)

Abstract

The current document provides a great evaluation of the data coming from the fMRI studies
on the neurocognitive impact of IA and smartphone addiction among young people. By
applying the PRISMA method, 21 studies published in the period of 2013-2023 were chosen
to investigate brain changes linked to cognitive control and reward processing. The results
show a strong relationship between IA and SPA and a major setback in the performance of
the neural networks responsible for executive functions and emotional regulation, especially
in the areas of the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC),
insula, amygdala, and parietal regions. Youngsters and young adults with IA had their
functional connectivity within the frontoparietal and cortico-subcortical circuits reduced,
along with the activity in the ACC and mPFC, which suggests less inhibitory control and an
impaired decision-making process. In a similar way, altered amygdala connectivity patterns
were detected, indicating emotional dysregulation and diminishing reward sensitivity. In one
area, task-related fMRI studies pointed to difficulties with response inhibition, risk
evaluation, and executive flexibility, while resting-state analyses brought to the surface
abnormal functional connectivity across cognitive control and default mode networks.
Although IA and SPA have common neuroanatomical correlates, current evidence does not
yet give any indications to clearly differentiate their effects on cognition. The review
emphasizes the prefrontal-limbic circuitry as the main mechanism behind the development of
addictions and urges for longitudinal, standardized neuroimaging studies to map out where
causal mechanisms and possible interventions lie more precisely. Understanding the neural
underpinnings of IA and SPA is essential for addressing their cognitive and psychological
impact on developing brains.
PAPER 10: “THE IMPACT OF ADDICTION ON THE BRAIN’S
REWARD CIRCUITRY, AND HOW THIS AFFECTS THE
MOTIVATION AND DECISION-MAKING PROCESSES: A REVIEW”
Rokaia Walid (2025)

Abstract

The paper investigates the neurobiological and psychological mechanisms of addiction,

particularly focusing on the impact of changes in the reward system of the brain on
motivation and decision-making. A comprehensive PRISMA methodology was used to
review articles from the literature published between 2014 and 2024 from databases like
PubMed, PsycINFO, and Google Scholar. The addiction is viewed as a long-term
neurobiological disorder that is characterized by the disruption of the mesocorticolimbic
dopamine pathway, which includes major areas such as the ventral tegmental area (VTA),
nucleus accumbens (NAc), prefrontal cortex (PFC), amygdala, and hippocampus. The review
points to dopamine as the most important factor in reward processing and reinforcement of
behaviours, followed by the use of substances. Substance users undergo a process of
maladaptive neuroplasticity which is characterized by heightened cravings, poor impulse
control, and lower sensitivity to natural rewards. All these neuroadaptations affect the PFC
and disrupt the decision-making circuits leading to more impulsive decisions and preference
for instant rewards over delayed ones which can be explained by the concept of delay
discounting. Furthermore, emotional instability and stress make these deficits even more
serious while environmental and social factors help to keep the addiction alive by reinforcing
compulsive behaviour. The results emphasize that the process of addiction goes through the
clearly defined stages—from trying the substance to becoming dependent—intertwined with
changes in the structure and function of the brain that continue to reinforce the negative
motivation patterns. The paper merges the neurobiological understanding with psychological
models and points to the necessity of comprehensive therapies that consider and work on both
cognitive control and the reward system's restoration. Ultimately, the paper emphasizes the
interplay between brain, behaviour, and environment in sustaining addiction and shaping
recovery pathways.
PAPER 11: “BRAIN AND SMARTPHONE ADDICTION: A
SYSTEMATIC REVIEW” C. Anbumalar And [Link] Sahayam (2024)

