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Substance use disorders
- 2. Why Do We Do The Things That We Do?Why Do We Do The Things That We Do? To satisfy basic drives, e.g. hunger.To satisfy basic drives, e.g. hunger. Because they bring pleasure.Because they bring pleasure. Because they will make some future thing thatBecause they will make some future thing that is pleasurable.is pleasurable. Because we feel “compelled” to.Because we feel “compelled” to. To avoid unpleasant consequences.To avoid unpleasant consequences. Most things are done because of a combinationMost things are done because of a combination of several of these things.of several of these things. There are neurotransmitter systems in the brainThere are neurotransmitter systems in the brain involved with pleasure, happiness & motivation.involved with pleasure, happiness & motivation.
- 3. Substance Use DisordersSubstance Use Disorders Often chemical.Often chemical. Characterized by inability to stop.Characterized by inability to stop. Life is organized around the addictiveLife is organized around the addictive behavior.behavior.
- 4. Substance Related DisordersSubstance Related Disorders The substance related disordersThe substance related disorders encompass 10 separate classes of drugs:encompass 10 separate classes of drugs: Alcohol; Caffeine; Cannabis;Alcohol; Caffeine; Cannabis; Hallucinogens; Inhalants; Opioids;Hallucinogens; Inhalants; Opioids; Sedatives; Hypnotics & Anxiolytics;Sedatives; Hypnotics & Anxiolytics; Stimulants; Tobacco and Others.Stimulants; Tobacco and Others. These 10 classes are not fully distinct.These 10 classes are not fully distinct. All drugs that are taken in excess have inAll drugs that are taken in excess have in common direct activation of the braincommon direct activation of the brain reward system.reward system.
- 5. Substance Related DisordersSubstance Related Disorders The pharmacological mechanisms byThe pharmacological mechanisms by which each class of drugs produceswhich each class of drugs produces reward are different but all producereward are different but all produce feelings of pleasure.feelings of pleasure. Individuals with lower levels of selfIndividuals with lower levels of self control, which reflect impairments ofcontrol, which reflect impairments of brain inhibitory mechanisms, arebrain inhibitory mechanisms, are predisposed to develop substance usepredisposed to develop substance use disorders.disorders.
- 6. DSM-V CriteriaDSM-V Criteria A maladaptive pattern ofA maladaptive pattern of substance use, leading tosubstance use, leading to clinically significantclinically significant impairment or distress, asimpairment or distress, as manifested by the following,manifested by the following, occurring at any time in theoccurring at any time in the same 12-month period.same 12-month period.
- 7. DSM-V CriteriaDSM-V Criteria The substance is often taken in larger amountsThe substance is often taken in larger amounts or over a longer period than was intended.or over a longer period than was intended. A persistent desire or unsuccessful efforts to cutA persistent desire or unsuccessful efforts to cut down or control substance use.down or control substance use. A great deal of time is spent in activitiesA great deal of time is spent in activities necessary to obtain the substance (e.g., visitingnecessary to obtain the substance (e.g., visiting multiple doctors or driving long distances), usemultiple doctors or driving long distances), use the substance (e.g., chain-smoking), or recoverthe substance (e.g., chain-smoking), or recover from its effects.from its effects.
- 8. DSM-V CriteriaDSM-V Criteria Important social, occupational or recreationalImportant social, occupational or recreational activities are given up or reduced because ofactivities are given up or reduced because of substance use.substance use. The substance use is continued despiteThe substance use is continued despite knowledge of having a persistent or recurrentknowledge of having a persistent or recurrent physical or psychological problem that is likelyphysical or psychological problem that is likely to have been caused or exacerbated by theto have been caused or exacerbated by the substance (e.g., current cocaine use despitesubstance (e.g., current cocaine use despite recognition of cocaine-induced depression, orrecognition of cocaine-induced depression, or continued drinking despite recognition that ancontinued drinking despite recognition that an ulcer was made worse by alcohol consumption).ulcer was made worse by alcohol consumption).
