Index

Sr Topic Page
No. no.
1 Introduction 1

2 Types of Drugs 2-3

3 Diseases related to drugs and their symptoms 4-7

4 Effect of alcohol, cannabis, LSD, and heroin on neurotransmission 8-11

and the process explained
5 Adverse effects and withdrawal symptoms of alcohol, cannabis, and 12-15
heroin, hallucinogens
6 Rehabilitation from alcohol, cannabis, heroin, and hallucinogen 16-18

7 Summary 19

8 Bibliography 20

Introduction
Recreational drug use is a widespread phenomenon that significantly impacts
public health and society. These substances, ranging from cannabis to cocaine to
MDMA, exert profound effects on the brain's neurotransmission processes.
Neurotransmitters are chemicals that facilitate communication between neurons,
influencing everything from mood and cognition to behavior and physiological
functions. By altering neurotransmitter activity, recreational drugs can induce
various short-term pleasurable effects and potentially long-term detrimental
consequences.
The interaction between recreational drugs and neurotransmission involves
complex mechanisms that can either mimic, enhance, or inhibit the action of
natural neurotransmitters. For instance, drugs like cannabis mimic
endocannabinoids, while substances like cocaine inhibit the reabsorption of
dopamine, serotonin, and norepinephrine, leading to increased levels of these
neurotransmitters in the brain. These alterations can result in euphoria,
heightened alertness, and altered sensory perceptions. However, the same
mechanisms that produce these effects can also lead to dependency, cognitive
deficits, and severe mental health issues with prolonged use.
Understanding the effects of recreational drugs on neurotransmission is crucial
for several reasons. It provides insights into the biological underpinnings of
addiction and substance abuse, informing the development of effective
treatments and interventions. Additionally, this knowledge can guide public
health policies and educational programs aimed at preventing drug abuse and
diminishing its consequences. This report delves into the specific effects of
various common recreational drugs, most widely used in India, on
neurotransmission, exploring their mechanisms of action and the short- and
long-term impacts on the brain and behavior. These drugs include alcohol,
cannabis, heroin, and LSD or hallucinogens.

Types of drugs:
 Depressants: These are drugs that slow or depress the functions of the
central nervous system and brain. Depressants attach to the brain’s
neurotransmitters and increase levels of gamma-aminobutyric acid
(GABA). When GABA levels increase, nerve cell signals are suppressed,
leading to a sense of deep relaxation. Examples of depressants
include alcohol, benzodiazepines, barbiturates, and hypnotics.

 Opioids: Drugs that are used to suppress physical pain are called
analgesics or opioids. Some opioids are naturally derived, such as the
poppy plant, while others are lab-created like fentanyl, oxycodone,
hydrocodone, etc. Opioids work by attaching to the opioid receptors in
 the brain, which then block pain signals from the nervous system.
Examples of opioids include heroin,
morphine, fentanyl, oxycodone, hydrocodone, and hydromorphone.

 Hallucinogens: Drugs that alter consciousness or the perception of

reality are called hallucinogens. These substances, sometimes called
psychedelics, can be naturally derived, such as certain plants or
mushrooms or lab-created. The psychoactive effects can include
detachment from reality, hallucinations, paranoia, violent behaviours,
distorted perceptions, euphoria, agitation, and fear. Examples of
hallucinogens include lysergic acid diethylamide (LSD), phencyclidine
(PCP), ketamine, mescaline, psilocybin, and high-potency cannabis.

Diseases related to drugs and their

symptoms:
1. Substance use disorder (SUD)
Definition:
Substance Use Disorder is a condition in which the use of one or more
substances leads to a clinically significant impairment or distress. This disorder
encompasses a range of substances including alcohol, cannabis, opioids, and
other drugs.
Symptoms:
 Craving for the substance
 Difficulty controlling its use
 Neglecting responsibilities at work, school, or home
 Continued use despite social or interpersonal problems
 Withdrawal symptoms when not using
 Tolerance (needing more of the substance for the same effect)
 Spending a lot of time obtaining, using, or recovering from the substance
 Giving up important activities in favor of substance use
 Using the substance in hazardous situations or manner

