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PSYB65 Final Exam Lectures 7-11

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University of Toronto Scarborough
Ted Petit

PSYB65: Human Brain and Behaviour Lecture 7 –Mechanisms of drug action, psychopharmacology of neural stimulants (Chapter 9, 15) Monday, November 5, 2012 Global Overview of How Drugs are Classified 1. Prescription drugs o Doctors prescribe them for you o What drugs are considered legal or illegal varies over time and across different countries 2. Over-the-counter drugs o Don’t need a prescription from a doctor o Example: in Canada, Codene can be bought through over-the-counter o In the US, it’s considered illegal to buy Codene from the pharmacy (must be prescribed by a doctor) 3. Social drugs o Social types that can be bought on a regular basis o Examples: Nicotine, alcohol, caffeine (coffee, tea, Coke, Pepsi, etc.) 4. Drugs that are not produced commercially or, if they are produced commercially, they are not produced for their psychoactive effects o No one manufactures it, so you can’t just go out to the store to buy it o Example: Marijuana o Example: Airplane glue –produced commercially but not produced for its psychoactive effects Tolerance and Withdrawal –Overview Tolerance  A concept that if a drug is taken repeatedly, most drugs show a decreasing behavioural effect o Basically, the more you take the drug, the less behavioural effect it has What causes tolerance to occur?  If you have drugs that alter a transmitter system, the more you stimulate/alter the system, the postsynaptic side of the system will compensate o Example: the more you stimulant a system, the more it will compensate by either reducing the number or sensitivity of the receptors  If you’re using something that slows the system down (like a depressant), you’re getting under-activity of the system, then the system will compensate by increasing the number or sensitivity of the receptors The Mechanism of Tolerance  Whenever you take a stimulant(drug) it will cause an excess amount of NT to be released so there is more transmitter substancehyper stimulation of synaptic receptors PLASTIC RESPONSE: reduce the number of the postsynaptic receptors and it will compensate for the over active stimulation, so then the postsynaptic neuron won’t fire regularly because it has its own regulation : so over time when you take the same amount of drug over time, you don’t get the same, strong enough effect behaviourally (decrease of sensitivity in the receptors) TOLERANCE: you take the same amount of drug and you don’t feel as high after a long period of time  It’s never permanent on the brain, cyanide is permanent Example of Cause with Stimulant  Whenever a drug (ex. stimulant) is taken normally, it will cause excess amounts of transmitters to be released due to different mechanisms – winds up with more transmitter substances stimulating the postsynaptic neurons (receptors)  As more and more neurotransmitters are released and there is hyper-stimulation of the receptors, receptors are bombarded; there is classic response from postsynaptic receptor that will result in the reduce the number of sensitive of the postsynaptic receptors  Will start reducing the number of receptors that it has to compensate for overactivation – postsynaptic will not fire as often (self-regulates / tones down sensitivity of receptors) Example of Cause with Depressant  Depressant is slowing down functional activity – decreases activation of postsynaptic cell – realizes that it is not hitting the normal number activity that it should, will start to increase in the number / sensitivity of postsynaptic receptor  Will respond by building more receptors to compensate for the depression of brain – same amount of drugs that will stop 4 receptors will not have to stop 8 receptors  Instead of person being depressed, the drugs will no longer have the same  dramatic event, won’t be relaxed as much  Depends on the drug that whether a tolerance effect may be produced Withdrawal –definition  If you have been taking the drug for over a long period of time (a very long time) and then you suddenly stop taking it  Once you stop, you obviously begin to have cravings for the drug o Example: smokers  In general, the behavioural effect of withdrawal is exactly the opposite of the effect of the drug itself  The effects can be quiet severe The Mechanisms of Withdrawal  The presynaptic isn’t bombarding the postsynaptic side  When a person comes off a drug, they postsynaptic cell is being under stimulated and will go below average stimulation  When someone who is taking a stimulant