- 9. ToleranceTolerance A need for markedly increased amounts ofA need for markedly increased amounts of the substance to achieve intoxication orthe substance to achieve intoxication or desired effect.desired effect. Markedly diminished effect with continuedMarkedly diminished effect with continued use of the same amount of the substance.use of the same amount of the substance.
- 10. WithdrawalWithdrawal Manifested by either of the following:Manifested by either of the following: - The characteristic withdrawal- The characteristic withdrawal syndrome for the substance.syndrome for the substance. - The same (or a closely related)- The same (or a closely related) substance is taken to relieve or avoidsubstance is taken to relieve or avoid withdrawal symptoms.withdrawal symptoms.
- 11. DependenceDependence Altered physiological state thatAltered physiological state that develop to compensate fordevelop to compensate for persistent drug exposure andpersistent drug exposure and that gives rise to a withdrawalthat gives rise to a withdrawal syndrome after cessation of drugsyndrome after cessation of drug exposure.exposure.
- 12. Alcohol Use DisordersAlcohol Use Disorders Alcohol Dependence & Abuse.Alcohol Dependence & Abuse. Alcohol Intoxication:Alcohol Intoxication: Clinically significant problematicClinically significant problematic behavioral or psychological changes, slurred speech,behavioral or psychological changes, slurred speech, incoordination, unsteady gait, nystagmus, impairment attentionincoordination, unsteady gait, nystagmus, impairment attention or memory, stupor or coma.or memory, stupor or coma. Alcohol Withdrawal:Alcohol Withdrawal: Autonomic hyperactivity, increased hand tremor, insomnia,Autonomic hyperactivity, increased hand tremor, insomnia, nausea or vomiting, transient hallucinations or illusions,nausea or vomiting, transient hallucinations or illusions, psychomotor agitation, anxiety & tonic clonic seizures.psychomotor agitation, anxiety & tonic clonic seizures. Diagnostic Markers:Diagnostic Markers: GGT; Gamma Glutamyl Transferase (› 35 units),GGT; Gamma Glutamyl Transferase (› 35 units), CDT; Carbohydrate Deficient Transferase (≥ 20 units),CDT; Carbohydrate Deficient Transferase (≥ 20 units), MCV; The Mean Corpuscular Volume.MCV; The Mean Corpuscular Volume.
- 13. Alcohol Induced DisordersAlcohol Induced Disorders Alcohol Intoxication.Alcohol Intoxication. Alcohol Withdrawal.Alcohol Withdrawal. Alcohol Intoxication Delirium.Alcohol Intoxication Delirium. Alcohol Withdrawal Delirium.Alcohol Withdrawal Delirium. Alcohol Induced Persisting Dementia.Alcohol Induced Persisting Dementia. Alcohol Induced Persisting AmnesticAlcohol Induced Persisting Amnestic Disorder.Disorder.
- 14. Alcohol Induced DisordersAlcohol Induced Disorders Alcohol induced Psychotic Disorder,Alcohol induced Psychotic Disorder, with Delusions.with Delusions. Alcohol induced psychotic Disorder,Alcohol induced psychotic Disorder, with hallucinations.with hallucinations. Alcohol induced mood disorder.Alcohol induced mood disorder. Alcohol Induced Anxiety Disorder.Alcohol Induced Anxiety Disorder. Alcohol Induced Sexual Dysfunction.Alcohol Induced Sexual Dysfunction. Alcohol Induced Sleep Disorder.Alcohol Induced Sleep Disorder.
- 15. Alcohol InducedAlcohol Induced Medical ComplicationMedical Complication Wernicke’s Encephalopathy.Wernicke’s Encephalopathy. Korsakoff’s Psychosis.Korsakoff’s Psychosis. Alcohol-Induced Dementia.Alcohol-Induced Dementia. Fetal Alcohol Syndrome.Fetal Alcohol Syndrome.