Abstract

This systematic review is an attempt to map out the neurofunctional correlates of smartphone
addiction with a particular emphasis on brain activation patterns and structural alterations
which are linked to the abusive use of mobile phones (PSU). A thorough search through
several databases, namely PubMed, Science Direct, Taylor & Francis, and Springer Link, led
to the identification of a total of 83 papers that satisfied the inclusion criteria of being
published in the years between 2012 and 2023, following the PRISMA guidelines. Out of the
initial pool comprising 28,896 records, 7 empirical studies were those that included
neuroimaging methods such as fMRI, EEG, and MRI for the evaluation of neural activity,
connectivity, and morphology respectively in individuals with PSU. Smartphone addiction
has been consistently linked across studies to the phenomenon of diminished cortical
activation and the reduced functional connectivity in prefrontal and temporal areas of the
brain—together defined as the main area of the brain for executive function, creativity, and
impulse control. Research has pointed to the anterior cingulate gyrus, fusiform gyrus, lateral
orbitofrontal cortex (OFC), and dorsolateral prefrontal cortex (DLPFC) as the sites for certain
abnormalities in brain structure and function that are reminiscent of the aforementioned
disruptions in emotional regulation, decision-making, and cognitive flexibility. Moreover, the
integrity of white matter in the corpus callosum is reduced along with superior cerebellar
peduncle (SCP) volume which are both factors that may have an impact on interhemispheric
communication as well as motor coordination. A possible link is drawn between a decrease in
connectivity involving OFC, nucleus accumbens, and middle cingulate cortex as well as
alterations in the processing of the reward system, mirroring the patterns observed in
substance-based addictions. In conclusion, the outcomes of this study tell us that an excessive
use of smartphones is responsible for the changes in the neurobiological systems that are
measurable and for these changes in the systems of emotional processing, attention, and
executive control. The review highlights the urgent need for longitudinal and cross-cultural
neuroimaging research to clarify causal mechanisms and inform targeted cognitive-
behavioural and neuroregulatory interventions promoting digital well-being.
PAPER 12: “A REVIEW ON: NEUROBIOLOGY OF ADDICTION AND
DOPAMINE ROLE ON DRUG ADDICTION” Preksha P. Saparia, Akshat
H. Patel (2023)

Abstract

This review study presents the diverse impact of dopamine as the primary neurotransmitter
over all human activities, cognitive processes, and feelings. Based on the results of
neurobiological, psychological, and clinical studies, the article explains how dopamine acts as
a chemical messenger with the brain trusted to regulate reward, motivation, attention,
movement, and even moods. Dopamine mainly acts through the four main areas of the brain:
the mesolimbic, mesocortical, nigrostriatal, and tuberoinfundibular pathways, where each of
them is responsible for different behavioural and physiological functions. The mesolimbic
and mesocortical pathways which originate from the ventral tegmental area (VTA) and
project to the nucleus accumbens and prefrontal cortex respectively, are involved in the
processing of reward, reinforcement learning, and control of executive functions; thus, the
neurobiological foundation for motivation and goal-directed behaviour is formed. The
imbalance in these dopaminergic systems is associated with various neuropsychiatric
disorders such as schizophrenia, Parkinson’s disease, depression, and addiction. The
excessive activation of dopamine receptors particularly in the mesolimbic pathway, leads to
the development of compulsive behaviours and drug dependence, while the decreased
dopamine transmission causes the individual to experience inability to feel pleasure and lack
of drive. The review further highlights the interplay between dopamine and other
neurotransmitters like serotonin, GABA, and glutamate, indicating the complexity of the
chemical’s participation in the process of neural communication and emotional stability. The
point is made very clear about dopamine’s role in learning and reinforcement when it is
shown how it encodes reward prediction errors which in turn teach the organism either to
behave adaptively or maladaptively. Overall, the review underscores dopamine’s centrality in
human functioning and its dual potential to support both healthy motivation and pathological
addiction. The paper concludes by advocating for integrative research combining
neuroimaging, pharmacological, and behavioural studies to advance understanding of
dopaminergic regulation and its therapeutic implications.
PAPER 13: “THE NEUROBIOLOGY OF SUBSTANCE USE AND
ADDICTION - EVIDENCE FROM NEUROIMAGING AND
RELEVANCE TO TREATMENT” Alexandra Hayes, Katherine Herlinger
(2020)