and comes off of it, they become depressed and eventually come back to normal. When they are withdrawing from the stimulant, they are tired, they are sad, exhaustion  A person who is on a depressant gets super stimulated (ie: shaking, seizures) and high and comes back to normal  Withdrawal from a depressant can be life threateningyou run the risk of the brain going into a seizures and becoming too active, you can’t take someone off a depressant cold turkey Diagram  If you give a person a stimulant, and then take it away, they will become depressed (tired)  If you give them a depressant (barbiturates, alcohol), and then take it away, they will have a excited period of time (hyperexcitable brain) agitation, good chance it can cause a seizures and death o Don’t ever take a person off depressants right away, because the consequences can be severe (can cause death) o Give them valium, that helps substitute the depressant without the behavioural effects Addiction  Applies to all drugs  Person enjoys and becomes depend on the drug o Implies that the person wants to have the drug, a behavioural or physical dependence on the drug, a requirement for the drug  However, there are different levels of addiction: (1) Psychological Addiction  The person has become behaviourally dependent on the particular drug o Very attached to the drug and can’t let go of it  Not a meaningful term, but has a slight meaning (2) Physical Addiction  On withdrawal, if you take the drug away, there has to be some physical withdrawal symptoms  Symptoms can be something that is measured o There is a clear physical indication that can be seen o Examples: sweating, changes in Galvan response, seizures, blood pressure, body temperature As a general rule: the more rapid the affect (behavioural) of the drug, the more addicting the drug is  EXAMPLE: cocaine grows on the coca tree, and people in Bolivia use the leaves to take the cocoa leaves and make a tea because it’s a light stimulantimported into Canada in very concentrated. CRACK cocaine: is much more concentrated, and gives an instant rush and injected cocaine becomes more addicting o Same chemical in a form with a powerful rapid effect, it can become very very addicting Stimulants  Activates the Central Nervous System  All of these stimulants cause an arousal in the cortical EEG o When they take a stimulant, the EEG will shift into an arousal state and they inhibit sleep Mild Stimulant –Caffeine  Many students ingest this stimulant  Found in coffee and tea  Inhibits sleep  Coffee has more caffeine than tea (they have many levels of caffeine depending on the type, but tea usually has less caffeine than coffee)  Many headache remedies has caffeine within them  Stimulates the digestive system  Tolerance: some tolerance does develop towards caffeine, but it’s very little  Withdrawal: headache (because caffeine stops headache), constipation (must be drinking 6-8 cups of coffee a day)  Toxicity: it’s not very toxic, it’s estimated 70-100 cups of coffee at one time can be toxic and it can kill you  Mechanism: it inhibits the breakdown of cyclic AMP (cAMP), it causes an increase in the amount of cAMP, this leads to an increase in glucose production which causes heighten cellular activity o Works with cellular activity rather than neurotransmitters Nicotine  Found in tobacco leaves (formed into cigars and cigarettes)  It mimics ACh , thereby stimulating at the postsynaptic neurons also known as nicotinic receptors  Other effects: also causes release of adrenaline, which causes an increase in heart-rate and blood-pressure  Tolerance: some does develop, but it’s not bad (example: smokers would smoke about ½ pack a day and maintain that)  Withdrawal: craving leads to depression  Toxicity: not very high, can be a problem for infants who have eaten/chew a cigar; it can cause death Cocaine  Comes from cocoa trees (found in mountain of Bolivian-Peru where it’s considered legal) o Mild stimulant –drink it in the morning where its grown; drunken like it’s coffee to wake up  Cocoa leaves contain about 2% cocaine  Causes an increase in heart rate and respiration  Tolerance: some does develop but it is not great  Withdrawal: period of emotional depression and physical appearance (tired and want to sleep all the time) and emotional depression(they feel sad) not life threatening  Toxicity: not toxic, unless it is used intravenously (injected) o If used intravenously in high dosesit can directly stop the heart from beating  Mechanism: primarily prevents the reuptake of norepinephrine o Norepinephrine sits around for a long time and stimulates postsynaptic neuron  