Exam II PDF

Title Exam II
Author Brook evans
Course Physiological Psych
Institution Clemson University
Pages 20
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exam 2 study guide ...


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Physiological Psych. Exam II Notes Pg. 78 ch. 3 ( skip ch 4) Ch. 5 ( drug and addiction ) up to pg.146 excluding the “role of genes” Ch.6 to pg 171

Central Nervous System I.

Spinal Cord o Outside part is myelinated  white matter o Cable of neurons  Carries signals from the brain to muscles and glands (periphery )  Carries sensory info from the periphery to the brain  Spinal cord is the “hub” for reflex arcs Reflex arc: section off spinal cord in a horizontal plane  Dorsal side and Ventral side  Outside is white matter while inner portion is gray matter in a butterfly shape  Ventral horns and dorsal horns of the gray matter  Dorsal root and ventral root of spinal cord o Separated by the type of fibers they carry o Dorsal root  sensory neuron fibers , contains a buldge which is the spinal ganglion o Receptor at the end of the fibers , carries signal up dorsal root and synapse at the interneuron and goes to a motor neuron toward to effector( produces observable response) at the end of the ventral root o Ventral root o Receptor  dorsal root ( sensory neuron) interneuron ventral root (motor neuron) effector

 Reflex arc o Neural pathway that controls a reflex act o “hardwear”  Reflex act o Simple automatic response to a sensory stimulus o Response because its muscle contraction or gland secretion o “behavior”

Spinal Cord o o o o

The spinal cord consists of the ventral roots, dorsal roots, gray and white matter Meninges ( membranes that wrap around spinal cord , there are 3 ) don’t worry about knowing the names CSF in between the two innermost meninges serving as extra cushion and protection Spinal cord runs through the vertebrae (spinal column) apart of skeletal system

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Intervertebral discs ( flexible outer portion while inner is a jellylike substance ; if too much pressure is placed on the discs, it can begin to buldge out and cause pain ex: sciatica; the pain is illusion as roots are being damaged by the pressure ) If the fluid escapes , it can accumulate and cause pressure and damage ; surgery needed ; it can cause paralysis

Blood-Brain Barrier o o o o

Vascular system ( veins and arteries bringing blood to CNS) CNS is control system for rest of body This barrier prevents toxins from entering brain The barrier is made up of the capillary membrane walls  Capillary membrane cells are so tightly packed that they form a barrier to most molecules  Fat soluble substances freely pass through the barrier  **Psychiatric medicines and other drugs are designed to be fat soluble , some of the most powerful/addictive are fat soluble, having immediate effects  Others use special transport proteins to get through ( amino acids, glucose)  Some areas of brain are not protected by blood brain barrier  The area postrema ( in medulla) induces vomiting when certain toxins are in blood

Peripheral Nervous System  PNS Cranial Nerves + Spinal Nerves or  PNS o

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Somatic  motor neurons that carry signals from CNS to skeletal muscles  Sensory neurons that bring in info  Aware Autonomic  Involuntary movement  Motor or sensory  Not aware ( HR, breathing, digestion, hormonal secretion…)  Activity of muscles ( smooth muscles, heart, glands)  Sympathetic o Speeding up body activity level o Increase HR, BP, respiration, sweat glands o Important in fight or flight situations o Originate from the middle of the spinal cord o Passes through sympathetic ganglion chain (simultaneous activation of organs- work as a unit)  Parasympathetic o Slows down bodily processes back down o Originate from ends of spinal cord

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NOT connected by a ganglion chain ( once danger is gone, there’s no need for it)

BOTH are active to some degree all the time ( its not that it’s the symppara; its whichever one is more active than the other at a certain time ) o Body’s activity reflects balance btwn the two

1. Cranial Nerves (12 pairs) Originate in the brain

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The image on canvas; do not need to recognize where nerve is but know what it does and its number 2. Spinal Nerves (31 pairs )

Development of the Nervous System o 3 parts (forebrain, midbrain and hindbrain) o If you divide the neural tube structure in two, there’s a dorsal and ventral portion 1. Proliferation  Neurons divide and multiply at extreme rate (stem cells)  Only occurs in ventricular zone 2. Migration  Neurons migrate to final location by climbing radial gilal cells  Ventricular zone fiber of gilal cell cortex  Migrating neurons follow chemical radiance to determine where to go 3. Circuit formation  Neurons send developing axons to make synapses with their target cells  Growth cone dev at tips of dev axons and move toward final targets using chemical/molecular signals