- 16. Caffeine Related DisordersCaffeine Related Disorders Caffeine Intoxication (≥ 250 mg):Caffeine Intoxication (≥ 250 mg): - Restlessness, Nervousness, Excitement,- Restlessness, Nervousness, Excitement, Insomnia, Flushed face, Diuresis, GITInsomnia, Flushed face, Diuresis, GIT disturbance, Muscle twitching, Tachycardiadisturbance, Muscle twitching, Tachycardia oror arrhythmia & psychomotor agitation.arrhythmia & psychomotor agitation. Caffeine Withdrawal:Caffeine Withdrawal: - Headache, Fatigue or Drowsiness, MoodHeadache, Fatigue or Drowsiness, Mood (Dysphoric – Depressed – Irritable), Difficult(Dysphoric – Depressed – Irritable), Difficult Concentration & Flu Like Symptoms.Concentration & Flu Like Symptoms.
- 17. Cannabis Related DisordersCannabis Related Disorders Cannabis Use Disorder.Cannabis Use Disorder. Cannabis Intoxication:Cannabis Intoxication: -- Clinically significant problematic behavioral orClinically significant problematic behavioral or psychological changes, Conjunctival injection,psychological changes, Conjunctival injection, Increased appetite, Dry mouth, Tachycardia.Increased appetite, Dry mouth, Tachycardia. Cannabis Withdrawal:Cannabis Withdrawal: -- Irritability, anger or aggression, Nervousness orIrritability, anger or aggression, Nervousness or anxiety, sleep difficulty, decreased appetite,anxiety, sleep difficulty, decreased appetite, Restlessness, Depressed mood & Physical symptomsRestlessness, Depressed mood & Physical symptoms..
- 18. Hallucinogen Related DisordersHallucinogen Related Disorders Phencyclidine & Other Hallucinogens UsePhencyclidine & Other Hallucinogens Use Disorder.Disorder. Phencyclidine Intoxication:Phencyclidine Intoxication: - Clinically significant problematic behavioral or- Clinically significant problematic behavioral or psychological changes, Nystagmus, Hypertension,psychological changes, Nystagmus, Hypertension, Tachycardia, Numbness, Ataxia, Dysarthria, MuscleTachycardia, Numbness, Ataxia, Dysarthria, Muscle rigidity, Seizures or Coma & Hyperacusis.rigidity, Seizures or Coma & Hyperacusis. Hallucinogen Persisting Perception Disorder:Hallucinogen Persisting Perception Disorder: - Following cessation of use.Following cessation of use. - Re-experience of the perceptual symptoms.Re-experience of the perceptual symptoms.
- 19. Inhalant Related DisordersInhalant Related Disorders Inhalant Use Disorder.Inhalant Use Disorder. Inhalant Intoxication:Inhalant Intoxication: - Clinically significant problematic behavioral or- Clinically significant problematic behavioral or psychological changes, Dizziness, Nystagmus,psychological changes, Dizziness, Nystagmus, Incoordination, Slurred speech, Lethargy, DepressedIncoordination, Slurred speech, Lethargy, Depressed reflexes, Psychomotor retardation, Tremor, Musclereflexes, Psychomotor retardation, Tremor, Muscle weakness, Blurred vision or diplopia, Stupor orweakness, Blurred vision or diplopia, Stupor or Coma & Euphoria.Coma & Euphoria. Inhalant Induced Psychotic Disorder.Inhalant Induced Psychotic Disorder. Inhalant Induced Depressive Disorder.Inhalant Induced Depressive Disorder. Inhalant Induced Anxiety Disorder.Inhalant Induced Anxiety Disorder.
- 20. Opioid Related DisordersOpioid Related Disorders Opioid Use Disorder.Opioid Use Disorder. Opioid Intoxication:Opioid Intoxication: - Pupillary constriction or dilatation,- Pupillary constriction or dilatation, Drowsiness or Coma, Slurred speech,Drowsiness or Coma, Slurred speech, Impairment in attention or memory.Impairment in attention or memory. Opioid Withdrawal:Opioid Withdrawal: - Dysphoric Mood, Nausea or Vomiting, Muscle- Dysphoric Mood, Nausea or Vomiting, Muscle Aches, Lacrimation or Rhinorrhea, PupillaryAches, Lacrimation or Rhinorrhea, Pupillary Dilation, Piloerection or Sweating, Diarrhea,Dilation, Piloerection or Sweating, Diarrhea, Yawning, Fever and Insomnia.Yawning, Fever and Insomnia.
