Lecture Notes on Amphetamines, Cocaine, and Opiates
Professor Nick, Lecture 1 Notes (11/18/25)
Amphetamine:
Parent compound of a family of synthetic psychostimulants.
Has two pharmaceutical forms:
Benzedrine
Dexedrine
Structurally related to dopamine (DA).
Commonly used in street drug culture; aids individuals with ADHD.
Natural Compounds Related to Amphetamine:
Ephedrine:
Derived from the herb Ephedra vulgaris.
Used as medicine in China for over 5000 years.
Reduces appetite and induces a feeling of heightened energy.
Marketed in weight loss supplements; banned by FDA in 2004 due to safety concerns.
Cathinone:
Found in khat, a shrub native to East Africa and the Arabian Peninsula.
Amphetamine Pharmacokinetics:
Administered orally, intravenously (IV), or subcutaneously (SC).
Slow gastrointestinal absorption; effects may take up to 30 minutes post a typical dose of 5-15 mg.
Methamphetamine:
More potent than amphetamine; available forms include oral, snorted, IV, or smoked.
Smoking typically involves a glass pipe or heating on aluminum foil.
Crystalline methamphetamine (methamphetamine hydrochloride) is particularly suitable for smoking.
Inexpensive to produce, with a high potential for addiction.
Chronic use or high doses may result in psychotic reactions or brain damage.
Mechanism: Excess dopamine leads to psychosis; push dopamine back into the presynaptic terminal.
Amphetamines influence the membrane transporter, reversing transporter flow.
Autonomic Compensation:
Reflex adaptation of the body to environmental cues, specifically parasympathetic responses.
Dopamine Effects:
Amphetamines primarily spill dopamine (the main effect).
Act as reuptake blockers as a secondary action.
Dopamine released in the nucleus accumbens, which plays a crucial role in addiction.
Limbic system: Associated with emotion and reward.
Basal ganglia: Controls smooth movement and motor control.
High dopamine = increased movement; low dopamine = rigidity.
Post-amphetamine injection leads to significant overflow and spikes in dopamine levels.
Amphetamines are utilized in treating ADHD; methylphenidate is another commonly used stimulant.
Some paradoxical effects: Psychostimulants may help ADHD individuals but seem counterintuitive compared to effects on the general population.
Dense presence of dopamine transporters in the basal ganglia indicates the drug's binding efficacy.
Neuroscientific Factors:
Important nuclei involved: substantia nigra.
Cessation of meth use allows recovery of presynaptic terminals; however, permanent damage can lead to conditions like Parkinson's disease.
Genetic predisposition may influence susceptibility to Parkinson’s disease.
MDMA:
Initially used by psychotherapists to enhance patient openness (circa 1970).
Differs from amphetamines by primarily enhancing serotonin (5-HT) rather than dopamine and norepinephrine (NE).
MDMA can stimulate some dopamine release but is less potent compared to serotonin.
Toxicity is associated with damage to serotonergic pathways in the brain.
Professor Nick, Lecture 2 Notes (11/20/25)
Cocaine:
An alkaloid derived from the leaves of the shrub Erythroxylon coca, primarily found in South America, especially in the northern and central Andes.
Historical usage: Inhabitants have been consuming coca leaves for over 5000 years by chewing them, often with alkaline substances (lime or ash) to enhance absorption.
Coca chewing persists among Bolivian miners for stamina during work hours.
Cocaine Composition and Extraction:
Coca leaves contain approximately 0.6 - 1.8% cocaine.
Initial extraction creates a coca paste with about 80% cocaine.
Cocaine can be converted to hydrochloride salt for various methods of intake:
Taken orally, intranasally, or via IV injection.
When heated with baking soda, it hardens into forms known as “crack” or “rock” cocaine, which is lipophilic and penetrates the blood-brain barrier rapidly when smoked.
Following administration, cocaine is swiftly metabolized and eliminated; half-life ranges from 0.5 - 1.5 hours, with effects lasting around 30 minutes for IV or smoked doses.
Breakdown products persist in the body longer than cocaine itself.
Mechanism of Action and Effects:
Cocaine's reinforcing, stimulating, and addictive properties stem from its impact on dopamine levels.
At high doses, cocaine inhibits voltage-gated sodium channels in axons, acting as a local anesthetic when applied topically.
Classified as a sympathomimetic drug:
Increases heart rate, causes vasoconstriction, hypertension, and hyperthermia.
While low doses may be manageable, high doses can lead to severe consequences including heart failure, stroke, or intracranial hemorrhage.
Professor Nick, Lecture 3 Notes (11/25/25)
Cocaine Abuse:
Approximately 10-15% of intranasal cocaine users may develop addiction.
Users may engage in binge patterns lasting up to 3 days with consumption of up to 150g of cocaine.
Chronic use results in tolerance and sensitization.
Schizophrenia:
Positive Symptoms:
Includes thought disorders, hallucinations, delusions of persecution, grandeur, and control.
Negative Symptoms:
Characterized by flattened emotional responses, lack of initiative and persistence.