Chapter 5 Psychoactive drugs  Drug : substance on enetering the body changes the body or its functioning (2) categories based on their effect on transmitters 1. Agonist o mimics or enhances the effect of a neurotransmitter (NT) o a) having same effect on receptor as NT, or o b) increasing the effect of NT on receptor o c) block reuptake or degradation of NT 2. Antagonist o blocks or reduces the effects of a NT o a) binding to a receptor w/o activating it o b) reducing availability of NT  psychoactive Drug o have psychological effects, such as anxiety or hallucinations  addictive drugs o

Addiction - preoccupied with obtaining drug - compulsive use of the drug -high tendency to relapse after quitting

Withdrawal -negative reaction when drug is stopped -symptoms often the opposite of drug effects tolerance -increasing amounts of the drug are needed to obtain the same effects -mostly due to reduction in number and /or sensitivity of receptors  opiates Opiates derived from opium poppy (opium, morphine, heroine, and codeine) Effects of opiates -analgesic (pain relieving) -hypnotic (sleep inducing -euphoria ( sense of happiness) -addictive potential Examples: Opium -opiate -abused since around 4000 B.C., originally eaten Morphine -opiate -early 1800s -> effective treatment of intense pain Heroine - synthesized from morphine Late 1800's -> initially sold as an over-the-counter analgesic - Highly soluble in lipids -> crosses blood-brain barrier easily -Danger of overdose (too pure, tolerance) Codeine Cough suppressant Dilute solutions of opiums Paregoric and laudanum were used to treat diarrhea and pain  opiates have mostly been replaced with safer synthetic versions called opioids o opioids are still subject to abuse o oxycontin for example o heroin is the most abused ( orgasm, drowsy relaxation and contentment)  conditioned tolerance

o o

tolerance is often associated with the drug taking surroundings and circumstances overdose can vary with environment

 the body produces it’s own natural opiods o

opiate drugs are effective because they mimic these endogenous ( generated within the body) opiods known as endorphins

 Depressants o

Reduce activity of CNS (Ethanol, barbiturates, benzodiazepines)

Ethanol Depressant that -acts as an antagonist of glutamate (most prevalent excitatory neurotransmitter); inhibits release of glutamate which causes the sedating effect -Increase of glutamate receptors seizures during withdrawl -acts as an agonist to GABA by binding to GABAa receptors (facilitates the opening of CL- channels -> hyperpolarization \of postsynaptic membrane) -increases GABA release ; alcohol specificallty affects the A subtype of gaba GABA a is a receptor complex, with 5 different kinds of receptor sites One receptor is for gaba, when activated, opens up cl channel, influx of cl which hyperpolarize the neuron -other receptors respond to alcohol, barbituarates and benzodiapeines ( why its dangerous to mix anti depressants and alcohol!) -addictive Withdrawal symptoms of ethanol: tremors, anxiety, mood and sleep disturbances (delirium tremens in the worst cases) Delirium tremens (hallucinations, tremors, and even death) *Barbiturates A depressant derived from barbituric acid that -acts as antagonist of glutamate -acts as agonist of GABA by binding to GABAa receptors o

Can open cl channels on their own without gaba

Complex action of barbiturates -High doses ->sedative and hypnotic -Low doses -> inhibits cortical centers that inhibit -behavior -> talkativeness

*Benzodiazepines -Similar to barbiturates but safer (Cannot open chloride channels on their own) -act at the benzodiazepine receptor -Produce anxiolytic (anxiety-reducing), sedative, anti-seizure, and musclerelaxing effects -reduce anxiety by suppressing the activity in the limbic system -Addictive -valium, Xanax, halcion, rohypnol  Stimulants o

Increase the activity of the CNS

Cocaine -Produces euphoria, increased alertness, relief from fatigue -Acts as agonist of dopamine and serotonin by blocking their reuptake Side effects of cocaine addictive, brain damage, seizures, and psychotic symptoms Withdrawal symptoms of cocaine depression and anxiety Amphetamines -Synthetic drugs (methamphetamine: speed, crank, crystal) -Produce euphoria, increase in confidence, alertness & concentration -Acts as agonist of dopamine and norepinephrine by increasing their release in the synaptic cleft -In high doses can cause hallucination, delusions and other psychotic-like symptoms Nicotine A stimulant that acts as agonist of acetylcholine (activates muscles, increases alertness) -addictive Short puffs stimulating effect Long puffsdepressant effect -agonist of acetylcholine Withdrawal symptoms of nicotine nervousness, anxiety, drowsiness, lightheadedness, headaches Caffeine -Produces arousal, alertness and decreased sleepiness -Acts as agonist of dopamine and acetylcholine by increasing their release in the synaptic cleft Withdrawal symptoms of caffeine headaches, fatigue, anxiety, shakiness, and craving

