Transcript STIMULANTS
STIMULANTS
Allen Fowler
Mycheal Scott
Psyc 472
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DEFINITION
Stimulants are a substance which tends to
increase behavioral activity when
administered
Elevate Mood
Increase Motor Activity
Increase Alertness
Decrease need for Sleep
Increase the brains metabolic and neuronal
activity
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PROCESSES
While all stimulants increase behavioral
activity the component processes involved
differ.
Neurotransmitter or receptor processes
Increase neurotransmitters release
Block reuptake
Inhibition of inhibitory neurotransmitters
disinhibition
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COMMONLY USED STIMULANTS
Caffeine
Nicotine
Amphetamine
Cocaine
Ephedrine
Ritalin
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CAFFEINE AND NICOTINE
Allen Fowler
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CAFFEINE
(picture courtesy Erowid web site)
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CAFFEINE
Most commonly consumed psychoactive
drug in the world
Average intake per person per day is
between 80 to 400 milligrams
Consumption of caffeine is not considered
drug abuse
No regulation on sale or use
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CAFFEINE CONTENT
Item
Coffee (5 oz)
Tea (5oz)
Cocoa (5oz)
Chocolate (1oz)
Chocolate milk (1oz)
Cola drink (12oz)
OTC stimulants
OTC analgesics (aspirin)
OTC cold remedies
Average (mg)
100
50
5
25
5
100+
100+
35-65
30
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EFFECTS
Caffeine elicits positive effects such as
Enhanced mental alertness
Sustained
intellectual effort
No substantial disruption of coordinated intellectual
thought or motor activity
Increased energy
A sense of well-being
Faster and clearer flow of thought
Reduced fatigue
Need for sleep is delayed
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Effects
Caffeine may adversely effect tasks involving
Heavy doses - 1.5 grams
delicate muscle coordination
Accurate timing
Arithmetic skills
Agitation
Anxiety
Tremors
Rapid breathing
Insomnia
Lethal dose – 10 grams
100 cups of coffee
100 OTC stimulant capsules
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Effects
Caffeine causes a slight stimulant action
on the heart
Increases the workload
cardiac
contractility
Increases cardiac output
Dilates coronary arteries
More oxygen to the heart
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Effects
Caffeine constricts cerebral blood vessels
Decreases blood flow by about 30%
Can relieve headaches
Bronchial relaxation
Increased secretion of gastric acid
Increased urine
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Effects
Chronic use associated with habituation
and tolerance
Quitting may cause withdrawal
Headaches
Drowsiness
Fatigue
Negative mood
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Reproductive Effects
Freely crosses the placenta to the fetus
Consumed by estimated 75% of pregnant women
Breast milk contains levels equal or higher in concentration than mothers
plasma
Safety still unresolved
One study shows 300 mg relatively safe
Another study shows 160 mg may cause growth retardation
Higher doses increased intrauterine growth retardation
300mg intake even in the month before doubled the risk of spontaneous abortion
Recent study shows 6-10 cups per day is associated with increased risk of
spontaneous abortion
Moderate consumption does not increase the risk
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Therapeutic Uses
Asthma
Narcolepsy
To help maintain daytime wakefulness
Migraine
Bronchial relaxation effects
Restricts blood flow in the cerebral cortex
Headache and other minor pain syndromes
In conjunction with aspirin
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Pharmacokinetics
Caffeine is rapidly and completely absorbed
Significant blood levels reached in 30-45 minutes
Levels peak in about 2 hours
Caffeine is freely and equally distributed through total
body water
Caffeine can be found in almost equal concentrations
throughout body and brain
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Pharmacokinetics
Caffeine has 3.5 to 5 hours half life
Extended half life for
Elderly
Pregnant
women
Up to ten hours
Infants
Decreased half life for smokers
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Pharmacokinetics
Caffeine is metabolized in the liver by the
CYP1A2 subgroup of enzymes into three
metabolites
Theophylline
Bronchial relaxation
Paraxanthine
Theobromine
Theophylline and Paraxanthine act similar to caffeine
About 10% is excreted unchanged
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Mechanism of Action
Major site of action
– Adenosine receptors
– Most potent at adenosine A1 and A2A
Caffeine works as an antagonism agent
– Blocks the adenosine receptor
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Mechanism of Action
– Adenosine is a neuromodulator
Modulatory effect increasing or decreasing the rate at which
neurons fire
Works in conjunction with the G protein processes
– Adenosine appears to exert sedative, depressant, and anticonvulsant
actions
Works to slow down the system
Important to sleeping
– Adenosinergic neurons form a diffuse system
No exclusively adenosinergic pathways
Adenosine stimulates GABAA inhibitory neurons
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Mechanism of Action
– Adenosine is created from the process by
which the body breaks down ATP for energy
ATP is used throughout the body for energy
Used for high energy bursts such as exercising
and running
Phosphates form a high energy bond
Cells break the phosphate bond to extrapolate the
energy