Abstract

The present review gives an overview of the human neuroimaging evidence that supports the
understanding of the neurobiology of substance usage and addiction and discusses the
implications of the findings for treatment. The functional imaging techniques (PET, task and
resting-state fMRI, MRS, and DTI) have shed light on the alteration of neural circuits
connected with reward, inhibition, stress/negative affect, emotion, and learning/memory—
these being the very circuits that correspond to the three phases of the drug addiction cycle
(binge/intoxication; withdrawal/negative affect; preoccupation/anticipation). The authors put
together diverse findings which reveal the dysfunction in the mesocorticolimbic pathway
(ventral tegmental area → nucleus accumbens → prefrontal cortex) along with reduced
striatal activity to non-drug rewards but increased cue-reactivity to drug-related stimuli, drop
in D2 receptor availability in the striatum and underactive control of the prefrontal cortex
(OFC, ACC, DLPFC). Neuroimaging signs such as dampened ventral-striatal activation in the
course of monetary reward anticipation and insular/dorsal-striatal responses during
risk/decision tasks have been pinpointed as possible predictors of susceptibility and relapse.
Besides, the authors scan the neuroadaptations involved in tolerance, withdrawal and craving,
and the use of imaging to investigate the mechanism of treatment, such as, the ability of
naltrexone to reduce cue-induced striatal activation and the promise of DRD3 antagonists to
restore reward processing in the case of addiction. The authors underline the present
methodological difficulties (limited sample sizes, variance, ROI vs network strategies,
shortage of PET tracers), the necessity for longitudinal, multi-centre cohort studies (e.g.,
ENIGMA, IMAGEN), and the potential of network-level and preregistered studies in the
field of imaging. Clinically, the review argues for biomarker-driven, individualized treatment
strategies that combine psychosocial, pharmacological and neuromodulator approaches to
target dysregulated circuits and reduce relapse risk.
PAPER 14: “IMPACT OF DRUG ADDICTION ON MENTAL HEALTH”
Wani M.A And Sankar.R (2016)

Abstract

This empirical research delves into the correlation between drug dependence and mental
health with a specific concern to age and gender diversity among the addicts. The researchers
took a sample of 60 people (30 of them adolescents and 30 adults, gender equally divided)
and used the P.G.I. Health Questionnaire N-1 by Varma, Wing, and Pershad, to measure the
overall mental health condition. The methodology comprised conducting a two-way analysis
of variance (ANOVA) considering two independent variables—age and gender—and one
dependent variable—mental health. The findings indicated that both age and gender effects
on drug addicts' mental health were statistically significant (p < 0.01). Adult addicts and
adolescents, on the other hand, were different with respect to their mental health, where
adults were healthier implying that they might have developed greater resilience or adaptive
coping over the years with substance dependence. Likewise, female addicts showed higher
mean mental health scores than their male counterparts suggesting that the gender-based
psychological and social factors might play a role in moderating addiction-related distress.
Additionally, the interaction between age and gender turned out to be significant at the 0.05
level which indicated their combined influence on the psychological well-being. The results
validate that mental health of addicts is not the same but rather influenced by the
demographic factors, thereby necessitating the introduction of age and gender-based
rehabilitation programs. The research states that drug addiction has a debilitating effect on a
person's psychological adjustment, emotional stability, and social functioning and that there is
a need for prevention strategies directed at the vulnerable groups—especially adolescent and
male addicts—to be successful in the long run and to avoid mental health deterioration.
PAPER 15: “ADDICTION BECOMES A BRAIN DISEASE” Roy A. Wise
(2000)