Addiction: the addictive qualities of cocaine depend on how you take it. (from leaves, from concentrated cocaine, or crack cocaine) stimulates the part of the brain that is activated by eating food and having sex o Level of addiction varies on the stage of the drug  Stimulate the whole medial forebrain bundle (reward mechanism in hypothalamus) o Causes alertness/awakeness, activates pleasure feeling  Many effects of cocaine are similar to the effects of amphetamine, they share similar mechanisms o Cocaine can be considered the milder form of amphetamines Amphetamine  Almost a stronger version of cocaine  Relatively new drug –discovered in 1932  Reduction in fatigue (more alert) and performance deficit (decrement) associated with fatigue  Very popular in Toronto, Canada –known as ecstasy (common form –used in clubs to stay awake all night))  Increases the activity in the medial forebrain bundle(also known as reward system) located in the hypothalamus (pleasure area –refer to lecture 1) o Gives euphoric feeling –performs better feeling of euphoria (feels great/ good)  Tolerance: depends on what it’s used for, o Appetite control –the appetite suppresses, tolerance developed quickly within 2-4weeks o ADD children –usually develop no tolerance (can stay at the same dosage for years, if any at all) o Mood elevating effect –can get some tolerance to that but usually takes a while (slow to develop)  Withdrawal o It’s a stimulant –causes depression o Fatigue o Somnolent: fatigue, tiredness o Are not life threatening o Usually lasts less than a week o An appetite suppressant –when you get off of it, you have a huge appetite  Mechanism of Action o Very powerful stimulant – has 4 mechanisms that drives noradrenergic system:  Causes norepinephrine to leak from the presynaptic terminal – in the absence of action potential (no AP)  Causes an increase in the release of norepinephrine when there is an action potential (AP used)  Blocks reuptake of norepinephrine (just like cocaine)  Directly mimics effects of norepinephrine on receptor sites  2 Primary Legal Uses of Amphetamine: o Hyperactivity in children: ADHD or ADD –short attention span, very distracted, restless, impulsive  Helps them focus  Most kids are given Ritalin (methylphenidate) –most commonly prescribed derivative of amphetamine  50-75% ADHD/ADD children do show some improvement, it’s fairly helpful  Kids can stay on Ritalin for years without growing tolerance, but it stunts growth (taken off during the summer in order for them to grow) o Appetite control –weight control  Rapid suppression in appetite  More of a problem for middle-aged women with weight problems  Tolerance for appetite suppression built up –has not effect after 2-4 weeks  In the 1970s: women would get a prescription from a doctor  The tolerance builds up and then has no effect on appetite after 2-4weeks causing women to addicted to amphetamine and overweight  Banned in 1973 for the use of appetite suppression  3 types of amphetamine: o D-amphetamine o L-amphetamine o Meth-amphetamine Social and Behavioural Effects of High Doses of Amphetamine (high levels over a long period of time)  Most commonly seen with amphetamine since it’s much stronger  High levels of cocaine can do the same things as amphetamine, cocaine is a milder form: o COMPLUSIVE BEHAVIOUR:  Becomes OCD –constantly checking things, doing things o COCAINE BUGS:  Most commonly seen in amphetamine but can be seen in cocaine  It feels like bugs that are crawling around underneath their skin, and they try to pick our these bugs, so the person will have scars and sores –delusional  Will have scars and sores where they have been scratching and cutting their skin o PARANOID PSYCHOSIS:  Visual and auditory hallucinations in a clear setting of consciousness  Similar to schizophrenia –increase in dompanergic system  Everything seems completely normal – assumes someone is behind their back talking to them (feel more paranoid)  What they hear is usually paranoid in nature – thinks people are plotting against them  Can become suspicious and hostile which leads to aggression and potential for violence PSYB65 Human Brain and Behaviour Lecture 8 - Psychopharmacology of drug action, depressants, opiates, and hallucinogens (Chapter 11, 16) Monday, November 12, 2012 Depressants  Placed into 3 major classifications: 1. Barbiturates 2. Non-barbiturates 3. Alcohol  Sometimes known as sedative hypnotics  Anything that causes the cortex to go into a more relaxed state 1. Barbiturates  Used to help people sleep/relax  Primary Method of Influence: o GABA  primary inhibitory amino acid neurotransmitter in the brain o Increase GABA, you slow things down  How do they work?  