Cumulative Questions_ Drugs PDF

**Cumulative Questions (various chapters in the text) - names of drugs within classes - definitions of dependence, tolerance, potency, therapeutic index , agonist, antagonist - mechanisms responsible for dependence and tolerance - names of drugs within classes e.g., be able to pick out a CNS stimula...

**Cumulative Questions (various chapters in the text) - names of drugs within classes - definitions of dependence, tolerance, potency, therapeutic index , agonist, antagonist - mechanisms responsible for dependence and tolerance - names of drugs within classes e.g., be able to pick out a CNS stimulant from a list of opiates - features of the different admin methods - drugs sites of action in CNS re: brain areas - general mechanisms of actions of drugs - general effects of cocaine, amphetamine, and ecstasy CNS Stimulants: Drugs that increase brain and spinal cord activity, enhancing alertness and energy, e.g: Caffeine: Increases alertness, reduces fatigue Amphetamines (e.g., Adderall): Treat ADHD, improve focus Cocaine: Illicit, boosts dopamine for euphoria Methylphenidate (Ritalin): Treats ADHD, enhances attention  Nicotine: Found in tobacco, stimulates cognitive function CNS Depressants: Drugs that slow down brain and spinal cord activity, inducing relaxation, sedation, or sleep, e.g: Benzodiazepines (e.g., Valium): Treat anxiety, promote calmness Barbiturates (e.g., Phenobarbital): Used for seizures, but less common due to overdose risk Alcohol: Common depressant that impairs coordination and judgment Z-drugs (e.g., Zolpidem): Treat insomnia by promoting sleep Antidepressants: Drugs used to treat depression by balancing brain chemicals (neurotransmitters like serotonin, norepinephrine, and dopamine), e.g: SSRIs (e.g., Fluoxetine): Increase serotonin levels. SNRIs (e.g., Venlafaxine): Increase both serotonin and norepinephrine. Tricyclic Antidepressants (e.g., Amitriptyline): Older class, affects multiple neurotransmitters. MAOIs (e.g., Phenelzine): Inhibit breakdown of neurotransmitters, but require dietary restrictions Antimanic Drugs: Drugs used to stabilize mood, primarily in the treatment of bipolar disorder, reducing mania and preventing mood swings, e.g: Lithium: The most common and effective treatment for mania. Anticonvulsants (e.g., Valproate): Used to stabilize mood by calming brain activity. Atypical Antipsychotics (e.g., Olanzapine): Treat acute mania and prevent mood fluctuations Barbiturates: Central Nervous System (CNS) depressants that were once commonly used for sedation, anesthesia, and treating seizures but are now less frequently used due to their high risk of overdose and addiction, e.g: Long-acting: Used for seizure control (e.g., Phenobarbital). Short-acting: Used for anesthesia or sedation (e.g., Thiopental). Intermediate-acting: Previously used for anxiety or sleep (e.g., Amobarbital) Benzodiazepines: CNS depressants used to treat anxiety, insomnia, seizures, and muscle spasms by enhancing the effect of the neurotransmitter GABA, which calms brain activity, e.g: Short-acting: Used for sleep and acute anxiety (e.g., Alprazolam which is Xanax) Intermediate-acting: Common for anxiety disorders (e.g., Lorazepam which is Ativan) Long-acting: Used for chronic anxiety and seizure disorders (e.g., Diazepam which is Valium) Anti-Psychotics: Drugs used to manage symptoms of psychosis (e.g., schizophrenia, bipolar disorder) by altering dopamine levels in the brain, e.g: Typical (First-generation): Primarily block dopamine receptors (e.g., Haloperidol) used to treat schizophrenia and acute psychosis  Atypical (Second-generation): Affect both dopamine and serotonin receptors, with fewer movement-related side effects (e.g., Risperidone, Clozapine) used to treat schizophrenia, treatment resistant schizophrenia, and bipolar disorder Psychedelics: Substances that alter perception, mood, and cognitive processes, often causing hallucinations and profound changes in consciousness, e.g: LSD (Lysergic acid diethylamide): Causes visual and sensory distortions. Psilocybin (Magic Mushrooms): Produces altered states of perception and mood. MDMA (Ecstasy): Affects mood and perception, often associated with euphoria and heightened