- 21. Heroin & MorphineHeroin & Morphine These act via an endogenous opioid system whoseThese act via an endogenous opioid system whose normal function is probably to suppress pain untilnormal function is probably to suppress pain until danger has passed.danger has passed. Injection of opiates causes a rise inInjection of opiates causes a rise in (NA dopamine)(NA dopamine).. However, lesions to the NA do notHowever, lesions to the NA do not impair opiate self-administration.impair opiate self-administration. Therefore, there must beTherefore, there must be a separate pathway.a separate pathway.
- 22. Sedative, Hypnotic or AnxiolyticSedative, Hypnotic or Anxiolytic Related DisordersRelated Disorders Sedative, Hypnotic or Anxiolytic Use Disorder.Sedative, Hypnotic or Anxiolytic Use Disorder. Sedative, Hypnotic or Anxiolytic Intoxication:Sedative, Hypnotic or Anxiolytic Intoxication: - Clinically significant problematic behavioral or- Clinically significant problematic behavioral or psychological changes, Slurred speech, Incoordination,psychological changes, Slurred speech, Incoordination, Nystagmus, Impairment in Cognition & Stupor orNystagmus, Impairment in Cognition & Stupor or Coma.Coma. Sedative, Hypnotic or Anxiolytic Withdrawal:Sedative, Hypnotic or Anxiolytic Withdrawal: - Autonomic Hyperactivity, Hand Tremor, Insomnia,- Autonomic Hyperactivity, Hand Tremor, Insomnia, Nausea or Vomiting, Transient Hallucinations orNausea or Vomiting, Transient Hallucinations or Illusions, Psychomotor agitation, Anxiety & GrandIllusions, Psychomotor agitation, Anxiety & Grand Mal Seizures.Mal Seizures.
- 23. Stimulant Related DisordersStimulant Related Disorders Stimulant Use Disorder.Stimulant Use Disorder. Stimulant Intoxication:Stimulant Intoxication: - Clinically significant problematic behavioral or- Clinically significant problematic behavioral or psychological changes, Tachycardia or Bradycardia,psychological changes, Tachycardia or Bradycardia, Pupillary dilation, Elevated or Lowered BP, Chills,Pupillary dilation, Elevated or Lowered BP, Chills, Nausea or Vomiting, Weight loss, PsychomotorNausea or Vomiting, Weight loss, Psychomotor disturbance, Muscle weakness, respiratorydisturbance, Muscle weakness, respiratory depression, chest pain, Arrhythmias, Confusion,depression, chest pain, Arrhythmias, Confusion, Seizures or Coma.Seizures or Coma. Stimulant Withdrawal:Stimulant Withdrawal: - Dysphoric Mood, Vivid unpleasant dreams, Sleep- Dysphoric Mood, Vivid unpleasant dreams, Sleep disturbance, Increased appetite, Psychomotordisturbance, Increased appetite, Psychomotor
- 24. Cocaine & AmphetaminesCocaine & Amphetamines Most effective reinforcer, especially freebase (crack).Most effective reinforcer, especially freebase (crack). Animals will self-administer until they die.Animals will self-administer until they die. Cocaine psychosis indistinguishable fromCocaine psychosis indistinguishable from schizophrenia.schizophrenia. No physical withdrawal but psychological effects includeNo physical withdrawal but psychological effects include depression and anhydonia.depression and anhydonia. They are highly addictive but do not produce a physicalThey are highly addictive but do not produce a physical dependence - only a behavioral dependence.dependence - only a behavioral dependence. Both are dopamine agonists.Both are dopamine agonists. Both inhibit dopamine reuptake but amphetamine mainlyBoth inhibit dopamine reuptake but amphetamine mainly stimulates release from terminal buttons.stimulates release from terminal buttons.