When the phosphates are pulled off the adenosine
is now free to have an effect in the body
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Mechanism of Action
A1 receptors inhibit excitatory neurons
–
–
–
–
Dopamine, glutamate, and ACh
secreting neurons
Reduces production of cAMP
Slows the activity of the kinase
Reduces occurrence of the action
potential
A2A receptors stimulate inhibitory
neurons
–
–
–
–
GABAA neurons
Stimulates production of cAMP
Increases activity of the kinase
Increases occurrence of the action
potential
picture courtesy “The Brain a Neuroscience Primer
”
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Mechanism of Action
Adenosine A receptors
1
– Inhibit the release of dopamine and glutamate
– Limit the release of acetylcholine
Blockade of A receptors
1
– Modest reward
– Increased vigilance and mental acuity
– Creates arousal effect
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Mechanism of Action
Adenosine A2A receptors
– Stimulate GABAA neurons of inhibitory
pathways
– Inhibit dopamine activity
Blockade of A2A receptors
– Increases the potency of endogenous
dopamine
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Mechanism of Action
Caffeine facilitates a disinhibition process
at adenosine receptor sites
Caffeine removes the negative effects of
adenosine from dopamine receptors
increasing dopamine activity
– Caffeine does not stimulate dopamine release
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NICOTINE
(picture courtesy Erowid web site)
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NICOTINE
Primary active ingredient in tobacco
One of the three most widely used
psychoactive drugs
Caffeine
Alcohol
Few or no therapeutic applications
Important because of widespread use and
toxicity
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Background Information
Indigenous to the Americas
1492 Columbus beaches in West Indies
Natives offer them tobacco as gift
1556 first plants taken to Europe
1571 believed to have curing properties for
36 different ailments
1575-1600 becomes “duty” of every man of
fashion – worth its weight in silver
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Background Information
1881 Cigarette rolling machine invented
1889 2.4 billion cigarettes produced annually in
U.S.
1904 3 billion cigarettes sold in U.S.
1912 13 billion cigarettes sold in U.S.
WWII through mid-1960’s smoking considered
cool
Now beginning to be shunned as unhealthy and
unwise
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Background Information
Responsible for the deaths of 1100 Americans
every day
Each day
6000 American teenagers try their first cigarette
3000 children become regular smokers
1000 of these will die from smoking related disease
9 in 10 smokers become addicted before age 21
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Background Information
½ of all people who have smoked have quit
% American adults who smoke has fallen
from 50 in 1965 to 25 in 1998
Smoking identified as the major
preventable cause death and disability
As far as 30 years ago
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Background Information
o
Nicotine is only one of about 4000
compounds released by burning tobacco
o
Adverse cardiovascular, pulmonary, and
carcinogenic effects are from the other
compounds
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Effects
Nicotine exerts powerful effects on
Brain
Spinal cord
Peripheral nervous system
Heart
Various other body structures
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Effects
Stimulation of the vomit center in the brain
stem and sensory receptors in the
stomach
Nausea in early stages of smoking
Tolerance develops rapidly
Reduces weight gain
probably by suppressing appetite
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Effects
Stimulates release of ADH (antidiuretic hormone)
causing fluid retention
Reduces activity of afferent nerve fibers from muscles
Higher doses
Reduction in muscle tone
May be partially involved with relaxation effect
Can induce nervousness and tremors
Seizures in toxic overdose
Smoking associated with increased occurrence of panic
attacks and panic disorders
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Effects
In the CNS nicotine increases
Psychomotor activity
Cognitive functioning
Sensorimotor performance
Attention
Memory consolidation
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Effect
Nicotine can improve performance on
vigilance and rapid information processing
Effects are greater for working memory rather
than long term memory
Nicotine exerts an antidepressant effect
High smoking rates among depressed
individuals may be an attempt at self
medication
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Effects
Nicotine exerts a potent reinforcing action
Indirect activation of midbrain dopamine
neurons
Greatest in early phases
Diminishes over time
Smoking is continued to avoid withdrawal
symptoms
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Reproductive Effects
Smoking during pregnancy increases rates
spontaneous abortion
Stillbirth
Early postpartum death
Preterm deliveries
Intrauterine growth retardation is increased 40%
2000 infant deaths per year attributed to
smoking
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Reproductive Effects
Smoking reduces oxygen delivery to the
fetus resulting in varying degree of fetal
hypoxia
Fetus does not receive as much oxygen
Smoking may result in irreversible
intellectual and physical deficiencies
Increased prevalence of ADHD
Lower IQ scores
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Tolerance
Nicotine does not appear induce a pronounced
degree of biological tolerance