empathy. DMT (Dimethyltryptamine): Causes intense, short-term hallucinations  Agonist/Direct Agonist: a drug or molecule that binds directly to a receptor and activates it, producing a biological response, i.e., it mimics the effect of the natural neurotransmitter or hormone at the receptor, e.g., morphine is a direct agonist at opioid receptors, producing pain relief by activating these receptors Partial agonist: binds to the receptor and activates it but not to the full extent-- it produces a weaker response, e.g., buprenorphine produces some pain relief but less than a direct agonist like morphine Antagonist: a substance that binds to a receptor but does not activate it-- it blocks or inhibits the receptors activation by other substances Additive: When two drugs are combined, and their effects add up E.g., if Drug A causes a 5-point increase in heart rate and Drug B causes a 5-point increase, together they cause a 10-point increase Superadditive (Potentiation): When two drugs combined produce a greater effect than the sum of their individual effects E.g., Drug A causes a 5-point effect, Drug B causes a 5-point effect, but together they cause a 15-point effect.  Competitive Agonist: A drug that binds to the same receptor site as another substance, competing for that spot. It can be displaced by a higher concentration of the original substance Noncompetitive Agonist: A drug that binds to a different site on the receptor, not the same one as the original substance, but still changes the receptor's function, even if the original substance is present Physiological Antagonist: A drug that causes an opposite effect to another drug by acting on a different receptor or pathway. For example, one drug may raise blood pressure, while the physiological antagonist lowers it Depolarization - What Happens: Depolarization occurs when the inside of the neuron becomes less negative (or more positive) than its resting potential How: This is usually triggered by opening sodium (Na+) channels. Na+ ions flow into the cell, making the inside more positively charged Result: If enough depolarization occurs to reach a certain threshold, it triggers an action potential, allowing the neuron to send an electrical signal down its axon Purpose: Excitatory signals increase the chance that a neuron will "fire" and pass along the signal to other neurons effect of drug: e.g., drugs like nicotine or certain stimulants (e.g., cocaine) can increase the release or effect of excitatory neurotransmitters, such as dopamine or acetylcholine ○ These drugs may open sodium (Na+) channels or mimic excitatory neurotransmitters, making the neuron more likely to depolarize and fire. ○ Increased neural activity, leading to feelings of energy, alertness, or euphoria Hyperpolarization - What Happens: Hyperpolarization makes the inside of the neuron more negative than its usual resting potential How: This can occur by opening potassium (K+) channels (K+ flows out of the cell) or chloride (Cl-) channels (Cl- flows into the cell), both of which increase the negative charge inside Result: This negative shift makes it harder for the neuron to reach the threshold needed for an action potential, decreasing its likelihood of firing Purpose: Inhibitory signals reduce the chance that a neuron will send a signal, helping to control or limit neural activity effect of drug: e.g., Depressants, like alcohol and benzodiazepines, enhance the action of GABA, the brain’s primary inhibitory neurotransmitter ○ These drugs open chloride (Cl-) channels or boost GABA’s binding, making the inside of the neuron more negative, leading to hyperpolarization. ○ Reduced likelihood of neuron firing, resulting in calmness, sedation, or muscle relaxation Tolerance: Occurs as a result of repeated use/administration of drug State of decreased effectiveness and/or need to increase dosage for same level of effect Varies as a function of drug effects Eventually dissipates Pharmacokinetic Tolerance: (metabolic tolerance) when the body gets better at breaking down a drug, so the drug doesn’t have as strong an effect as it did before → This usually happens because the liver produces more enzymes (cytochrome P450) to process the drug faster Drug movement*** Essentially more of the drug is needed to feel effects Can create cross-tolerance Pharmacodynamic Tolerance: (physiological tolerance) occurs when the body’s cells, especially in the brain, become less sensitive to a drug over time. This means that the same amount of the drug has a weaker effect because the body’s cells aren’t responding to it as strongly Drug change*** In pharmacodynamic tolerance, the body adapts to drugs by changing the number or sensitivity of receptor sites on nerve cells: 1. Nerve cells send signals by releasing chemicals called neurotransmitters, which attach to receptor sites on nearby cells. 