Abstract

Through a comprehensive review of the literature, the author points out the major
neurobiological developments that have led to drug addiction being recognized as a chronic
brain disorder characterized by neuroadaptive transformations in the brain's reward and
motivational systems. Wise gives a summary of the research which was presented in the
workshop on The Neurobiology of Addiction held at the Juan March Foundation, indicating
how addiction research has moved from the consideration of physical withdrawal and liver
damage to that of the neural pathways responsible for reinforcement and compulsion. The
paper combines the results of neuroimaging, electrophysiology, genetics, and molecular
neuroscience, and tells the story of how addictive drugs take possession of the
mesocorticolimbic dopamine system which consists of the ventral tegmental area (VTA),
nucleus accumbens, and prefrontal cortex and was originally designed for natural rewards
like food and social interaction. It becomes evident that dopaminergic signalling is
responsible for reward prediction and motivational salience rather than simply pleasure, and
Schultz’s reward-prediction error model which shows this can be used as an example. In
addition, Robinson’s findings point out that drug effects are dependent on the environment
and context, thus setting has a very strong impact on the dopaminergic response and
sensitization. Besides, Wise proceeds to talk about the interaction between glutamate and
dopamine in the nucleus accumbens, wherein he particularly points out their contribution to
processes like conditioned reinforcement and the development of the addiction. Nestler,
White, and Caron's molecular and genetic studies provide evidence of how the process of
drug addiction is accompanied by the creation of lasting changes in gene expression (such as
ΔFosB accumulation, GluR2 upregulation, etc.) and synaptic plasticity which make the
person engage in more and more compulsive drug seeking. In the following parts, the topics
of tolerance, sensitization, and stress-induced vulnerability are discussed, illustrating the
interaction of stress and genetic factors in increasing the risk of addiction. The paper
concludes that addiction arises from maladaptive learning within neural circuits governing
motivation, reward prediction, and memory—transforming voluntary drug use into
compulsive behaviour through long-lasting neuroplasticity. This perspective firmly situates
addiction within neuroscience, redefining it as a disorder of brain circuitry rather than moral
weakness or simple behavioural choice.

PAPER 16: “THE NEUROBIOLOGY OF ADDICTION:

UNDERSTANDING THE BRAIN BASIS OF CRAVING AND RELAPSE”
Dr. Pradeep Ramchandra Pawar (2018)

Abstract

The present article reviews extensively the neurobiological mechanisms that cause craving
and relapse in addiction. It also describes how the brain's reward, stress, and memory systems
are interconnected. The paper relies on the latest neuroscientific studies to explain the way
prolonged drug use disturbs the functioning of neurons in various areas including the
mesocorticolimbic dopamine pathway consisting of the VTA, nucleus accumbens, and
prefrontal cortex, which in turn affects the processing of rewards, decision making, and
motivation. It goes on to present the three-phase model of addiction as consisting of the three
stages: binge/intoxication, during which the release of dopamine strongly supports drug-
seeking behaviour; withdrawal/negative affect, wherein the balance of dopamine, opioid, and
glutamate systems is disturbed causing the person to experience anhedonia and stress; and
preoccupation/anticipation, in which the drugs’ and the person's emotional states help to
trigger craving and relapse because they are already associated with drugs. The review sheds
light on the amygdala and hypothalamus being involved in stress responses, the hippocampus
being responsible for the drug cues’ associative memory, and the prefrontal cortex being in
charge of the lack of cognitive control. Genetic vulnerabilities, environmental pressures, and
concurrent psychiatric disorders are pointed out as main factors contributing to the addiction
risk. By combining data from neuroimaging, behaviour studies, and neurochemistry research,
the author underlines that the addicted person is kept in the loop of compulsive use due to the
harmful neuroplasticity of the reward and stress systems. In the end, the author links the
biological knowledge of addiction to psychological treatment by suggesting acceptance and
commitment therapy (ACT) that combines pharmacotherapy targeting the dopamine, opioid,
and glutamate systems with psychotherapeutic methods like cognitivist, behavioural, and
mindfulness-based therapies. A holistic, individualized approach addressing biological,
psychological, and environmental determinants is positioned as essential for effective relapse
prevention and long-term recovery.
PAPER 17: “NEUROPLASTICITY AND ADDICTION:
UNDERSTANDING BRAIN REWIRING DURING SUBSTANCE USE
AND RECOVERY” T M. Andrew Bickel (2024)