> Psychedelics -Cause perceptual distortions (of objects, time, self, often accompanied by euphoria) -Addictive -LSD, Ecstasy, Angel Dust, Marijuana

LSD -psychedelic -similar to serotonin, binds to serotonin receptors

Ecstasy (MDMA) -psychedelic -causes release of dopamine and serotonin -kills serotonin neurons in monkeys

Angel Dust (PCP) -psychedelic -Produces schizophrenia-like symptoms in humans -Inhibits glutamate receptors -Increases activity of dopamine pathway Marijuana -psychedelic -dried and crushed leaves of indian hemp plant -major psychoactive ingredient is THC ( concentrated in the dried resin of the plant (hashish)) -active ingredient acts an agonist of NT anadamide and 2-AG by binding to their receptors (cannabinoid receptors) -> widely distributed in CNS * anadamide and 2AG may play an important role in the regulation of mood, memory, appetite and pain perception

Withdrawal symptoms of marijuana anxiety, irritability, stomach cramps

Addicition I.

The neural basis of addiction and reward o Withdrawal Avoidance hypothesis: addicition caused by desire to avoid withdrawl ( does not explain use of drug before dependence happens ) o Addiction and withdrawal occur at different places in the brain and are independent of each other o Withdrawal is not necessary for addiction and avoidance of withdrawal is not an explanation for addiction  PeriVentricular /PeriAqueductal Gray o Bozarth and Wise 1984: Injected drug into area in rats, showed withdrawal symptoms o Inserted needles into area, connected to switch for rat to press drug o Addicition depends on something else, one hypothesis is that of reward…. o Reward: positive effect of an object or condition on a user ( mostly behavior effects and accompianed by feelings of pleasure) o

II.

Mesolimbocortical dopamine system : location of major drug reward system o It begins in the midbrain (mesencephalon) and projects to the limbic system and prefrontal cortex o The most important structures in the system : nucleus accumbens, medial forebrain bundle, and ventral tegmental area o The amydgala and hippocampus are also involved with reward but not as important o Leisoning of the nucleus accumbens reduces reward effects for many drugs

Dopamine and reward o Virtually all of the abused drugs increase dopamine levels in the nucleus accumbens including opiates, barbiturates , alcohol, THC, PCP, MDMA, nicotine and even caffeine o Evidence that increase in dopamine plays role in addicition o Food,water, and sexual sitmulation also can increase dopamine levels in the nucleus accumbens o Also , electrical stimulation o Electrical stimulation of the brain , animals and sometimes humans, learn to press a lever to deliver mild electrical stimulation to brain areas where stimulation is rewarding o Thought to reflect a natural reward process b/c self stimulation rate in the posterior hypothalamus varies with experimenter sexual motivation o Most sensitive areas are where the density of dopaminergic neurons are the greatest ( medial forebrain bundle for example) o Drugs and electrical stimulation are powerful motivators of behavior

Research has shown PET scans reveal chronic drug users have dimished dopamine release and numbers of dopamine receptors o This decrease may not be a consequence of chronic drug use o Non chronic drug users also had low numbers of D2 type recptors of dopamine o Those who found the drug unpleasant had the highest number o So, lowered dopamine receptors probably precedes drug experience and creates a “reward defiencieny syndrome” that accounts for some addicts lowered responsiveness to rewards in general and predisposes the individual to drug abuse o This view has received experimental support o Thanos and collegues: insert D2 into rat nucleus increase in receptors decrease in alcohol intake o Dopamine cannot account for all reward!! o Reward effect of alcohol relies strongly on opiate receptors Opiate receptors ( naloxone and naltrexone) to prevent relapse  Wise  Dopamine is crucial for the rewarding effects of cocaine and amphetamine ; important but perhaos not crucial for the effects of opiates , nicotiein, cannabis, ethanol ; and questionable are the barbiturates, benzos, and caffeine Dopamine, learning, and brain plasticity o Reward is an essential factor in early drug taking but it is doubtful that reward maintains long term drug abuse o Later stages of addiction ( craving and withdrawal symptoms) involve lifelong changes in brain functioning o Learning research: o As learning proceeds in the lab, a rewarding stimulus initially produces dopamine release then ceases to do so o Instead, that capability shifts to stimuli that precede the reward such as an auditory tone that signals the period when lever pressing will produce the reward o Dopamine release does occur at the time the reward would be expected if the reward is omitted o Dopamine system responds to the unpredictability of rewards o Dopamine not only signals rewards but also signals errors in predicition o Contemporary learning theory: learning only occurs when the reward is unexpected or better than expected or when the reward is omitted or is worse than expected o The ability to detect errors in predicition is critical for learning o Reinforcer : any object or event that increases the probability of the response that preceeds it o Learning changes behavior by modifying the brain connections which is why drugs still produce reactions years after the last use and why some addicitons last a lifetime  Amphetamine or cocaine can increase dendrite length and increase complexity of nucleus accumbens and prefrontal cortex o