Barbiturate binds to GABA receptors in the brain o Decreases activity in the brain since it is inhibitory  Barbiturates are synergistic with other sedatives/sedatives hypnotic (they put you to sleep) o Also with anxiolytic drugs (drugs that take away anxiety, ie valium) o Also with anticonvulsant (slow down brain activity)  All of these are mechanisms that we use to calm the brain down, slow down neural firing  Therefore, barbiturates are synergistic with these drugs  Almost all are synergistic – for drugs to be synergistic, they have to work in very similar mechanisms, and that they can add to each other or cancel each other out (cancel the withdrawal effects of each other) o What does synergistic mean?  If you put them together, they’re additive (not independent); they add to each other; multiplies the effects  For example you take aspirin and snort cocaine, they will not add together (not synergistic)  If you take a barbiturate and one beer, it is equivalent to taking 3 beers o Deadly to mix barbiturates with alcohol depresses the brain to sleep and then it leads to death  Most will prevent the withdrawal effects of the other  Are prescribed normally for sleep induction (induces people to go to sleep)  Most commonly used in elderly individuals – their sleep-wake cycles are abnormal/irregular o Largest group of people taking barbiturates o Its prescribed o Less time spend in REM sleep  Although induces sleep, reduces REM sleep  Withdrawal o Strongest depressant  when you come off it, it leads to seizures  Never take them off it right away, it can cause death, so you need them to take drug substitutes to help them slowly get off the drug  Brain becomes hyper-excitable  May result in seizures and death – depends on how much and how long  Alcohol will stop the withdrawal symptoms from barbiturates; other drugs works as well (its synergistic) Alcohol • CNS depressant • Made by yeast - yeast digests sugar and excretes alcohol • Causes more problems and damage than any other drug in society • Problems with alcohol in society o Accounts for the largest number of admittance to mental hospitals / psychiatric wards (40%) o Accounts for 55% of all arrests (either had been drunk or been drinking) o Accounts for 50-75% of all homicides o Accounts for 50% of all driver deaths o Accounts for 20-30% of all suicides • Experiment: United States passed a law in which people could not manufactured or sell alcohol (jan 1920- dec1933 o Known as prohibition o Percentages decreased for a little while in society but didn’t last long  Drop in % in all alcohol related problems (homicides, death, arrests, etc.) o By 1930, all of the numbers (statistics) had gone right back up to where they were before prohibition – people started drinking again (alcohol related problems) and other problems occurred as well  Instead of making ethyl alcohol (in wine beer), they made methyl alcohol and drank that  Lead to blindness permanently, or they died because it was lethal  The government did not inspect these, so they were not as safe as the ethyl alcohol o Lesson learnt: If anyone wants a drug, they can find a way to get it  If it is not produced and inspected by the government, it might not be as safe  Educate people about drinking and the consequences of the negative side effect of it o The numbers were back up and there were additional problems:  Prohibition of alcohol resulted in manufacturing of alcohol that is not pure – methyl alcohol causes blindness (we drink ethyl alcohol) Physiology of Alcohol (Chemistry / Reaction Mechanism)  Directly absorbed through the stomach wall – one of the fastest source of energy that is available to humans (doesn’t require breaking down)  Contains a tremendous high amount of energy – 200 calories / per ounce of alcohol or 7 calories per gram  Its metabolic pathway is such that it cannot be stored as fat – can still get fat because the body starts using alcohol as its energy source and stores everything else as fat  Causes the brain to decrease in anti-diuretic hormone (ADH) o Causes more excretion of fluids o Drink a little and pee a lot  leads to dehydration  CNS Effects o Not fully understood o Partially affects GABA-ergic system, works on metabolism, alter membrane excitability (not clear which is responsible for CNS depressant effects) – might be combination of all three  Behavioural Effects o Exact result of cortical result depends on the dose level o At low levels (1-2 drinks at the most), causes (disinhibition); excitation in cortical EEG – at low amounts if inhibits /depresses inhibitory centers