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9.18.19 Didactic STIMULANTS- PART I Michael H. Baumann, Ph.D. Designer Drug Research Unit (DDRU), Intramural Research Program, NIDA, NIH Baltimore, MD 21224 Chronology of Stimulant Misuse 1. 1980s: Cocaine 2. 1990s: Ecstasy 3. Summary 2 Topics Covered for Each Substance Chemistry Formulations and Methods of Use Pharmacokinetics and Metabolism Desired and Adverse Effects Chronic and Withdrawal Effects Neurobiology Treatments 1980s: Cocaine Cocaine, a Plant-Based Alkaloid Andean Cocaine is Trafficked Globally UNODC World Drug Report, 2012 Formulations and Methods of Use Cocaine Free Base (i.e., Crack) Smoking of free base “rock” using pipes Cocaine HCl Intravenous injection of solutions using needle and syringe Intranasal snorting of powder Pharmacokinetics and Metabolism Pharmacokinetics Smoked drug reaches brain within seconds Intravenous drug reaches brain within seconds Intranasal drug reaches brain within minutes Metabolism Ester hydrolysis to benzoylecgonine Ecgonine methyl ester Cone, 1995 Rate Hypothesis of Drug Reward Smoked and Intravenous Routes Faster rate of drug entry into the brain Enhanced subjective and rewarding effects Intranasal and Oral Routes Slower rate of drug entry into the brain Reduced subjective and rewarding effects Desired Effects Enhanced Mood and Euphoria Increased Attention and Alertness Decreased Need for Sleep Appetite Suppression Sexual Arousal Adverse Effects Psychosis Tachycardia, Arrhythmias, Heart Attack Hypertension, Stroke Hyperthermia, Rhabdomyolysis Multisystem Organ Failure Tolerance- Blunted Effects Acute Tachyphylaxis or “First Dose” Effect Cardiovascular Effects Euphoria and sexual arousal But no longer-term tolerance Anorexia 13 Sensitization- Enhanced Effects Seizures Psychosis Paranoid delusions Visual, auditory and tactile hallucinations Virtually indistinguishable from schizophrenia Stereotypical Behaviors 14 Withdrawal Effects Anhedonia and Depressed Mood Increased Appetite Anergia and Fatigue Vivid or Unpleasant Dreams Insomnia or Hypersomnia Molecular Sites of Action SLC6 Monoamine Transporters Dopamine transporter (DAT) Norepinephrine transporter (NET) 5-HT transporter (SERT) Other sites Sodium channels DATs mediate DA uptake DATs are membrane proteins cytoplasm DATs are responsible for uptake of released dopamine (DA) Drugs that disrupt DAT function increase synaptic DA DAT Increases in DA are rewarding synapse Cocaine Blocks DAT (Inhibits DA Uptake) Vesicles Presynaptic DA cell VMAT D2 DAT Synapse D2/3-type Postsynaptic cell D1-type Cocaine Increases Synaptic DA in Rats Saline 600 Saline 6000 Cocaine Cocaine ** 400 3 4000 ** 3 1 ** ** ** 200 * 2000 1 DA (% basal) (% DA * * Activity (% basal) (% Activity 0 0 -40 0 40 80 120 -40 0 40 80 120 Time (min) Time (min) Baumann et al., 1994 Cocaine is Self-Administered by Rats 8 0 A c t i v e C o c a i n e I n a c t i v e 6 0 4 0 2 0 0 A 1 A 6 E 1 E 6 D a y Schindler et al., 2016 Treatment for Cocaine Dependence Pharmacotherapy No FDA-approved medication for cocaine dependence Psychologically-Based Therapies Cognitive Behavioral Therapy Group and Community Therapies Twelve Step Programs Dopamine Agonists - FAIL Amato et al. 2011 1990s: Ecstasy Ecstasy (MDMA), a synthetic club drug MDMA is a ring-substituted amphetamine Methamphetamine 3,4-Methylenedioxymethamphetamine (MDMA) Formulations and Methods of Use Powders, tablets and capsules Oral ingestion of tablets or capsules most common Some intranasal and intravenous use “Bumping”, or repeated doses over time “Stacking”, or multiple doses at once “Binge and crash” cycling Pharmacokinetics And Metabolism Pharmacokinetics Cmax reached within 2 h of oral ingestion Non-linear drug accumulation at doses > 3 mg/kg Metabolism N-demethylation to form MDA (bioactive) O-demethylenation to form hydroxylated metabolites de la Torre et al., 2004 MDMA metabolism is complex Baumann et al., 2007 Desired Effects Combined effects of a stimulant and hallucinogen Enhanced mood and energy Heightened or altered sensory perception Feelings of empathy and closeness to others Cardiovascular stimulation Adverse Effects Psychosis Sympathetic stimulation Palpitations and heart attack Hypertension Serotonin Syndrome Hyperthermia and dehydration Treat with hydration, cooling, and sedation Avoid b-blockers, which may worsen and hypertension Withdrawal Anhedonia and depressed mood Lethargy and fatigue for several days Sleep disturbances No indication for treatment Molecular Sites of Action SLC6 Monoamine Transporters 5-HT transporter (SERT) Dopamine transporter (DAT) Norepinephrine transporter (NET) Other sites Vesicular Monoamine Transporter 2 (VMAT2) 5-HT2A receptors SERTs mediate 5-HT uptake SERTs are membrane proteins cytoplasm SERTs are responsible for uptake of released 5-HT Drugs that disrupt SERT function increase synaptic 5-HT SERT Increases in 5-HT are not synapse rewarding (e.g., SSRIs) MDMA is a SERT substrate (5-HT releaser) Vesicles Presynaptic 5-HT cell VMAT 5-HT1B Synapse SERT 5-HT1A-type Postsynaptic cell 5-HT2A-type MDMA Increases 5-HT more than DA 4 0 0 1 2 0 0 S a l i n e ) S a l i n e l ) l a a M D M A * s M D M A s 3 0 0 9 0 0 a a b b * 2 0 0 * * % 6 0 0 ( % * * * ( * T A 1 0 0 H 3 0 0 - D 5 0 0 - 4 0 0 4 0 8 0 1 2 0 - 4 0 0 4 0 8 0 1 2 0 T i m e ( m i n ) T i m e ( m i n ) Baumann et al., 2008 Neurotoxic Potential MDMA acutely increases synaptic 5-HT SERT-mediated 5-HT release (i.e., reverse transport) MDMA chronically decreases tissue 5-HT Depletion of serotonin stores Inhibition of 5-HT synthesis Neurotoxicity? 1. Cocaine is the prototypical dopaminergic stimulant that acts by blocking DAT 2. MDMA acts as a mild stimulant and hallucinogen due to its SERT-mediated 5-HT release 37 .
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