2. Alcohol use disorder (AUD)

Definition:
Alcohol Use Disorder is a chronic disease characterized by an inability to
control alcohol consumption despite adverse social, occupational, or health
consequences.
Symptoms:
 Craving for alcohol
 Inability to limit drinking
 Spending a lot of time drinking or recovering from drinking
 Neglecting responsibilities
 Continued use despite social or interpersonal problems
 Giving up important activities
 Using alcohol in hazardous situations
 Tolerance
 Withdrawal symptoms (e.g., shaking, sweating, nausea, seizures,
hallucinations)
 Persistent desire or unsuccessful attempts to cut down or control alcohol
use
 Continued use despite physical or psychological problems
3. Cannabis use disorder
Definition:
Cannabis Use Disorder is characterized by a problematic pattern of cannabis use
leading to significant impairment or distress.
Symptoms:
 Craving for cannabis
 Increased tolerance
 Withdrawal symptoms (e.g., irritability, sleep difficulties, decreased
appetite, anxiety)
 Using more cannabis than intended
 Inability to cut down or control use
 Spending a lot of time obtaining, using, or recovering from cannabis
 Giving up important activities
 Continued use despite social or interpersonal problems
 Neglecting responsibilities
 Using cannabis in hazardous situations

4. Opioid use disorder

Definition:
Opioid Use Disorder is characterized by a problematic pattern of opioid use that
leads to significant impairment or distress.
Symptoms:
 Intense cravings for opioids
 Inability to control or reduce use
 Tolerance
 Withdrawal symptoms (e.g., muscle pain, sweating, agitation, insomnia)
 Spending a lot of time obtaining, using, or recovering from opioids
 Neglecting responsibilities
 Continued use despite physical or psychological problems
 Using opioids in hazardous situations
 Giving up important activities

5. Hallucinogen use disorder

Definition:
Hallucinogen Use Disorder is characterized by a problematic pattern of
hallucinogen use leading to significant impairment or distress.
Symptoms:
 Taking larger amounts of hallucinogens or using them for a longer period
than intended
 Unsuccessful effort to cut down or control hallucinogen use
 Spending a great deal of time obtaining, using, or recovering from the
effects of hallucinogens
 Craving to use hallucinogens
 Recurrent hallucinogen use failing to fulfill major role obligations at
work, school, or home
 Important social, occupational, or recreational activities are given up or
reduced because of hallucinogen use
 Recurrent hallucinogen usage in situations where it is physically
hazardous
 Hallucinogen use is continued despite knowledge of having a persistent
or recurrent physical or psychological problem
 Tolerance

Effect of alcohol, cannabis, LSD, and

heroin on Neurotransmission and the
process Explained
1. Heroin: It acts on opioid receptors: Miu (µ), Kappa (k), and Delta (δ).
MORs—mu-opioid receptors are in the cerebral cortex, thalamus,
accumbens nucleus (part of the forebrain). The activation of the MOR
produces supraspinal and spinal analgesia (painlessness), increased
prolactin release, respiratory depression, decreased gastrointestinal
motility, sedation, miosis, euphoria (by binding of endorphins), drug
dependence (by repetitive triggering euphoria and stimulus), and
immunosuppression. By the time the addictive behavior develops, poor
decision-making and impaired cognition shift away from goal-oriented
behaviors and lead to compulsive drug use. KORs—kappa opioid
receptors—are in the hypothalamus and bind to dynorphins and trigger
dysphoric and sedative effects, which can trigger anti-reward effects
(dysphoria). KOR activation reduces dopamine release. DORs—delta-
opioid receptors—are in the basal ganglia. These opioid receptors bind to
encephalins and induce anxiolytic (anti-anxiety) effects.
 HEROIN