in the brainstem, therefore the rest of the brain is allowed to become more active (cortex is activated)  At low levels of alcohol, people are actually able to function better at tests – reflexes are faster than those whom are completely sober – inhibition of inhibitory centers allow faster reaction in a given amount of time o At high levels, it depresses the cortex (become sloppy)  Continual drinking will depress activity in medulla which depresses respiration (may result in death) --> Can be prevented you will vomit (it’s a reflex)  Long Term Effects – long term at very high levels o Drinking heavily, drunk everyday for the past 4 years o Atrophy of the brain – especially in dendrites – dendrites look like shrivelled up (happens in cortex and cerebellum)  Severe enough to be seen on CAT scan – reduction in size  Withdrawal Effects – depends on severity o Hallucination, tremors, convulsions (seizures), possibly death o Is as severe and as likely to cause death as someone who has come off of narcotics (heroine / morphine)  Tolerance – some tolerance does develop o Appears that primary mechanism is through the increase in the level of liver enzymes  Fetal Alcohol Syndrome o No effects if a pregnant woman drink 1-2 times a day (very low levels) o Caused by the person drinking during pregnancy at reasonably high levels of alcohol o Infant will go through withdrawal from alcohol – within 6-8 hours of birth will go through withdrawal symptoms o Long term effects:  Third highest cause of mental retardation/ deficiency (50%)  30% of them not only show mental retardation but multiple physical handicaps – primarily facial distortions and permanent growth: crossed eyes, small eye openings, small head, cleft pallet, ear abnormalities, heart disease, permanently retarded growth Opiates  Aka. Narcotics  Chemicals that either come from opium poppy or synthesized by humans or made by scratch  Have been used since 4000BC  Primarily used as painkillers(analgistic), stops diarrhea (stops motility) o Most powerful painkiller and last resort for cancer patients to reduce pain (morphine sulphate)  In 1874, Bayers Laboratory attached 2 acetyl groups to morphine (morphine derived from raw opium)and came up with heroine  Heroine 3 times more potent than morphine  More fat soluble than morphine – can cross the blood brain barrier more faster/quickly  Once in the brain, the heroine is changed back into morphine  More addicting – 3 times as powerful as morphine  Cannot overdose/die directly from heroine, unless it is mixed with other drugs such as alcohol or not safe  Do not stop the perception of pain – people can still feel the pain but opiates stop the emotional perception of pain o People still feel the pain but the pain doesn’t bother them o Morphine blocks the emotional pain  Depresses respiration and causes constriction of the pupils(with fairly high doses this occurs)  Opiates work? --> In CNS, opiates mimics post-synaptically the endorphins (stimulate endogenous opiates)  Tolerance o Very rapid to the opiates  Withdrawal o Diseurophia –bad feeling, feel yucky/terrible o Causes stomach cramping and sweating Psychedelics  Examples: Marijuana, LSD, Magic mushrooms, etc  Primary Function / Primary Behavioural Effect: Alters perception  None of the drugs in this category are physically addicting  Although can be psychologically addicting (meaningless term)  No withdrawal symptoms at social levels of use  All psychedelics work through serotonin –usually divided into groups based on structures o Mescaline: found in the cactus in south western parts of US/Mexico (naturally occurring)  Binds to and activates serotonergic receptors  At low doses, it’s euphoric  At high doses, causes hallucinations  Causes pupil dilation, increase in blood pressure, pulse rate and body temperature Psilocybin  Found in mushrooms (Magic Mushrooms) – grows naturally  Structure very close to serotonin  Activates serotonergic receptors  Effects very close to LSD but milder – is like a milder version of LSD  Shows cross-tolerance with LSD LSD  Dilysergic acid diethylamide  Primary effect: Visual Hallucinations  Serotonin agonist or stimulant (based on research)  Research indicates it increases glutamate in the cortex  causes excitation in the cortex  Synthesized from a mold that grows on grain o The mold is highly toxic –be careful when synthesized  Very, very powerful chemical: 1 oz LSD is equivalent to 300,000 adult doses (1 normal adult dose is 1 drink – only 1 dose is required to start a person relaxing)  Tolerance is developed very quickly – the same dose of LSD is completely ineffective after 3-4 days  