2. Some drugs block these receptor sites, reducing the effect of the neurotransmitter. 3. The body senses this change and responds by creating more receptor sites or making existing ones more sensitive—this is called upregulation. 4. If a drug stimulates (rather than blocks) these receptor sites, the body may reduce the number or sensitivity of receptors in response—this is called downregulation. These changes help the body maintain balance but also make the drug less effective over time Dependence: compulsive use of drugs despite adverse consequences Psychological dependence: experiencing a cluster of unpleasant physical and psychological effects upon termination of drug use E.g., presence of withdrawal symptoms/abstinence syndrome E.g., the effects experienced opposite of drug effects E.g., severity, length, timing of withdrawal influenced by dose, moa, and rate of elimination Primary psychological dependence: Driven by a direct desire for the drug’s pleasurable or rewarding effects. The person seeks the experience or “high” the drug provides  Secondary psychological dependence: Driven by a need to manage or escape negative feelings or stress. The drug use is primarily about coping with discomfort rather than seeking positive effects Cross Dependence: phenomenon in which use of a drug (typically from same class) stops withdrawal symptoms Reverse Tolerance: occurs when a person becomes more sensitive to a drug over time, meaning that smaller doses start to have a stronger effect than they initially did. This can happen because repeated use of the drug causes changes in the brain or body that make it respond more intensely, rather than building tolerance e.g., someone who drinks alcohol might initially need a lot to feel its effects, but with reverse tolerance, they might later feel drunk from just a small amount Cross-tolerance: tolerance to one drug can diminish the effect of another drug— often seen between members of the same class of drug, e.g., opioids, morphine, heroin, oxycodone Acute tolerance: tolerance that has developed during a single administration An example of acute tolerance is alcohol, as BA level rises a person feels increasingly intoxicated but the subjective effect of intoxication peaks before BA level does and the subjective effect of intoxication disappears before all of the alcohol leaves the person's body Behavioral Tolerance: through experience with a drug, an organism can learn to decrease the effect that the drug is having Habituation: With repeated use, a person starts to feel less of the drug’s effects because they get used to it. It’s like how you might stop feeling the heat after being in the sun for a while. Over time, the drug feels less intense Specific tolerance refers to the decrease in the effect of a drug when taken repeatedly, but only for the specific effect it has on a particular receptor or system Psychological Dependence VS Physical Dependence - Psychological: individual feels a mental or emotional need for the drug, often experiencing cravings or a strong desire to use it to cope with stress, emotions, or certain situations Physical: The body adapts to the drug, leading to withdrawal symptoms (e.g., shaking, nausea, seizures) if the drug is reduced or stopped Addiction - Characterized by tolerance, psychological, and physical dependency, and organ changes 3 C's: compulsion, loss of control, continued use despite adverse consequences Withdrawal - Not associated with severe or medically serious withdrawal syndrome  Initial high is followed by a crash that can be relieved by taking another dose Withdrawal