Abstract

The present study delves into the complex interplay between neuroplasticity and addiction,
and the focus is primarily on how the brain's wiring is profoundly altered during substance
addiction, and how, later on, during recovery, the same brain's ability to rewire and heal can
be utilized for further recovery. Bickel characterizes neuroplasticity as the capacity of the
brain to alter neural connections depending on the experiences and training it receives, or the
injuries it suffers, and places addiction in this context as a disorder of overreactive plasticity.
The mixed-methods strategy adopted by the researchers consists of a systematic literature
review plus an interpretation of recent neuroimaging and clinical studies. The paper illustrates
how the prolonged use of drugs impairs the functioning of the mesolimbic dopamine system
and affects the network related to the latter, whose main functions include reward,
motivation, decision-making and emotional regulation. Observations of functional MRI and
PET scans point out that the addiction process lasts for a long time, leads to the strengthening
of neural connections that sustain craving and compulsive use, and, at the same time, the
inhibition of the activities of the prefrontal brain regions which are critical for controlling
impulses and regulating oneself. Moreover, the authors emphasize that the process of
recovery involves the reversal of these maladaptive patterns by way of the processes of
neuroplastic healing. It is established by virtue of empirical research that the such methods as
cognitive-behavioural therapy (CBT), mindfulness-based interventions (MBIs),
neurofeedback, transcranial magnetic stimulation (TMS), and medication (e.g., naltrexone,
buprenorphine) not only facilitate but also participate in the activity of the prefrontal cortex
and reward circuits whereby the process of neurologic positive change is achieved. These
methods make one's emotions more manageable, lessen the recurrence of relapses, and boost
one's ability to think flexibly. However, there are limitations to neuroplastic recovery such as
structural damage which is still there, and the different individual responsiveness, and age,
addiction severity, and treatment duration are factors that will influence this. The paper
depicts neuroplasticity as a two-fold process, one being the mechanism responsible for the
development of addiction and the other the way leading to its resolution; thus, it claims that
the understanding and targeting of brain rewiring can make treatment strategies for substance
use disorders and long-term recovery support come to a new level.

PAPER 18: “DOPAMINE, BEHAVIOR, AND ADDICTION” Roy A. Wise

and Chloe J. Jordan (2021)

Abstract

This review thoroughly investigates the decisive function of dopamine in the process of
learning, motivating, and also addicting. Evidence that dopamine is critical in the
development of both reward and punishment associated behaviours is summarized by Wise
and Jordan (2021). The findings indicate that the animals deprived of dopamine manifest only
unconditioned reflexes and do not develop any goal-directed actions, which illustrates the
dependency of such learning on dopamine. Two primary modes of firing in the dopaminergic
neurons are the basis of these actions: burst-firing which allows the plasticity and long-term
potentiation (LTP) of the synapse between the glutamatergic inputs and GABAergic outputs
in the striatum and pacemaker-firing which maintains the tonic level of dopamine and
controls the motivational arousal. The review makes it clear that the motivational drive has a
U-shaped pattern in relation to dopamine levels—both the lack and the high level of
dopamine hinder the goal-directed behaviour. The authors also discuss the methods by which
addictive drugs take advantage of these neural circuits. Stimulants like amphetamine and
cocaine markedly augment the release of dopamine and their reinforcing effects are clearly
dependent on dopamine, whereas to a lower extent, opiates, nicotine, and alcohol are
regarded as moderately dependent, and cannabinoids, benzodiazepines, barbiturates, and
caffeine show more varied or weaker associations. Dopamine's contribution goes beyond
merely the processing of reward to the forecasting and waiting of results which accounts for
how the environmental signals that are related to drugs can both activate craving and turn into
a source of discomfort in certain settings. All in all, the paper points out that nearly every
learned motivated behaviour relies on dopaminergic signalling and that contrasting how
various addictive substances manipulate dopamine-dependent plasticity could lead to a better
comprehension of the neurobiological basis of addiction.
PAPER 19: “ADDICTION” Terry E. Robinson Andkent C. Berridge (2003)