2. Alcohol: It is a CNS depressant that manifests its effects by its action on

the GABAergic, opioidergic, dopaminergic, and serotonergic systems,
generating inhibition in the CNS, manifested as sedation, loss of
inhibition, and relaxation. The sedative effects of alcohol can be
explained by drastically enhancing GABAergic neurotransmission and
inhibiting the excitatory N-methyl-D-aspartate or NMDA receptors.
Acting on the µ receptor (as seen in Heroin) induces effects such as
pleasure, satisfaction, and increased interest in alcohol consumption. A
meta-analysis study assessing the dose-response effect of alcohol on
blood pressure resulted in a finding that acute alcohol consumption leads
to a decrease in blood pressure, an effect that usually lasts up to 12 hours.
The possible explanation for this effect is the increase of vasodilation
induced through NO, CH3CHO, and insulin-increased production. High
doses of alcohol could lead to the reduction of a vasoconstrictor that
inhibits sodium reabsorption in the proximal and distal tubules of the
kidney.
 Whiskey
3. Tryptamines: They are tryptamine hallucinogens, the most popular being
LSD—lysergic acid diethylamine, and include monoamine alkaloids that
act on the 5HT2A receptor and inhibit serotonin reuptake. Although
studies have demonstrated the potential therapeutic use of classic
serotoninergic psychedelics in mood disorders and depressive symptoms,
adverse effects need to be considered. Other hallucinogenic drugs, such
as LSD, act by binding strongly to human serotonin receptors, dopamine
receptors, and adrenergic receptors generating hypertension, heart rhythm
disorders, severe hyperthermia, convulsions, visual disturbances,
synaesthesia, extreme mood disorders, depersonalization, disorders of
perception of time and space.

4. Cannabis: It is a complex drug that can depress, excite, and impair the
central nervous system, therefore having a distinctive pharmaco-
toxicological profile. This contains various chemical compounds, with the
most notable one being δ -9-tetrahydrocannabinol or THC. Cannabis
manifests its psychoactive effects, such as euphoria and relaxation, by
acting on the endocannabinoid system, i.e. the CB1/CB2 cannabinoid
receptors. The repetitive use of cannabis can be attributed to the
 interaction between THC and CB1 receptors situated on inhibitory
GABAergic interneurons in the reward pathway. This interaction results
in a reduction in the release of GABA, leading to the disinhibition of
dopaminergic neurons. Consequently, there is an elevation in dopamine
levels, like the effects observed with opioid drugs of abuse.
Synthetic cannabinoids: This represents a class of substances of abuse
that mimic the effects of cannabis and are included in the complex group
of new psychoactive substances. Their mechanism of action can be
explained by the action of the cannabinoid system, CB1/CB2 receptors.
Synthetic cannabinoids activate CB1 receptors which lower cellular
cAMP and thus elicit cannabimimetic responses. They induce THC-like
effects but have stronger and longer-lasting effects. Synthetic
cannabinoids cause agitation, irritability, confusion, hallucinations,
delusions, and psychosis.

Adverse effects and withdrawal

symptoms of alcohol, cannabis, and
heroin, hallucinogens
1. Heroin
Adverse Effects:
 Acute intoxication with opioids manifests through a diverse array of
symptoms and effects on the body. Individuals exhibit sedation, a state of
drowsiness, and reduced arousal.
 Nausea and vomiting contribute to feelings of discomfort and
gastrointestinal distress.
 Dizziness and euphoria can appear. This pleasurable sensation contributes
to the addictive potential of these substances.
  Pruritus and flushing can be observed along with constipation, and
opioids’ ability to slow down intestinal motility. Bradycardia and
hypothermia also occur.
 Miosis is a classic sign of opioid intoxication and can aid in recognizing
opioid overdose. The most critical and potentially life-threatening effect
of opioid intoxication is respiratory depression. Opioids suppress the
CNS, including the respiratory centres in the brain, leading to slowed and
shallow breathing. Severe respiratory depression can result in respiratory
arrest and can be fatal if not promptly addressed.
Withdrawal Symptoms:
o Flu-like symptoms (e.g., muscle aches, sweating, chills)
o Anxiety and restlessness
o Irritability
o Insomnia
o Dilated pupils
o Nausea, vomiting, diarrhea
o Yawning
o Drug cravings
These symptoms can be severe and may lead to relapse if not managed properly.
2. Alcohol
Adverse Effects:
 When individuals consume alcohol in excessive amounts, they experience
a range of symptoms: mild visual disturbances leading to impaired vision,
blurring, difficulty in focusing, and altered perception of the surrounding
environment.
 Euphoria can contribute to a sense of relaxation, lowered inhibitions, and
increased sociability. Tachycardia, irregular heartbeat, and palpitations
also occur.
 Due to alcohol’s vasodilatory effects, which cause blood vessels to
expand, resulting in heat dissipation, increased body heat and a feeling of
warmth.
 Gastrointestinal effects are nausea and vomiting. In extreme cases,
alcohol poisoning can lead to respiratory arrest and heart failure, posing
significant risks to an individual’s life.
Withdrawal Symptoms:
o Tremors (shakes)
o Anxiety
o Nausea and vomiting
 o Headache
o Insomnia
o Sweating
o Elevated heart rate and blood pressure
o Hallucinations (visual/auditory/tactile)
o Seizures (in severe cases)
o Delirium tremens (DTs) characterized by confusion, hallucinations,
agitation, and autonomic instability
3. Cannabis and synthetic cannabinoids
Adverse Effects:

 Acute cannabis intoxication includes euphoria and disinhibition, injected

eyes, mydriasis, mild blood sugar extremities, fine tremors, impaired
thinking and concentration, obsessions, delusions and hallucinations,
delirium, panic, psychosis, lack of coordination, disorganized thinking,
tachycardia, and orthostatic hypotension. The severity of these acute
symptoms depends on the administration route, intravenous
administration of THC leading to more severe symptoms than inhaled
administration, but on the administered dose as well.
 Individuals who experience acute intoxication with synthetic
cannabinoids exhibit vomiting, convulsions and tremors can occur. These
involuntary muscle movements and shaking can be alarming and indicate
a significant neurological impact. Behavioral changes manifest as
aggression and agitation. This altered state of mind can lead to
unpredictable and potentially dangerous actions along with slurred
speech. High blood pressure contributes to cardiovascular stress and
potentially leads to complications if not addressed promptly. Respiratory
symptoms, such as wheezing and shortness of breath also occur.

Withdrawal Symptoms:
o Irritability
o Anxiety
o Insomnia
o Decreased appetite
o Restlessness
o Depressed mood
o Physical discomfort (e.g., abdominal pain, headache)
o Vivid dreams or nightmares
o These symptoms are typically milder compared to those of other
substances but can still be distressing for some individuals.
 4. Tryptamine hallucinogens (LSD)
Adverse Effects:
 Acute intoxication with tryptamines can result in affected perception,
cognition, and physiological functions. Individuals experiencing
tryptamine intoxication may encounter visual hallucinations, de-
personalization, and alterations in sensory perception.
 In addition to perceptual effects, acute tryptamine intoxication can lead to
various physiological symptoms. Anxiety, increased blood pressure,
headaches, and nausea, often accompanied by a feeling of queasiness or
the urge to vomit are observed.
 A meta-analysis study analyzed the post-acute psychological effects of
psychedelics, and no evidence that these increase the risk for adverse
effects was obtained. The use of hallucinogens can trigger episodes of
schizophrenia and lead to profound alteration of the consumer’s behavior.
 In addition, the consumer’s behavior can present physical and mental
decline while presenting social implications, tachycardia, loneliness, fear,
suicidal tendencies, mydriasis, hypertension, hyperthermia, tachycardia,
piloerection, hyperreflexia, panic attacks, psychotic states, and
flashbacks.
Withdrawal Symptoms:
o Depression
o Anxiety
o Irritability
o Fatigue
o Sleep disturbances
o Cognitive issues
o Craving
o Mood swings
o Paranoia
o Memory problems
o Increased sensitivity to sensory input
o Nightmares or vivid dreams
o Reduced appetite
o Anhedonia (inability to feel pleasure)
o Emotional instability

Rehabilitation from alcohol, cannabis,

heroin, and hallucinogen
1. Alcohol Use Disorder (AUD)
Medications:
 Acamprosate helps reduce cravings and withdrawal symptoms.
 Disulfiram creates unpleasant effects when alcohol is consumed, acting as
a deterrent.
 Naltrexone blocks the euphoric effects of alcohol and reduces cravings.
Psychotherapeutic Methods:
 Cognitive Behavioral Therapy (CBT): Helps individuals recognize and
change problematic patterns of thinking and behavior related to alcohol
use.
 Motivational Interviewing (MI): A client-centered approach that helps
individuals resolve ambivalence about changing their alcohol use
behavior.
 12-Step Facilitation Therapy: Based on the principles of Alcoholics
Anonymous, it encourages engagement with a support group and
adherence to its principles.