- 25. Cocaine Action
- 26. Tobacco Related DisordersTobacco Related Disorders Tobacco Use Disorder.Tobacco Use Disorder. Tobacco Withdrawal:Tobacco Withdrawal: - Irritability, Frustration, Anger,- Irritability, Frustration, Anger, Anxiety, Difficulty Concentrating,Anxiety, Difficulty Concentrating, Restlessness, Depressed Mood,Restlessness, Depressed Mood, Insomnia.Insomnia. Other Tobacco Induced Disorders:Other Tobacco Induced Disorders: - Tobacco Induced Sleep Disorder.Tobacco Induced Sleep Disorder.
- 27. Etiology of SubstanceEtiology of Substance Use DisordersUse Disorders Biological Models.Biological Models. Psychological Models.Psychological Models. Socio-Cultural Models.Socio-Cultural Models.
- 28. The Ventral Striatum (Nucleus Accumbens) Human Monkey Rat
- 36. The Reward PathwayThe Reward Pathway & Addiction& Addiction Natural Rewards:Natural Rewards: FOODFOOD WATERWATER SEXSEX NURTURINGNURTURING
- 38. AddictionAddiction A State in which an organismA State in which an organism engages in a compulsive behavior.engages in a compulsive behavior. The Behavior is reinforcingThe Behavior is reinforcing (Rewarding or Pleasurable).(Rewarding or Pleasurable). Loss of control in limiting intake.Loss of control in limiting intake.
- 39. ToleranceTolerance A State in which an organismA State in which an organism no longer responds to a drug.no longer responds to a drug. A Higher dose is required toA Higher dose is required to achieve the same effect.achieve the same effect.
- 40. DependenceDependence A State in which an organismA State in which an organism functions normally in the presencefunctions normally in the presence of a drug.of a drug. Manifested as physicalManifested as physical disturbance when the drug isdisturbance when the drug is removed (removed (WithdrawalWithdrawal).).
- 42. Psychological ModelPsychological Model Psychological Models:Psychological Models: - Addictive Personality.- Addictive Personality. - Psychological Vulnerability.- Psychological Vulnerability. - Self Medicating.- Self Medicating. - Personality Issues (Anti-Social, C.D., etc..).- Personality Issues (Anti-Social, C.D., etc..). - Self Esteem.- Self Esteem. Psychoanalytic Models:Psychoanalytic Models: - Oral.- Oral. - Maternal Depravation.- Maternal Depravation. - Sexual Adequacy.- Sexual Adequacy. - Sexual Identity.- Sexual Identity.
- 43. Drug Self-Administration Protocol In Rats This is a way of testing to see whether a rat finds a drug rewarding
- 44. Pleasure & The “ Pleasure Centre ” The Experiment by Olds & Milner
- 45. Tension & Stress Reduction ModelTension & Stress Reduction Model Low tolerance for tension.Low tolerance for tension. Stimulus augmenting.Stimulus augmenting. Drugs (CNS) reduce tension =Drugs (CNS) reduce tension = people use it and get thispeople use it and get this response = Reinforcementresponse = Reinforcement..
- 46. Socio-Cultural ModelsSocio-Cultural Models Cultural Circumstances -Tension.Cultural Circumstances -Tension. Attitude toward drug taking.Attitude toward drug taking. Cultural; substitutes as means ofCultural; substitutes as means of satisfaction.satisfaction. Alienation – Anomie.Alienation – Anomie.
- 47. Risk FactorsRisk Factors Adolescence.Adolescence. Academic Failure.Academic Failure. Family History of Drug Use.Family History of Drug Use. Risk Taking Behavior.Risk Taking Behavior.
- 48. Cost of Drug AbuseCost of Drug Abuse Absenteeism.Absenteeism. Low Productivity.Low Productivity. Accidents.Accidents. High Medical Costs.High Medical Costs.