symptoms appear within 1/2 hour for cocaine, few hours for amphetamines Withdrawal symptoms include ranging depression and suicidal thoughts, insomnia, vivid and unpleasant dreams, appetite loss Initial withdrawal lasts ~ a week but depression, sleep and eating issues can persist for months Amphetamine withdrawal symptoms include cognitive impairment, anxiety, panic, drug craving Mechanisms of Action Amphetamines- Block re-uptake of DA, NE, and 5-HT: ○ DA = Dopamine, NE = Norepinephrine, 5-HT = Serotonin. ○ The drug blocks reuptake of these neurotransmitters, meaning it prevents them from being taken back into the neuron after they’ve been released. ○ This leads to increased levels of these neurotransmitters in the synaptic cleft, intensifying their effects. Binds to receptors/substrate recognition sites on MAT: ○ MAT = Monoamine Transporters (these include DAT (dopamine transporter), NET (norepinephrine transporter), SERT (serotonin transporter), and VMAT2 (vesicular monoamine transporter 2)). ○ The drug binds to these transporter sites on neurons to block reuptake. ○ Reuptake Blockers: By binding to these transporters, the drug prevents the neurotransmitters from being reabsorbed, leading to their accumulation in the synaptic cleft. Act as Competitive Reuptake Inhibitors (CRI): ○ The drug competes with neurotransmitters (like DA, NE, and 5-HT) for binding to the transporter proteins. ○ It binds to the MAT in its inward position (when it's ready to take the neurotransmitter back into the neuron), preventing reuptake and allowing neurotransmitters to stay in the synapse longer. Amphetamine Effects: ○ Increases neurotransmitter release: Amphetamines cause neurons to release more neurotransmitters like dopamine, norepinephrine, and serotonin. ○ Cause spontaneous leakage: They also make neurotransmitters leak out of the storage vesicles into the synapse without the neuron firing an action potential. ○ Induce release and block reuptake of glutamate: Amphetamines also affect glutamate, which is another neurotransmitter, by both inducing its release and blocking its reuptake. Effects on VMAT2 and MAO: ○ Bind to VMAT2: The drug binds to VMAT2 (vesicular monoamine transporter 2), causing neurotransmitters to build up inside the axon terminal.  ○ More neurotransmitter release: When an action potential occurs, more neurotransmitter is released because there is more in the axon terminal. ○ Inhibit MAO: The drug also inhibits MAO (monoamine oxidase), which is responsible for breaking down neurotransmitters. This increases the availability of neurotransmitters. Special Target: Mesotelencephalic Dopamine Pathway: ○ Mesotelencephalic pathway = A pathway in the brain that involves dopamine transmission. ○ It projects to the limbic system and nucleus accumbens, both of which are involved in reward, motivation, and pleasure. ○ This pathway is a key target for drugs like amphetamines and cocaine, which increase dopamine in these areas, leading to feelings of euphoria and reinforcing drug use Metabolization & Elimination Amphetamines- Excretion and Urine Acidity: ○ Urine pH: the excretion rate of amphetamines depends on urine acidity. Acidic urine leads to faster excretion, while basic (alkaline) urine slows elimination. ○ Other Excretion Pathways: amphetamines can also be excreted through sweat and saliva. Half-life: ○ L-amphetamine: 11–14 hours ○ D-amphetamine: 9–11 hours ○ Methamphetamine: 9–13 hours Metabolites: ○ Behaviorally Active Metabolites: Amphetamines have behaviorally active metabolites that can be detected for 2–3 days after drug use Physiological/Acute Effects Amphetamines-  activate sympathetic nervous system “fight or flight” → increase heart rate, increase respiration, increase body temp, elevate BP, increase blood flow to muscles and decrease blood flow to visceral organs Psychological Effects - Feelings of Euphoria (intense with IV and smoking), Giddiness, enhanced self-esteem/confidence Increased talkativeness Feelings of invincibility → methamphetamines Reduced sleep/increased mental alertness; subjective experience of improved or clarity of thought Increased sexual arousal Mechanisms of Action Cocaine - Block reuptake of DA, NE, and 5-HT: ○ DA = Dopamine, NE = Norepinephrine, 5-HT = Serotonin. ○ The drug blocks reuptake of these neurotransmitters, meaning it prevents them from being taken back into the neuron after they’ve been released. ○ This leads to increased levels of these neurotransmitters in the synaptic cleft, intensifying their effects. Binds to receptors/substrate recognition sites on MAT: ○ MAT = Monoamine Transporters (these include DAT (dopamine transporter), NET (norepinephrine transporter), SERT (serotonin transporter) ○ The drug binds to these transporter sites on neurons to block reuptake. ○ Reuptake Blockers: By binding to these transporters, the drug prevents the neurotransmitters from being reabsorbed, leading to their accumulation in the synaptic cleft. Act as Competitive Reuptake Inhibitors (CRI): ○ The drug competes with neurotransmitters (like DA, NE, and 5-HT) for binding to the transporter proteins. ○ It binds to the MAT in its inward position (when it's ready to take the neurotransmitter back into the neuron), preventing reuptake and allowing neurotransmitters to stay in the synapse longer. Cocaine blocks NA+ (Sodium) Ion Channels: Cocaine also blocks sodium channels on neurons, which prevents them from firing properly. This effect contributes to its anesthetic properties and may alter the communication between neurons, leading to its stimulating effect Special Target: Mesotelencephalic Dopamine Pathway: ○ Mesotelencephalic pathway = A pathway in the brain that involves dopamine transmission. ○ It projects to the limbic system and nucleus accumbens, both of which are involved in reward, motivation, and pleasure.  ○ This pathway is a key target for drugs like amphetamines and cocaine, which increase dopamine in these areas, leading to feelings of euphoria and reinforcing drug use Metabolization & Elimination Cocaine - Excretion: Cocaine is excreted through urine, sweat, and saliva, with minimal amounts excreted unchanged-- meaning the drug leaves the body in the same form it was originally taken, without being metabolized or broken down by the liver or other organs Half-life: Oral: Around 1 hour. Intranasal: Between 30 minutes and 5 hours. Intravenous: Between 15 minutes and 3.5 hours. Detection in Urine: Cocaine itself can typically be detected in urine for up to 12 hours after intravenous use. Metabolites of cocaine, particularly benzoylecgonine, can be detected for up to 10 days in chronic users  Interaction with Alcohol: Cocaine metabolically interacts with alcohol, creating a metabolite called cocaethylene, which can enhance and prolong the effects of cocaine and increase toxicity Cocaine Effects - Physiological/Acute Effects - activate sympathetic nervous system “fight or flight” → increase heart rate, increase respiration, increase body temp, elevate BP, increase blood flow to muscles and decrease blood flow to visceral organs Psychological Effects - Feelings of Euphoria (intense with IV and smoking), Giddiness, enhanced self-esteem/confidence Increased talkativeness Feelings of invincibility → methamphetamines Reduced sleep/increased mental alertness; subjective experience of improved or clarity of thought Increased sexual arousal Effects on Driving - Poor decision making Decreased reaction time Hallucinations & Paranoia Aggressive driving Fatigue after initial effects Differences Between Cocaine and Amphetamines Duration of Effects Cocaine: Shorter-lasting (15–30 minutes) Amphetamines: Longer-lasting (4–10 hours depending on type and use) Mechanism of Release Cocaine: Primarily inhibits reuptake of dopamine and norepinephrine Amphetamines: Prevent reuptake and increase the release of dopamine and norepinephrine directly Medical Uses Cocaine: Rarely used, but can be a local anesthetic in some medical contexts. Amphetamines: Used for ADHD, narcolepsy, and obesity. Physical Risks Cocaine: Higher risk of sudden cardiovascular events (e.g., heart attack, stroke) Amphetamines: Risks are more often from long-term use, affecting the heart and brain Forms and Methods of Use Cocaine: Usually snorted or smoked (as crack) Amphetamines: Commonly taken orally or injected, with a slower onset than smoked crack cocaine MDMA affects three main neurotransmitter systems - 1. Serotonin: MDMA releases large amounts of serotonin and blocks its reuptake, creating feelings of euphoria, empathy, and sensory enhancement. The eventual drop in serotonin can lead to a "comedown." 