2. Cannabis Use Disorder (CUD)

Medications:
There are currently no approved medications specifically for treating CUD, but
certain medications may be used to manage co-occurring conditions like anxiety
or depression.
Psychotherapeutic Methods:
 Cognitive Behavioral Therapy (CBT): Helps individuals identify and
change problematic thoughts and behaviors related to cannabis use.
 Motivational Enhancement Therapy (MET): A counseling approach that
focuses on increasing an individual's motivation to change their cannabis
use behavior.
 Contingency Management: Provides tangible rewards for maintaining
abstinence or meeting treatment goals.
3. Opioid Use Disorder (OUD)
Medications:
 Methadone: A long-acting opioid agonist that helps reduce withdrawal
symptoms and cravings.
 Buprenorphine A partial opioid agonist that reduces cravings and
withdrawal symptoms while producing less euphoria than full agonists.
 Naltrexone: Blocks the effects of opioids, reducing cravings and
preventing relapse.
Psychotherapeutic Methods:
 Cognitive Behavioral Therapy (CBT) helps individuals identify and
modify thoughts and behaviors that contribute to opioid use.
 Contingency Management offers incentives for maintaining abstinence
from opioids and participating in treatment.
 Supportive Therapy provides emotional support and encouragement for
individuals undergoing opioid addiction treatment.

4. Hallucinogen Use Disorder (HUD)

Medications:
 Antidepressants are selective serotonin reuptake inhibitors (SSRIs) or
other types of antidepressants may be used to manage co-occurring
depression or anxiety.
 Antipsychotics may be prescribed to manage severe symptoms of
psychosis or hallucinations, especially during acute intoxication.
 Benzodiazepines are used short-term to manage severe anxiety or
agitation but are typically not recommended for long-term use due to the
risk of dependence.
 Mood Stabilizers are medications like lithium or anticonvulsants that can
help manage mood swings, particularly if there is a co-occurring mood
disorder.

Psychotherapeutic Methods:
 Cognitive Behavioral Therapy (CBT) helps individuals understand and
change patterns of thinking and behavior related to hallucinogen use,
reducing cravings and preventing relapse.
 Motivational Interviewing (MI)Encourages individuals to find the
motivation to make positive changes through a non-judgmental and
supportive approach.
 Contingency Management (CM) uses positive reinforcement, such as
rewards or incentives, to encourage abstinence from hallucinogens.
 12-Step Programs like Narcotics Anonymous (NA) provide peer support
and a structured approach to recovery through a series of steps promoting
personal growth and accountability.
 Mindfulness-Based Therapies are techniques like mindfulness meditation
and Mindfulness-Based Stress Reduction (MBSR) that help manage
stress and cravings by promoting a non-reactive awareness of thoughts
and feelings.
 Family Therapy involves family members to improve communication,
address family dynamics contributing to substance use, and provide a
support system for recovery.
 Psychoeducation educates individuals about the effects of hallucinogens
and the risks associated with their use, helping them make informed
decisions and develop healthier coping strategies.

Summary
Recreational drugs can profoundly alter neurotransmission, leading to
significant short-term and long-term effects on the brain and behavior.
Understanding the mechanism of each drug or at least drug class is
imperative to help the victims rehabilitate and recover easily from addiction
and its implications.

Drug use is still rampant in India, preying on anyone from ages 14 to 75. The
DRI has seized 3,800 kilograms of heroin worth 26,000 crore rupees in a
measly 3 years. Only 25% of the population who wished to escape this
vicious cycle was given treatment while the 75% are still in the dark.
This is an emerging problem and needs to be addressed. This project has
aimed to do just that and has explored the scientific side of recreational
drugs, their effect on neurotransmission, and their adverse consequences.

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