- 49. Pathways To AddictionPathways To Addiction 4 Stages in a Relationship with Drugs4 Stages in a Relationship with Drugs 1. Experimentation 2. Active Seeking 3. Preoccupation 4. Addiction
- 50. Crime & DrugsCrime & Drugs Illegal.Illegal. Affect Behavior.Affect Behavior. Drug users more likely to commitDrug users more likely to commit crimes.crimes. Frequency of use increasesFrequency of use increases criminal activity.criminal activity.
- 52. Genome Protein Expression Neuronal Circuits DRUGS OF ABUSE Social Behavior ADDICTION Requires A Systems Approach ADDICTION Requires A Systems Approach
- 53. Remember...Remember... • Addiction is an illness noAddiction is an illness no one chooses to have.one chooses to have. • Addiction is involuntaryAddiction is involuntary & marked by a resistance& marked by a resistance to give up drugs.to give up drugs.
Notas del editor
- Slide 25: Snorting vs smoking cocaine: different addictive liabilities Historically cocaine abuse involved snorting the powdered form (the hydrochloride salt). When cocaine is processed to form the free base, it can be smoked. Heating the hydrochloride salt form of cocaine will destroy it; the free base can be volatilized at high temperature without any destruction of the compound. Smoking gets the drug to the brain more quickly than does snorting. Show the audience why this happens. Snorting requires that the cocaine travels from the blood vessels in the nose to the heart (blue arrow), where it gets pumped to the lungs (blue arrow) to be oxygenated. The oxygenated blood (red arrows) carrying the cocaine then travels back to the heart where it is pumped out to the organs of the body, including the brain. However, smoking bypasses much of this--the cocaine goes from the lungs directly to the heart and up to the brain. The faster a drug with addictive liability reaches the brain, the more likely it will be abused. Thus, the time between taking the drug and the positive reinforcing or rewarding effects that are produced can determine the likelihood of abuse.
- Slide 3: Brain regions and neuronal pathways Certain parts of the brain govern specific functions. Point to areas such as the sensory (orange), motor (blue) and visual cortex (yellow) to highlight their specific functions. Point to the cerebellum (pink) for coordination and to the hippocampus (green) for memory. Indicate that nerve cells or neurons connect one area to another via pathways to send and integrate information. The distances that neurons extend can be short or long. For example; point to the reward pathway (orange). Explain that this pathway is activated when a person receives positive reinforcement for certain behaviors ("reward"). Indicate that you will explain how this happens when a person takes an addictive drug. As another example, point to the thalamus (magenta). This structure receives information about pain coming from the body (magenta line within the spinal cord), and passes the information up to the cortex. Tell the audience that you can look at this in more detail.
- Slide 30: Summary; addictive drugs activate the reward system via increasing dopamine neurotransmission In this last slide, the reward pathway is shown along with several drugs that have addictive potential. Just as heroin (morphine) and cocaine activate the reward pathway in the VTA and nucleus accumbens, other drugs such as nicotine and alcohol activate this pathway as well, although sometimes indirectly (point to the globus pallidus, an area activated by alcohol that connects to the reward pathway). While each drug has a different mechanism of action, each drug increases the activity of the reward pathway by increasing dopamine transmission. Because of the way our brains are designed, and because these drugs activate this particular brain pathway for reward, they have the ability to be abused. Thus, addiction is truely a disease of the brain. As scientists learn more about this disease, they may help to find an effective treatment strategy for the recovering addict.
- Slide 7: The synapse and synaptic neurotransmission Describe the synapse and the process of chemical neurotransmission. As an electrical impulse arrives at the terminal, it triggers vesicles containing a neurotransmitter, such as dopamine (in blue), to move toward the terminal membrane . The vesicles fuse with the terminal membrane to release their contents (in this case, dopamine). Once inside the synaptic cleft (the space between the 2 neurons) the dopamine can bind to specific proteins called dopamine receptors (in pink) on the membrane of a neighboring neuron. This is illustrated in more detail on the next slide.