Abstract

Robinson and Berridge (2003) thoroughly discuss the phenomenon of addictive substances
that make the unaware user move from voluntary smoking to the compulsive one through
these very changes in their brain and mind. They consider the interplay between four primary
theoretical approaches: (1) the classic pleasure-withdrawal (opponent process) model, which
claims that addiction is due to the alternating phases of high and low feelings; (2) drug-made
learning theories, which propose that drugs make the user form the wrong kinds of stimulus-
response or stimulus-stimulus connections; (3) their own incentive-sensitization theory,
which claims that the repeated use of a drug leads to the sensitization of the mesolimbic
dopamine systems responsible for assigning "incentive salience" to drug-related cues; hence a
very strong "wanting" arises that can be separated from "liking"; and (4) frontal cortical
dysfunction models, which underline impairments in decision-making and lack of inhibitory
control. The authors support the idea that the incentive-sensitization model is the most valid
one in explaining the persistence and relapse in addiction, as it happens through the
incorporation of sensitized dopamine and glutamate circuits in the nucleus accumbens and
prefrontal cortex that become hyper-reactive to drugs or drug-related stimuli. These changes,
reinforced by context and learning, create an overwhelming urge for the drug even after the
cessation of withdrawal symptoms. The review provides a synthesis of neurobiological,
behavioural, and psychological evidence, arriving at the conclusion that the pathological
enhancement of incentive motivation, not hedonistic pleasure or habit learning alone, is the
driving force behind addiction.
PAPER 20: “THE PSYCHOLOGICAL SCIENCE OF ADDICTION”
Elizabeth Gifford & Keith Humphrey (2007)

Abstract

Gifford and Humphreys (2007) thoroughly describe the role of psychological science in
addiction understanding and treatment considering behavioural, social, neurobiological, and
clinical applied aspects. The authors claim that addiction is a process of dynamic interaction
between humans and their environment, and hence the focus of the understanding should not
shift purely to the physiological or the intrapersonal side of the matter. The authors also
present the role of psychology in integrating various levels of analysis including laboratory
research on conditioning and reinforcement to practical work in treatment and prevention.
The main issues are the necessity of motivation, learning, and social context in developing or
changing addicted behaviours. Behavioural and economic models show how reinforcement
processes determine substance use, while cognitive-behavioural theories account for the
persistence of non-adaptive habits. Besides, the psychological aspect is made very visible in
the review of its support in the neuroscientific study of addiction, especially in the case of the
understanding of how learned associations and stress-related neuroadaptations in
dopaminergic and prefrontal circuits influence craving, relapse, and inhibitory control. The
authors push for a "functional" approach that ties together theory and practice, linking
disciplines by integrating findings to increase the effectiveness and publication of treatments.
Over the years, psychology has been criticized for its strengths as well as weaknesses,
particularly in the area of the overemphasis of intrapersonal variables and the consequent
neglect of social or contextual influences. To sum up, the authors claim that the psychological
science—the study of the individual in context—will always be the unique proponent of a
multi-dimensional, progressive, and pragmatic addiction-related understanding, which is
important in times of crisis.
SUMMARY

The literature review regarding addiction's effects on the brain has concluded that addiction is
not merely a problem of behaviour or a matter of morality; rather, it is a complicated
neuropsychological disorder that develops from brain modifications influencing cognitive,
emotional, motivational, and decision-making processes. One of the main points across the
studies is that pioneering substances and actions disturb the mesocorticolimbic dopamine
system, which comprises the ventral tegmental area (VTA), nucleus accumbens (NAc), and
prefrontal cortex (PFC). The disruption brings about the phenomenon of high dopamine
liberation, skewed reward processing, and the addiction of one being drug-dependent
(Volkow & Koob, 2015; Wise & Jordan, 2021). In the course of withdrawal, tempering
occurs, innate rewards are, so to speak, deprived of their attractiveness, and cues in the
environment take up strong roles as craving and relapse triggers.

