Brain in Human Life - Addiction and Mental Health Topic Review PDF
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This document is a topic review on neurochemistry as it pertains to addiction and mental health. It covers neurotransmitter classifications and functions, and explains the effects of neurotransmitters on presynaptic and postsynaptic neurons. Various aspects, including drug actions, routes, and treatments are also included.
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Neurochemistry Handout Quiz #2 General Study Set - Addiction and Mental Health by Camy Burnston's Key Concepts by Camy Chemistry of Behavior Study Set by Chris Mental Health Study Set by Chris Addiction (Wee) Study Set by Chris 1. Understand how neurotransmitters are classified based on structure...
Neurochemistry Handout Quiz #2 General Study Set - Addiction and Mental Health by Camy Burnston's Key Concepts by Camy Chemistry of Behavior Study Set by Chris Mental Health Study Set by Chris Addiction (Wee) Study Set by Chris 1. Understand how neurotransmitters are classified based on structure and function. Give examples. Classifications - Synthesized in presynaptic neurons - Released when APs reach axon in terminal - Recognized by receptors - Blocking its release interferes with a cell's ability to affect a postsynaptic cell, causing changes in the latter. Structure - Amino acid NTs - GABA, Glutamate - Peptide NTs - (neuropeptides) oxytocin, vasopressin, opiates (enkephalin, endorphin) - Amine NTs - acetylcholine, serotonin, catecholamines = dopamine, norepinephrine - Gas NTs - nitric oxide, carbon monoxide Function - Excitatory/Inhibitory - Excitatory example: Glutamate binds to AMPA and NMDA receptors and releases EPSPs - Inhibitory example: GABA’s receptors are ionotropic and allow Cl- into cell - Peptides: many peptides act as NTs, and opioid peptides mimic opiate drugs (ex, morphine) 2. Explain what it means to be an inhibitory or excitatory neurotransmitter. - Inhibitory neurotransmitters (like GABA) inhibit neural firing (hyperpolarize) by opening Cl- channels. - Excitatory neurotransmitters (like Glutamate or norepinephrine) excite the neuron (depolarize) through the influx of sodium ions into the cell. 3. Defined these terms: Exogenous: Foreign substance from external source (ex: drug) Endogenous: Internal substance made within the body (ex: neurotransmitter) Ligand: any substance that binds to a receptor (could be endo/exogenous) Neurotransmitter: chemical messenger carrying signals between neurons, muscles, and glands through the synapse Drug: chemical substance (exogenous) that produces biological effects in a living organism Agonist: a chemical that mimics neurotransmitters (enhances their effects) Antagonist: a chemical that blocks NT action Reuptake-inhibitor: increases the amount of NTs by preventing them from being reabsorbed by the presynaptic neuron 4. Understand the different routes of drug administration and their relative effectiveness/ease of taking the drug. (1) Ingestion: requires a higher dose for oral (much of the substance will get digested) (2) Injection: faster, doesn’t have to go through the digestive system (3) Inhalation: needs a higher dose; the patient swallows lots of drugs (4) Absorption (through mucous membranes): effective very quickly 5. Give examples of drug action on the presynaptic neuron. - Transmitter production: drugs may block synthetic enzymes - Ex. Choline acetyltransferase (ChAT) is the enzyme that synthesizes ACh; drugs could increase or decrease ChAT activity - Transmitter release: inhibit or facilitate the release of NT from the axon terminal - Ex. Botox blocks ACh release - Ex. Amphetamine increases catecholamine release - Transmitter clearance: Drugs called reuptake inhibitors can block the reuptake of the transmitter, while others allow the transmitter to accumulate by blocking enzymes - Ex. Amphetamine, Cocaine block reuptake of catecholamines - Ex. Prozac and other SSRIs (selective serotonin reuptake inhibitors) block the reuptake of Serotonin - Ex. Acetylcholinesterase inhibitors - Ex. MAO inhibitors to treat depression 6. Give examples of drug action on the postsynaptic neuron. - Can affect transmitter receptors - Receptor antagonists - Receptor agonists - Can affect cellular processes/regulate receptors - up-regulating or down-regulating receptor densities - altering cellular processes (e.g., Lithium to treat depression) Here is a list of chemicals to know: 1. Be familiar with these neurotransmitters by name and structure (peptide, amino acid derivative, catecholamine, etc.): Acetylcholine: Amine NTs, ACh is composed of an acetate and choline Nicotinic receptors (ionotropic) Muscarinic receptors (metabotropic) Dopamine: Amine NTs, catecholamine (derived from the amino acid tyrosine) Dopamine receptors (D1, D2, D3, D4, D5), all of which are metabotropic Serotonin: Amine NTs, monoamine (derived from the amino acid tryptophan) 5-HT receptors (several subtypes, both ionotropic and metabotropic). Glutamate: Amino Acid NTs, excitatory Both ionotropic receptors and metabotropic receptors GABA: Amino Acid NTs, inhibitory Both ionotropic receptors and metabotropic receptors Opioids (endorphin, enkephalin): Peptide NTs Opioid receptors (metabotropic) 2. Be able to describe/identify the mechanism of action (i.e., how they work) for these exogenous substances: Benzodiazepines: (anxiolytics) act as neuromodulators to enhance the effects of GABA Caffeine: adenosine receptor antagonist; caffeine (stimulant) blocks adenosine’s inhibition of glutamate = disinhibition Cocaine: blocks reuptake of dopamine, causing an accumulation of dopamine in the synaptic cleft. LSD: serotonin receptor agonist Monoamine oxidase inhibitors (MAO-Is): Prevents the breakdown of monoamines at the synapses. This leads to increased levels of monoamines in the synaptic cleft. Nicotine: Nicotinic Acetylcholine Receptor Agonist: Nicotine acts as an agonist at nicotinic acetylcholine receptors (ionotropic) Prozac: Inhibits serotonin reuptake into the presynaptic cell SSRIs: Serotonin selective reuptake inhibitor (same mechanism as Prozac) Topic Review for Addiction and Mental Health 1. Be familiar with the terminology related to addiction and mental health. - Addiction: a chronic dysfunction of the brain system that involves reward, motivation, and memory 2. Describe the characteristics of someone who is experiencing addiction. - be unable stay away from the substance or stop the addictive behavior - display a lack of self-control - have an increased desire for the substance or behavior - dismiss how their behavior may be causing problems - lack an emotional response 3. Name and describe the major theoretical models of substance abuse 1) Moral Model: abuser lacks moral character or self-control 2) Disease Model: abuser requires medical treatment 3) Physical Dependence Model: abusers use drugs to avoid withdrawal symptoms like dysphoria (strong negative feelings) 4) Positive Reward Model: drug use is a behavior controlled by positive rewards 4. List the brain areas associated with reward and drug cravings. - Nucleus accumbens: some axons that terminate here originate in the ventral tegmental area (VTA) involved in the reward pathway - Insula: brain region in the frontal cortex (people with damage to the insula have been able to stop smoking effortlessly) 5. Explain why not everyone who takes drugs becomes addicted to them (that is, explain why there are individual differences in susceptibility to becoming addicted). Major risk factors for addiction - Biological factors: being male - Poor family life - Personality factors: poor emotional control - Environmental factors: living in neighboorhoods with high rates of addiction 6. Describe the different treatments for addiction. - Some quit on their own - Counseling/social interventions: 12 step program AA - Lessening the discomfort of withdrawal and drug craving : anti- nausea meds, rTMS (= repetitive Transcranial Magnetic Stimulation) - Providing alternate to the addictive drug: agonists or partial agonists to wean addicts off the drug (nicotine patch) - Directly blocking actions of the addictive drug: Narcan (naloxone), opiate receptor antagonist is used to block heroin action - Block brain’s reward circuitry: DA receptor blockers blunt activity of DA reward system, so addictive drugs lose pleasurable qualities - Immunization to render drug ineffective 7. Explain what the DSM is and some of the “issues” related to its use. - Diagnostic statistical manual, big book of all mental disorders - It's been wrong in the past 8. Describe the symptoms of depression, bipolar disorder, and the different types of anxiety disorders discussed in class. (Note: not everyone who has the condition will experience all these symptoms). - Depression - Unhappy mood, Loss of interests, reduced energy, Changes in appetite and sleep patterns, Difficulty in concentration, Restless agitation or torpor, Pessimism and thoughts of death (brain changes: increased activation in frontal lobes during cognitive tasks and amygdala during emotional processing) - Bipolar-alternating depression and mania, men and women are equally affected (enlarged ventricles and reduced gray matter) - Anxiety - Phobic disorders- intense irrational fears centered on an object, activity or situation that the person avoids - Panic disorders- recurrent transient attacks of intense fearfulness - Generalized anxiety disorder- persistent, excessive anxiety and worry - OCD- recurrent, unwanted thoughts and engages in repetitive behaviors without any reason or ability to stop 9. Explain what concordance rates tell us about how a condition is inherited. In genetics, concordance is the probability that a pair of individuals will both have a certain characteristic (phenotypic trait) given that one of the pair has the characteristic. In twin studies, concordance rates are interpreted by comparing rates between identical and fraternal (non-identical) twins. 