Physical indicators: Enlarged ventricles may signify tissue loss in the brain—acute symptoms indicate greater brain damage.
Historical Treatments:
Prior to the mid-1950s, effective treatments for schizophrenia were scarce.
Insulin shock therapy was one approach.
Significant progress arrived with the discovery of chlorpromazine in 1950, initially utilized as an antihistamine.
Chlorpromazine was demonstrated to reduce hallucinations and delusions while increasing activity in previously catatonic patients.
Dopamine Receptor Blockers:
Chlorpromazine and haloperidol function by blocking postsynaptic dopamine receptors.
Excess dopamine is linked with psychosis and increased movements.
Over time, antagonists can lead to an upregulation of postsynaptic receptors, exacerbating psychotic symptoms once the medication wears off, resulting in dyskinesia.
The dynamics of two dopamine systems underscore the significance of D2 antagonist properties, which do not activate addiction pathways because they block the dopamine signal.
Professor Nick, Lecture 4 Notes (12/2/25)
Dopamine Pathways and Movement:
Key pathways include the substantia nigra to the basal ganglia; loss of dopamine here leads to increased rigidity.
Depression Diagnosis:
DSM criteria involve:
Depressed mood
Anhedonia (loss of pleasure)
Reduced energy
Severe depression can exhibit psychotic symptoms like hallucinations and delusions.
High prevalence observed, with studies indicating that around 75% of women report depressive symptoms (higher frequency than men).
Comorbidity with Alcohol:
Mixing alcohol with depression is deemed dangerous; it can exacerbate symptoms.
Bipolar Disorder:
Prescription rates for antipsychotics are rising.
Bipolar I disorder occurs more frequently in males than females.
Dopamine and Behavioral Activation:
Consuming dopamine-stimulating media (e.g., social media) may drive dopamine circuits.
Increasing serotonin levels can contribute to elevated feelings of joy.
Neurotransmitter Interaction in Depression:
Involve several key neurotransmitters such as DA, NE, and 5-HT (serotonin), all penetrating the frontal cortex and anterior cingulate cortex, which act as a comprehensive emotional map.
Substance P: Related to pain responses, SSRIs can help mitigate perseveration symptoms.
Psychotherapy: The application of the Mirror Neuron Hypothesis validates therapeutic empathy.
The amygdala plays a critical role in threat perception and emotional responses.
Early Antidepressant History:
MAOIs (Monoamine Oxidase Inhibitors) emerged as the first antidepressants; they increase neurotransmitter levels post-release and were serendipitously developed for tuberculosis treatment.
Professor Nick, Lecture 5 Notes (12/4/25)
Opiates:
Considered the most effective painkillers available; they alleviate pain, induce relaxation, and foster sleep without inducing unconsciousness—except at high doses (risk of coma and death).
Opium is obtained from the opium poppy, California being a notable region for cultivation.
Notable side effect: Severe constipation.
Active Ingredients:
The primary compound in opium is morphine, alongside others like codeine and thebaine.
Heroin: A semi-synthetic opioid that converts to morphine upon reaching the brain.
Opioid Mechanisms:
Opioid receptors are G-protein coupled and function by:
Opening K+ channels and closing Ca++ channels, modulating vesicle release by inhibiting GABA neurons in the VTA (ventral tegmental area) and promoting dopamine (DA) release.
Key opioid receptor subtypes include:
Mu, Delta, Kappa: Each exhibiting different distributions and effects throughout the brain and spinal cord.
Tolerance and Dependence:
Long-term opiate use leads to tolerance, indicated by downregulation of dopamine receptors and upregulation of GABA receptors.
Endorphins and Exercise:
Exercise promotes the release of endogenous opiates, often described as a “runners’ high”.
Victims of overdose often die due to respiratory depression (insufficient oxygen intake).
Methadone:
High affinity for opioid receptors; however, low impact on dose-response effects, making it a useful maintenance therapy for opioid dependence.
Marijuana:
Contains over 60 distinct compounds collectively termed cannabinoids.
Enhanced tetrahydrocannabinol (THC) levels are linked with increased psychoactive effects.
Cannabis can be ingested in various forms; notable is THC's prolonged half-life when stored in fat tissues despite rapid plasma level decline.
Mechanism: Cannabinoids activate CB1 receptors, inhibiting a spectrum of neurotransmitter releases, including glutamate and GABA.
Anandamide: A key endogenous cannabinoid worth remembering.
Users of marijuana exhibit tolerance and withdrawal symptoms.
A strong correlation exists between marijuana use and the development of schizophrenia.
Hallucinogens:
Certain hallucinogenic plants can be consumed raw or prepared.
LSD: Synthesized from ergot fungus on grains.
Hallucinogens typically do not induce addiction or withdrawal signs.
Ketamine: A white powder associated with bodily sensation hallucinations, functioning as a non-competitive antagonist that blocks excitatory circuits in the brain.
Used surgically to induce anesthesia but with potential for hallucinations to occur post-administratively.