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Prolonged drug use decrease dopamine activity, deactivation of behavioral inhibition areas  Hippocampus involved with learning and environmental stimuli such as drug taking Changes in brain are also due to neural pathology  Disrupted prefrontal cortex loss of control over behavior  Dysfunction in the orbitofrontal area which monitors the value of reinforcers and seen in people with OCD  Pathological changes between the communication of nucleus accubens and the prefrontal cortex Addict returns to drug taking when stress or drug related stimuli trigger increases in dopamine release in the prefrontal cortex ( produces a compulsice focus on drugs) and glutamate release in the nucleus accumnbens ( cranks up the drive to engage in ddrug seeking)

Treating drug addiction  First step is Detoxification o o I.

Withdrawal from alcohol is potentially life threatening Medical intervention is necessary

Treatment strategies  Agonist treatments o Replace an addiciting drug with another drug that has a similar effect o Most common defense against drug cravings o Ex: nicotine gum and patches provide controlled amounts of the drug o Opiate addiction is often treated with a synthetic opiate called methadone ( made in wwII, named adolphine after Adolf Hitler)  Antagonist treatments o Involve drugs that block the effects of the addicting drug o Success depends entirely on the addict’s motivation o Ex: drugs that block opiate receptors such as naltrexone are used to treat opiate addicitions and alcoholism because they reduce the pleasurable effects o Can also interfere with the dopamine reward system o Ex: Baclofen reduces dopamine activity in the ventral tegmental area by activating GABA(B) receptors on dopaminergic neurons; this drug reduced cocaine cravings and rat’s self administration of cocaine, meth, heroine, alchol and nicotine o Ex: rimonabant drug interferes with the dopamine pathway by blocking cannabinoid receptors  Aversive treatments o Cause a negative reaction when the person takes the drug

Ex: Antabuse interferes with alcohol so that when a person drinks it makes them sick ; adding silver nitrate to chewing gumor loenges makes tobabcco taste bad o Success depends on addict’s motivation  Antidrug vaccines o Consist of molecules that attach to the drug and stimulate the immune system to make antibodies that will degrade the drug o Reduce the amt of cocaine that reaches the brain by 80% and nicotine by 65% o Only a percentage of addicts reach the necessary level of antibodies Effectiveness and acceptance of pharmacological treatment o

II.

Chapter 6

Motivation and the Regulation of internal states 

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Motivation : “ to set in motion” ; the set of factors that initiate, sustain, and direct behaviors o Motivation is a concept psychologists have invented and imposed on behavior o There is no single “ motivation center” in the brain Theoretical approaches to motivation o Greeks relied heavily on instinct in their attempts to explain human behavior  Instinct: complex behavior that is automatic and unlearned and occurs in all the members of a species ( ex: migration and maternal behaviors) o Instinct does not equal reflex o Ex of instincts: spiders building webs o William McDougall ( 1908) :popularized the idea of instincts; proposed that human behaviors such as reproduction, gregarioisness, and parenting are instinctive  Drive theory: the body maintains a condition of homeostasis , in which any particular system is in balance or equilibrium

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Any depletion of nutrients or disruption to any system causes an aroused condition or drive, which impels the individual to engage in appropriate action such as eating, drinking or seeking warmth Drive theory falls short when you start to look at more complex ; only useful when determining basic tissue needs  Incentive theory: recognizes that people are motivated by external stimuli not just internal needs ( ex: money is an incentive)  Arousal theory: people behave in ways that keep them at their preferred level of arousal ; different ppl have different optimal levels of arousal

 Drive theory ( revised) -

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Drives= conditions of the tissues (old theory) Drive...


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