10. Describe the various treatments for depression, bipolar disorder, and the anxiety disorders discussed in class. - Depression- ECT, rTMS, MAO inhibitors, tricyclics, SSRIs, CBT, Ketamine, vagal nerve stimulation, deep brain stimulation - Bipolar- lithium to increase grey matter - Anxiety- Benzodiazepines are anxiolytic drugs, used to treat anxiety (bind to GABA receptors and enhance GABA’s inhibitory actions.) Serotonin agonists and SSRIs can also treat anxiety. - OCD- CBT, SSRIs, deep brain stimulations, lesions to pathways involved 11. Explain the sex differences that have been observed for depression. - May reflect: patterns of help seeking, hormone difference and postpartum depression 12. Differentiate between “compulsions” and “obsessions” Compulsions are behaviors, while obsessions are thoughts. KEY CONCEPTS (Burnston) Health and Disease Naturalism: facts about health and disease are facts about the physical world (faults lie in the body, diseases should be “fixed”) Constructionism: facts about health and disease are relative to what we value as a society (fault is in society, diseases are just mismatches between society and body) Neurodiversity Neurodiversity: The claim that there are no inherently disordered kinds of brain or mental conditions, only neural differences that can be harmful or beneficial depending on context (constructivist view of mental disorder) - It has anti ableism elements - Analogies: left-handedness, homosexuality, biodiversity Addiction MEDICAL V MORAL MODEL Medical Model — drug addiction is a disease/disorder, comprising compulsive use based on physical causes Moral model — drug users choose to use drugs for the pleasure Psychedelics Neuro-existentialist anxiety: due to the internalization of the idea that we are just the result of causal occurrences in our brains “Manifest” v. “Scientific” image: Our introspective understanding of the world, v. the picture of the world that science gives us Ego dissolution: Lessening of focus on or interest in the self; lessening of perception of boundaries between self and other. Pickard — What We’re Not Talking About when We’re Talking About Addiction Summary: The Brain in Human Life Review Questions for Quiz #2 1. True/False: All neurotransmitters have the same structure. 2. What EFFECT in the postsynaptic neuron is produced by the release of an inhibitory neurotransmitter? hyperpolarization 3. What are the building blocks of peptide neurotransmitters? (Hint: they are the basic unit of all peptides or proteins!) Aminos acids 4. Explain the difference between the terms “endogenous” and “exogenous” and give an example of each. 5. The term “nicotinic” refers to which neurotransmitter? 6. If an agonist produces an EPSP in the postsynaptic cell, what effect does an antagonist produce? 7. Swallowing a pill is getting the drug into the body through which ROUTE OF ADMINISTRATION? 8. Compare i.v. vs oral administration of a drug in terms of speed of action and relative amount needed to be taken to have same desired effects. 9. The Blood-Brain Barrier is made up of tight junctions between endothelial cells that make up blood vessels and extensions of _____________. 10. What does Choline Acetyl Transferase (ChAT) do? 11. Why should someone who is taking Benzodiazepines not drink alcohol? 12. Compare the effects of Prozac to LSD in terms of mechanism of action and result. 13. Which drug prevents catecholamines from re-entering the presynaptic neuron after it has bound to the postsynaptic neuron? Amphetamines/Cocaine 14. What is the DSM? 15. What information can be obtained from Concordance Rates? 16. Name and describe some non-pharmaceutical treatments for depression. 17. Name and describe some pharmaceutical treatments for depression. 18. How does depression differ from bipolar disorder? 19. T/F Despite having psychological symptoms, the brain is unaffected by mood disorders. 20. Differentiate among these three types of anxiety disorders: Generalized Anxiety, Panic, Phobic 21. Describe the mechanism of action for Benzodiazepines. 22. How do compulsions differ from obsessions? 23. Thought question: Why might there be so many conditions that are co-morbid with OCD?