2. Dopamine and Norepinephrine: MDMA boosts dopamine (euphoria) and norepinephrine (alertness, heart rate). This contributes to stimulation and energy 3. Oxytocin and Cortisol: MDMA increases oxytocin (bonding hormone) and cortisol (stress hormone), enhancing feelings of closeness but also stress after-effects 4. MDMA also stimulates the hypo-thalamic-pituitary-adrenal axis, amplifying the levels of the stress hormone cortisol Metabolization & Elimination MDMA - Excretion: MDMA is excreted via urine, with minimal amounts excreted unchanged-- meaning the drug leaves the body in the same form it was originally taken, without being metabolized or broken down by the liver or other organs Half-life: ~8 hours 40 hours for ~95% of drug to be eliminated Metabolites: Metabolized to MDA Psychological Effects MDMA - Increased wakefulness Increased endurance E.g., in documentary when the characters could dance all night long, felt extroverted Heightened sense of emotional closeness to others Heightened self-awareness Feelings of peace and tranquility Adverse Psychological Effects - Psychosis-like state E.g., in docu, the girl who said she felt like she was seeing demons in her apartment ecstasy is both a CNS stimulant and hallucinogen, creates feelings of empathy, connectedness, etc but also paranoia, anxiety etc Pronounced anxiety Depersonalization and derealization Depression Cognitive deficits Sleep disturbances Biological Effects - Pupil dilation Headache Dizziness Muscular tension Jaw clenching and grinding Dose-dependent cardiovascular effects, e.g., increased blood pressure Medical Risks associated with MDMA - Hypothermia Due to prolonged exertion, as well as being in a warm environment Elevated levels of serotonin Acute Hyponatremia Low plasma sodium level due to dilution of blood with water Occurs as a result of excess water intake MDMA causes secretion of antidiuretic hormone, which promotes water retention by kidneys Hepatitis Severity ranges from mild to severe Repeat users may suffer from jaundice Long-lasting alterations to both dopamine and serotonin brain systems General Routes of Administration - Inhalation: Process: Breathing in drugs for absorption in the lungs (e.g., smoking marijuana, crack, nicotine) Mechanism: Diffusion governs gas movement between inhaled air and blood ○ Higher concentration in air: Drug moves into the blood ○ Higher concentration in blood: Drug moves into the exhaled air Differences: Vapor vs. Smoke:  ○ Smoke: Particles don’t revaporize; must be eliminated by other means ○ Vapor: May allow some re-exhalation Advantages: Fast absorption: Dense blood vessels in the lungs Disadvantages: Smoking: 1. Respiratory problems (e.g., lung cancer) 2. Quick, short-lasting effects 3. Irritation (lungs, throat, mucus/dry throat) Vapor: 1. Respiratory problems (e.g., lung cancer) 2. Quick, short-lasting effects 3. Irritation (lungs, throat, mucus/dry throat) 4. Chronic use can lead to cognitive impairments (e.g., attention, memory issues) and personality changes Snorting: Drugs (e.g., cocaine, heroin, tobacco) are sniffed into the nostrils (snorting). Process: ○ Drug dissolves in the moist mucous membranes of the nasal cavities. ○ Absorption occurs into the bloodstream. ○ Some drug may enter the lungs or run down the throat into the stomach and digestive tract Disadvantages: Nasal Irritation: Can cause discomfort or damage to the nasal mucosa. Variable Absorption: Absorption can be inconsistent due to factors like nasal congestion or the presence of mucus. Risk of Overdose: Fast absorption may lead to a higher risk of overdose if users take more than intended. Limited Amount: Only a small amount of drug can be effectively absorbed through the nasal passages at one time. Additional Advantages: Rapid Onset: Effects can be felt quickly, often within minutes, due to the efficient absorption in the nasal mucosa. Avoids First-Pass Metabolism: Bypasses the gastrointestinal tract and liver, which can break down the drug before it enters circulation. Convenience: Non-invasive method that doesn't require needles, making it easier for some users to administer compared to injections Oral Administration (p.o, Latin for "per os" which means "by mouth"): Process: ○ Drug enters the stomach, where strong acids and enzymes break it down. ○ Liquid moves to intestines, where absorption occurs (most efficient due to capillaries).  ○ Absorption involves passing through intestinal wall into capillaries. Factors Affecting Absorption: Stomach contents: Full stomach slows absorption. Lipid solubility: Affects how drug absorbs into fatty tissue. Forms: Tablets, pills, liquids, or mixed in food (e.g., LSD, marijuana, alcohol). Advantages: ○ Safest, cheapest, and most convenient. ○ Allows time for expelling the drug (e.g., vomiting). Disadvantages: ○ Slower absorption than inhalants. ○ Delayed feedback (risk of overdose if more is taken). ○ Variability in absorption. ○ Irritation from some substances (nausea, vomiting). Alternative Absorption Methods Types: ○ Buccal (against cheek) ○ Sublingual (under tongue) ○ Intrarectal (inserting into the rectum) Advantages: ○ Useful when oral intake isn't possible (e.g., unconscious patients). Disadvantages: ○ Potential irritation of skin/membranes. ○ Variability in absorption Brain Interaction - Pons Location: Located above the medulla and below the midbrain. Function: Connects different parts of the brain; involved in regulating sleep and arousal, and relaying information between the cerebellum and the cerebrum. Role in Drug Effects: Affects sedative and anesthetic drug action by influencing sleep and wakefulness. 2. Medulla Location: Located at the base of the brainstem, connecting the brain to the spinal cord. Function: Controls autonomic functions such as heart rate, blood pressure, and respiration. Role in Drug Dependency: Opioids and other depressants can depress medullary function, affecting vital signs and potentially leading to overdose. 3. Cerebellum Location: Located at the back of the brain, beneath the occipital lobes. Function: Coordinates voluntary movements, balance, and motor learning. Role in Drug Effects: Alcohol and other sedatives impair coordination and balance by affecting cerebellar function. 4. Reticular Formation (Reticular Activating System - RAS)  Location: A network of neurons located throughout the brainstem. Function: Regulates wakefulness, sleep-wake transitions, and alertness. Role in Drug Effects: Stimulants increase activity in the RAS, enhancing alertness, while depressants decrease activity, leading to sedation. 5. Thalamus Location: Located above the brainstem, at the top of the brain's central core. Function: Acts as the brain's relay station for sensory and motor signals; regulates consciousness and alertness. Role in Drug Effects: Drugs affecting sensory perception can modulate thalamic activity, impacting sensory processing. 6. Hypothalamus Location: Located below the thalamus, part of the limbic system. Function: Regulates homeostasis, including hunger, thirst, temperature, and circadian rhythms; controls the pituitary gland. Role in Drug Dependency: Many addictive substances alter hypothalamic functions, influencing cravings and reward pathways. 7. Hippocampus Location: Located in the medial temporal lobe. Function: Involved in memory formation and spatial navigation. Role in Drug Effects: Substance use can impair memory and learning due to its effects on the hippocampus, contributing to dependency. 8. Midbrain Location: Located above the pons and below the thalamus. Function: Involved in vision, hearing, motor control, sleep/wake cycles, and temperature regulation. Role in Drug Effects: Drugs like stimulants can enhance dopaminergic activity in the midbrain, influencing reward and motivation. 9. Periaqueductal Gray Area Location: Surrounds the cerebral aqueduct in the midbrain. Function: Involved in pain modulation and defensive behavior. Role in Drug Effects: Opioids exert their analgesic effects primarily through the periaqueductal gray area. 10. Ventral Tegmental Area (VTA) Location: Located in the midbrain. Function: Produces dopamine and is critical for the reward system. Role in Drug Dependency: Drugs of abuse increase dopamine release from the VTA, reinforcing addictive behaviors ​