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Study Questions Test 2.docx

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Department
Psychology
Course
PSB 2000
Professor
Berkley
Semester
Fall

Description
Study Questions Test 2 PSB2000 Drug Actions and Substance Abuse •In general, all drugs of abuse cause dopamine release in the nucleus accumbens. Okay, not a question, but KNOW THAT! •Stimulants: know some examples of stimulant drugs. What neurotransmitters do they increase? What are some behavioral effects? o Amphetamine (AMPH), cocaine, Ritalin (for ADHD), ecstasy o Increase dopamine, especially in nuclus accumbens o raise seratonin and norepinephrine release o raise excitement, activity, alertness, mood o lower fatigue –Cocaine: what is its method of action (ie, what does it do at a synapse)? o Cocaine blocks reuptake of serotonin, dopamine, and norepinephrine o Binds to DAT (dopamine transporter) blocking reuptake of dopamine o DAT maintains proper dopamine levels by removing excess dopamine from synapse o End effect is increase dopamine in synapse – “high” o Stored dopamine is depleted somewhat “crash” and depression –What does ritalin do at the synapse? How is it different from cocaine? o Ritalin has same effect as cocaine on dopamine, but different time- course and dose (ritalin increases and decreases slower; take less ritalin at a time as compared to cocaine) o Different from cocaine bc of o Dose o Oral administration o Slow release formulas o More gradual effect: no sudden high –What does ecstasy do at the synapse? What are the effects of long-term use neurons? What are some psychological/cognitive effects? Know examples of hormones that ecstasy affects and the behavioral result. o Ecstasy (MDMA) increases Da release…at high doses it also increases serotonin release. o At high doses stimulates serotonin release (reverses seretonin transmporter) hallucinogenic effects, decrease in depression, and anxiety o Large injections destroys dopamine and serotonin neurons thinner cell layers in some brain areas o Neurons may recover after few months of not using o Human users: more depression, anxiety, sleep problems, memory deficits, attention problems, and impulsiveness; even after 1-2 years of quitting o Hormones o Increase in oxytocin release  Social attachment stuff o Increase in vasopressin release  Antidiuretic; stimulates you to drink water •What is serotonin syndrome? Understand why drug interactions could cause it. o Serotonin syndrome: too much serotonin released into body bc of too much of a serotonin agonist or bc mixing drugs that act in come capacity as serotonin agonists •What type of receptor does nicotine use? What is the effect of long-term nicotine use on dopamine cells? o Increases dopamine release in nucleus accumbens o Stimulates nicotinic Ach receptor on VTA neurons, exciting them o Cells become less responsive than usual after repeated nicotine use (tolerance)  other pleasures (including nicotine itself) become less reinforcing •Opiates: know some example. What receptor do they use? What is the endogenous ligand of those receptors (in other words, we don’t have those receptors so we can use heroine…why do we have them)? How do opioids increase dopamine in n. accumbens? What is methadone, how does it work and why is it used clinically? o Examples: Morphine, heroine, methadone o Receptor: opioid receptors (aka endorphin receptors) o Why do you even have those?? So you can appreciate the effects of heroin?? Hint: Endorphins= endogenous morphines You have opioid/endorphin receptors b/c your brain makes its own opioids (called endorphins) that are helpful in pain control o On GABA neurons in VTA (GABA usually inhibits dopamine neurons in VTA that project to NA; inhibit the GABA neurons = disinhibition of dopamine neurons) o Methadone is taken to combat opoid addiction o Similar to heroine and morphine, but no ‘high’ o Taken as pill, enters brain and blood slow  no rush o Metabolized slowly, no crash •Cannabinoids: How do they increase dopamine in n. accumbens? What is their effect on glutamate and GABA? What are some medicinal uses? What are some psychological effects? What are some withdrawal symptoms reported by heavy smokers? o Indirectly increase dopamine in NA o Inhibits BABA in VTA more dopamine to nucleus accumbens o Retrograde transmitters that temporarily decrease transmitter release. o Decrease release of both glutamate (excitatory) & GABA (inhibitory) o Medicinal uses: decreases nausea, decrease pain, increase appetite by axn in hypothalamus; combats glaucoma o Psychological effects: intense sensory experiences and illusion of time passing slowly o Can impair memory and cognition o Heavy smokers report withdrawl symptoms (anxiety, depression, stomach pain, craving, loss of appetite, sleep problems) •Hallucinogens: What is the psychological effect? What neurotransmitters are effected? What receptor do they use? o LSD, psilocybin (mushrooms), PCP; o stimulate serotonin 2A receptors at inappropriate times or for longer than usual o stimulates Dopamine release in Nucleus accumbens o distorts perception o chemically resemble and stimulate serotonin receptors •Alcohol: What does it do to GABA transmission, and how? What does it do to glutamate transmission? o Binds to site on some GABA reAeptors, o Combines with GABA to produce longer than normal effects of GABA (opens Cl- channel wider than usual) o Glutamate receptor antagonist (depressant) o Increases stimulation at both dopamine and opiate receptors including in nucleus accumbens •What do you know about the self-administration animal model? o Drugs that are self administered by rats have high abuse potential in humans o Self administration is used for preclinical assessment of the abuse liability of new pharmaceutical agents o Rats bar press for cocaine o At first, rat stops if bar pressing leads to painful shock o after much cocaine self administration it will bar press equally fast with or without shock •What is tolerance? How does the brain respond to other natural reinforcers when tolerance has developed to a drug? o A decrease in the effectiveness of a drug that is administered repeatedly o As tolerance develops to the drug, the individual becomes less responsive to other types of reinforcement as well o Also as tolerance develops, withdrawl symptoms occur without