Neuroimaging studies (Volkow et al., 2003; Hayes & Herlinger, 2020) have revealed that
long-term substance use impacts not only the structure but also the functioning of the brain.
Among the effects of chronic substance use are; shrinkage of gray and white matter in the
prefrontal cortex, depletion of D2 receptors in the striatum, and disruption of communication
between the cognitive control and emotional regulation areas. With such neural plasticity
come the consequences of less inhibition, bad choices, and even more stress (Goldstein &
Volkow, 2011; Koob & Le Moal, 2008). In addition, both chemical and behavioural
addictions, among which are smartphone and internet addiction, are characterized by similar
neurofunctional traits—most importantly, Decreased Activation of Prefrontal Regions and
Over-activation of Reward-Related Areas such as the Amygdala and Nucleus Accumbens
(Parial, 2025; Anbumalar & Sahayam, 2024).

Theoretical viewpoints are also in agreement with the idea that learning and memory systems
play a significant role in the perpetuation of addiction. Robinson and Berridge’s (2003)
incentive-sensitization theory explains how repeated drug exposure sensitizes dopamine
circuits, producing strong “wanting” without necessarily increasing “liking.” In the same
way, stress-based models point out that using drugs over a long time period switches on the
brain’s antireward systems and negative emotions become the main reason for keeping drug
use (Koob & Le Moal, 2008). Psychological models, such as cognitive-behavioural and
attachment theories, support this viewpoint by arguing that emotional dysregulation,
impulsivity, and early attachment disruptions are causes of addiction and relapse
(Unterrainer, 2025; Manseur, 2025).

Neuroplasticity—the brain’s ability to change—has been recognized as both a factor and a

possible healing path by the latest studies. Cognitive Behavioural Therapy (CBT),
mindfulness-based therapies, neurofeedback, and transcranial magnetic stimulation (TMS)
are all examples of interventions that can help restore prefrontal regulation and thus rebalance
the reward system (Bickel, 2024). Overall, these studies point out that addiction is a complex
condition with the underlying causes being continuously interplay of biological,
psychological, and social factors over time.
CONCLUSION

In conclusion, the body of research reviewed demonstrates that addiction profoundly alters
the brain’s structure and function, affecting motivation, reward processing, stress response,
and executive control. These neurobiological changes explain why addicted individuals
struggle to regulate behaviour even when aware of the harm. However, understanding
addiction purely as a brain disease is incomplete; it is equally a psychological and social
phenomenon. Environmental context, learned associations, emotional regulation, and
attachment history all shape how addiction develops and persists (Gifford & Humphreys,
2007; Heilig et al., 2021).

The evidence supports a biopsychosocial model, recognizing addiction as a disorder of both

brain and behaviours. This integrated approach encourages treatment strategies that target
neural dysfunctions—through medication or neurostimulation—alongside behavioural
therapies that rebuild coping skills, cognitive flexibility, and social connection. Prevention
efforts should also focus on early education, emotional resilience, and family-based
interventions to mitigate risk factors in vulnerable populations.

Ultimately, addiction is a manifestation of the brain’s capacity for maladaptive learning and
plasticity, but that same plasticity offers hope for recovery. With sustained support, therapy,
and social rehabilitation, the brain can rewire itself toward healthier functioning. The ongoing
synthesis of neuroscience and psychology thus provides a deeper, more compassionate
understanding of addiction—not as moral failure, but as a reversible disorder of motivation,
control, and connection.
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