Increased use in early stages which usually levels off
as smoking is continued
Smokers adjust nicotine intake to maintain 20 to 40
nanograms per milliliter of plasma
Does induce physiological and psychological
dependence
Habituation
Rebound effect
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Withdrawal Symptoms
Intense nicotine craving
Irritability
Anxiety
Anger
Difficulty concentrating
Restlessness
Impatience
Increased appetite
Weight gain
Insomnia
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Therapy
Nicotine replacement therapy doubles
successful quit rates
Skin patches
Gum
Nicotine nasal spray
The use of Zyban has also been shown to
increase successful quit rates
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Pharmacokinetics
Easily absorbed in the body
Lungs
Buccal and nasal mucosa
Skin
Gastrointestinal tract
Nicotine is suspended in the minute particles (tars) in
smoke
Orally administered blood levels of nicotine are
comparable to smoking
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Pharmacokinetics
Only about 20% of the nicotine in a cigarette is inhaled
and absorbed into the bloodstream
Nicotine which is not immediately absorbed is rapidly
metabolized by the hepatic enzyme CYP2A6
Inhalation allows controllability of dose
Frequency of breaths
Depth of breaths
Time in lungs
Number of cigarettes
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Pharmacokinetics
Nicotine is thoroughly distributed in the body
The liver metabolizes 80 to 90% before excretion to the
kidneys
No barriers to nicotine distribution
Rapid brain penetration
Crosses placental barrier
Appears in all bodily fluids
Primary metabolite is cotinine
The elimination half life in chronic users is about 2 hrs
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Mechanism of Action
Nicotine activates specific acetylcholine
(ACh) receptors known as nicotinic
receptors
Nicotinic receptors are located throughout
the body
– Skeletal muscle
– Sympathetic and parasympathetic neurons
– CNS
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Mechanism of Action
ACh is released, broken down, and
reabsorbed very quickly (microsecond)
allowing the receptor to respond to new
Ach
ACh receptors work as a fast first
messenger system
– Attached directly to ion channels
– Binding has an immediate response
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Mechanism of Action
picture courtesy pharyngula.org
Nicotine replaces ACh at nicotinic receptor
Beats out the ACh at the binding site
Works as an agonist
Opens ion channel allowing depolarization to occur
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Peripheral Nervous System
Activation of nicotinic receptors in the PNS
Increases blood pressure and heart rate
Causes the release of epinephrine from the adrenal
glands
Increases the tone, secretions, and activity of the
gastrointestinal tract
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Central Nervous System
Nicotinic receptors are widely distributed and may be
present at the presynaptic terminals of neurons which
secrete
Dopamine
Acetylcholine
Glutamine
Activation by nicotine facilitates the release and
increases the action in the brain of these
neurotransmitters
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Central Nervous System
Dopamine levels are increased in the
Ventral tegmentum
Nucleus accumbens
Forebrain
Stimulation of these areas account for the
behavioral reinforcement, stimulant,
antidepressant, and addictive properties of
nicotine
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Central Nervous System
Increases in acetylcholine contribute to the
cognitive potentiation and memory facilitation
properties of nicotine
Facilitation of glutaminergic neurotransmissions
contribute to the improvement in memory
functioning
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Smoking Diseases
Smoking accelerates the
depositing of fat in the arteries
Increased risk of heart attack and
stroke
Smoking weakens the immune
system
Smoking irritates the lining in the
lungs impairing respiration
Smokers cough
Emphysema
picture courtesy quantumclinic.com
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Smoking Diseases
Lung cancer
90-95% of male
deaths
70-75% of female
deaths
Cancer of the mouth
and throat
Chewing tobacco
Picture courtesy quantumclinic.com
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Smoking Diseases
Cardiovascular disease
Carbon monoxide decreases amount of oxygen
delivered to the heart while nicotine increases the
workload
Carbon monoxide and nicotine increase narrowing
(atherosclerosis) and clotting (thrombosis) in the
coronary arteries
Increased risk of coronary heart disease
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Smoking Diseases
About 4000 Americans per year die from
lung cancer caused by second-hand
smoke
37000 deaths per year from heart disease
caused by second hand smoke
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Sources
Julien, Robert M. (2001). A Primer of Drug Action (ninth ed.).
Caffeine and Nicotine (pp 220-248). NY, New York: Worth
Publishers.
Tompson, Richard M. (2000). The Brain: A Neuroscience Primer
(third ed.). NY, New York: Worth Publishers.
http://www.erowid.org/psychoactives/psychoactives.shtml
http://home.howstuffworks.com/caffeine.htm
http://www.nida.nih.gov
http://pharyngula.org/~pzmyers/neuro/synapse/index.php?print
http://www.quantumclinic.com/quitsmoking/quit-smoking-stopaddiction-cigarettes-nicotine-lung-cancer-photos.htm
http://www.ccc.nottingham.ac.uk/~mqzwww/adenosine.html
http://www.pbs.org/wgbh/nova/cigarette/nicotine.html
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