- Slide 17: Opiates binding to opiate receptors in the nucleus accumbens: increased dopamine release This is a close-up view of a synapse in the nucleus accumbens. Three types of neurons participate in opiate action; one that releases dopamine (on the left), a neighboring terminal (on the right) containing a different neurotransmitter (probably GABA for those who would like to know), and the post-synaptic cell containing dopamine receptors (in pink). Show that opiates bind to opiate receptors (yellow) on the neighboring terminal and this sends a signal to the dopamine terminal to release more dopamine. [In case someone asks how--one theory is that opiate receptor activation decreases GABA release, which normally inhibits dopamine release--so dopamine release is increased.]
- Slide 27: Dopamine binding to receptors and uptake pumps in the nucleus accumbens; the action of cocaine Explain that cocaine binds to sites in areas of the brain that are rich in dopamine synapses such as the VTA and the nucleus accumbens. Review dopamine transmission in the close-up of a synapse in the nucleus accumbens. Point to dopamine (inside the terminal) that is released into the synaptic space. The dopamine binds to dopamine receptors and then is taken up by uptake pumps back into the terminal. Now show what happens when cocaine is present (yellow). Cocaine binds to the uptake pumps and prevents them from transporting dopamine back into the neuron terminal. So more dopamine builds up in the synaptic space and it is free to activate more dopamine receptors. This is the same effect that you showed in an earlier slide with morphine, where morphine increased dopamine release from the terminal to produce more dopamine in the synaptic space.
- Slide 8: Dopamine neurotransmission and modulation by endogenous opiates Using the close-up of a synapse, continue using dopamine for your example of synaptic function. Explain that it is synthesized in the nerve terminal and packaged in vesicles. Reiterate the steps in neurotransmission. Show how the vesicle fuses with the membrane and releases dopamine. The dopamine molecules can then bind to a dopamine receptor (in pink). After the dopamine binds, it comes off the receptor and is removed from the synaptic cleft by uptake pumps (also proteins) that reside on the terminal (arrows show the direction of movement). This process is important because it ensures that not too much dopamine remains in the synaptic cleft at any one time. Also point out that there are neighboring neurons that release another compound called a neuromodulator. Neuromodulators help to enhance or inhibit neurotransmission that is controlled by neurotransmitters such as dopamine. In this case, the neuromodulator is an "endorphin" (in red). Endorphins bind to opiate receptors (in yellow) which can reside on the post-synaptic cell (shown here) or, in some cases, on the terminals of other neurons (this is not shown so it must be pointed out). The endorphins are destroyed by enzymes rather than removed by uptake pumps.
- Slide 11: The reward pathway Tell your audience that this is a view of the brain cut down the middle. An important part of the reward pathway is shown and the major structures are highlighted: the ventral tegmental area (VTA), the nucleus accumbens and the prefrontal cortex. The VTA is connected to both the nucleus accumbens and the prefrontal cortex via this pathway and it sends information to these structures via its neurons. The neurons of the VTA contain the neurotransmitter dopamine which is released in the nucleus accumbens and in the prefrontal cortex (point to each of these structures). Reiterate that this pathway is activated by a rewarding stimulus. [Note: the pathway shown here is not the only pathway activated by rewards, other structures are involved too, but only this part of the pathway is shown for simplicity.]
- Slide 23: Addiction vs dependence As you have just explained, different parts of the brain are responsible for the addiction and dependence to heroin and opiates. Review the areas in the brain underlying the addiction to morphine (reward pathway) and those underlying the dependence to morphine (thalamus and brainstem). Thus, it is possible to be dependent on morphine, without being addicted to morphine. (Although, if one is addicted, they are most likely dependent as well.) This is especially true for people being treated chronically with morphine for pain, for example associated with terminal cancer. They may be dependent--if the drug is stopped, they suffer a withdrawal syndrome. But, they are not compulsive users of the morphine, and they are not addicted. Finally, people treated with morphine in the hospital for pain control after surgery are unlikely to become addicted; although they may feel some of the euphoria, the analgesic and sedating effects predominate. There is no compulsive use and the prescribed use is short-lived.
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