the drug, so stop using it as much for pleasure but to avoid displeasure (withdrawl) •Why do people experience cravings to a drug even after withdrawal symptoms have subsided? o People learn that a substance is strongly reinforcing during a period of severe stress o Receiving drug during withdrawl is powerful (during stressful time) o After having abstained; humans show more drug seeking during periods of stress or after being reminded of it •What is sensitization? What does it mean that cocaine causes sensitization in the nucleus accumbens? o An increase in the effectiveness of a drug that administered repeatedly o Can occur in nucleus accumbens o Repeated cocaine use  increased dopamine release in nucleus acc. o Repeated injection of cocaine  sensitization of movement irregularities; no change in tolerance to euphoric effects o With each use; also increased drug seeking behavior o At same time, n. accumbens responds less strongly to other pleasureable things (even sex) •How is the prefrontal cortex involved in decreased reinforcement from other pleasurable things? o Prefrontal cortex usually stimulates n. accumbens  facilitate nucleus accumbens response to reinforcing experiences o lots of drug use is inhibitory to prefrontal cortex  prefrontal cortex cant stimulate NA to facilitate reinforcement o drug is reinforcing (lots of dopamine coming from VTA); nothing else is (no reinforcement from Prefrontal cortex) •Define alcoholism. What are the differences between Type I and Type II alcoholism? o Alcoholism: continued use of alcohol despite medical or social harm, even after having made a decision to quit or decrease drinking o –largest health problem after heart disease and cancer o Type 1/Type A: o Later onset o Gradual onset o Fewer genetic relatives with alcoholism o Equal quantity between men and women o Less severe o Type 2/Type B o Earlier onset (usually before 25) o More rapid onset o More genetic relatives with alcoholism o Men outnumber women o Often severe o Often associated with criminality •What 2 genes could be involved in alcoholism? o Gene for a dopamine receptor o Longer version of gene makes less sensitive receptors o People w/this version experience stronger cravings for more alchohol after one drink o Gene for enzyme that breaks down dopamine o COMT (ccatechol-O-methyl transferase); breaks down all catecholamines (Da, NE, Epi) o One version of gene makes enzyme that is more active than the other; people w/ more active enzyme breaks down dopamine faster  less reinforcement from things that increase dopamine •What are some risk factors for becoming an alcoholic? o people described in childhood as impulsive, risk taking, easily bored, sensation seeking, outgoing o sons of alcoholics have specific traits relating to how alcohol affects them and their neuroanatomy o smaller amygdala on right •What are the medications used for alcoholism and how do they work? What is the major limiting factor to their efficacy? I’ll give you this one: they only work in people who are very motivated to quit drinking. o Antabuse o Antagonizes AD by binding to it; so alcohol makes you sick o Helps maintain the commitment not to drink o Needs lots of social support Spinal Cord and PNS •Know the parts of the spinal cord (dorsal horn, ventral horn, dorsal root, ventral root, central canal, dorsal root ganglion). Be able to label them on a figure. o •Know the Bell-Magendie law and understand how that incorporates the dorsal and ventral horns and roots. Understand that a spinal nerve has a sensory and a motor component, o The entering dorsal roots carry sensory info to the brain and the exiting ventral roots carry motor info to the muscles and glands o Dorsal = sensory o Ventral = motor •Could you recognize what a sensory neuron looks like compared to what a motor neuron looks like? o top is motor neuron; bottom is sensory neuron o •What are dermatomes? What disease is associated with them? o Segment of skin/muscle/bone associate with a spinal nerve o Each nerve innervates (defines) a dermatome o Associated with shingles •Generally speaking, what is a reflex? Describe the stretch reflex. How is that different from the flexor reflex (I’ll give you this one: the flexor reflex uses an interneuron in the spinal cord, so it is polysynaptic). How are reflexes “modifiable”? o Involuntary, stereotyped response to a sensory input o Modifiable: some reflexes are suppressed or enhanced deendign on our behavior o Stretch reflex: o Monosynaptic o Muscle contradiction in rsponse to stretch o Recriprocal inhibition •Does the spinal cord look the same in all critters? In other words, does out spinal cord look just like a bird’s? A snake’s? o Spinal cords o Look different at different levels o Different in different critters o Has long ascending and descending tracts carrying motor and sensory info o Meningeal covering •What do we mean when we talk about the “3 long tracts” in the spinal cord? You don’t need to know them by name. o Corticospinal tract for movement o Anterolateral system (spinothalamic tract) for pain and temperature o dorsal columns for nonpainful touch and proprioception •Does the spinal cord look exactly the same at every level? o NO •What structures comprise the CNS and what structures comprise the PNS? o CNS: brain and spinal cord o PNS: all nerves and ganglia outside brain and spinal cord •How is the PNS subdivided? What are the distinct roles of the somatic, enteric, sympathetic and parasympathetic nervous systems? o PNS divided into autonomic NS and Somatic NS o Somatic NS: nerves that convey info from sense organ to CNS and from CNS to muscles (motor and sensory) o •Understand the differences between the sympathetic and parasympathetic nervous systems in terms of (1) when each one is activated, (2) placement of ganglia (as well as location of preganglionic neurons), (3) length of fibers, (4) neurotransmitters used, (5) physiological effects. o Sympathetic NS: axons activate organs for “fight or flight” o Sympathetic ganglia are closely linked and act ‘in sympathy’ with each other o Chain outside spinal cord  Thoracic and lumbar regions o Long presympathetic; short post o Parasympathetic NS: o faciliatates vegetative, nonemergency functions o para means beside or related to; opposite action of sympathetic NS
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