Cross-tolerance between LSD, Psilocybin and Masculine Marijuana • Derived from cannabis plant • Have 4 active isomers – 4 active ingredients that vary by the different marijuana that’s obtained  Major Isomer: Delta-9-THC (THC: Tetrahydro cannabinol) • Toxicity: No human deaths that have been ever reported as a result of over dosage of marijuana o It is estimated that it would take (estimated lethal dose) is 40,000 times the effective dose – very harmless drug, almost impossible to kill yourself • It tends to make people less aggressive • Central Nervous System Effects: o Endogeneous receptors in the brain o Mimics a natural neurotransmitters that occur in our brains – indo-cannabinoids  Stimulates naturally occurring marijuana transmitters in our brain • Tolerance: o Slight tolerance at extremely high levels o No tolerance at social levels o Research shows that when people first try marijuana, instead of developing tolerance, they develop sensitivity – takes a while for the person to feel it • Withdrawal --> High levels users –Runny nose • Effects: Euporhic –feel good o At high levels, can be hallucinogenic (at concentrated levels) o Impairs immediate memory while the person is on the drug (temporary) o Can cause psychomotor and cognitive deficits – time distortions (difficult for people to accurately judge time) o No evidence of long term neurological damage associated with marijuana or with any of the other psychedelic drugs PSYB65 Human Brain and Behaviour Lecture 9: Cerebral dominance and the neuropsychology of language (Chapter 4, 15) Monday, November 19, 2012 Historical Overview of Humans  Early awareness of differences between the right and left hemispheres came from observation during war when they had a very large population that had wounds in their head from bullet wounds  Looked at whether the bullet wound was in the left or right hemisphere and see how the patient responded  Most of information derived during individuals who have brain damage during wars (WWII)  Results gained were primarily from adults first real grasp of lateralization were from adults whom had bullet wounds to the head  Whenever the brain damage was in the left hemisphere in the recovery process the following were observed: Damage to the Left and Right Hemisphere –Adults (over the age of 20)  Left Hemisphere Damage (ie., gunshot wound to the left hemisphere) o 100% of the patients showed some aphasic symptoms (language and speech problems)  Aphasic = no language o Approx. 30% of these patients will show some recovery – varies  The ones whom showed recovery were either left-handed or ambidextrous (both handed) individuals  The least amount of recovery were in the right-handed individuals o These results during these periods of war were the first indication that there was specialization in language and this specialization was related to handedness o Since right-handed people had the most problem, with left hemisphere damage, it clearly indicated that left hemisphere is important for language in everybody o Left side is damaged, right handed people lose language  Right Hemisphere Damage o Patients showed very little aphasic/language problem – relatively, rarely led to complete aphasia  Small percentage of people who did show aphasia were left-handed or ambidextrous  Most patients showed recovery from language problems o Right-handed people did not show aphasia o Right side is damage, right handed people DO NOT LOSE language o Suggests that in right-handed people (majority of the people), language problem was located on the left hemisphere; in left-handed / ambidextrous, language is bilaterally represented (language problems in both hemispheres) o In left-handed / ambidextrous individuals, damage to either hemisphere results in language problems , but show good recovery from right side damage  For left-handed people, since language is on both hemispheres, there is compensation for damage on either hemisphere o Suggests that left-handed people have some language on both sides  For right-handed people, damage to left hemisphere results in language problems, and there is no compensation because language is only limited to 1 hemisphere Children (younger than age 5) with brain damage  In children, under the age of 5, damage to either side of the hemispheres has equal possibility of producing aphasic symptoms o Research suggested that some language is found in both hemispheres  Recovery: o 100% of the kids will show some degree of recovery – both sides are both capable of language and so either side can compensate for language loss o Ch
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