Drugs and Individual Behavior Week 3 Class Notes
Drugs and Individual Behavior Week 3 Class Notes PSYCH 3102
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This 6 page Class Notes was uploaded by McKenna Keck on Friday September 9, 2016. The Class Notes belongs to PSYCH 3102 at University of Northern Iowa taught by Dr. Linda Walsh in Fall 2016. Since its upload, it has received 15 views. For similar materials see Drugs and Individual Behavior in Psychology at University of Northern Iowa.
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Date Created: 09/09/16
Drugs & Individual Behavior Week 3 Tuesday, September 6, 2016 Continued from Week 2 Notes… I’ve taken this dose of drug before, but time I’m not getting the same effect. ■ CrossTolerance & CrossDependence ● Tolerance to a drug often extends to other (usually chemicallyrelated) drugs. ● When physical dependence occurs, other chemicallyrelated drugs can “satisfy” that dependency & prevent withdrawal. ○ May Be Due to Drug to Drug Interactions ■ Drug Interactions: having more than 1 drug in your system can change the experienced effects ■ The presence of another drug may alter absorption, distribution, metabolism, elimination, and/or receptor interactions. ■ Some interaction examples: ● Additive (1+1=2) Effects of 2 analgesics in Excedrin add together ○ Like ibuprofen & aspirin together ● Synergistic (1+1=3) Taking alcohol & another depressant can lead to more than the sum of their effects (synergism) ○ Like alcohol & sleeping pills together ● Potentiating (0+1=2) Tagamet, Zantac, birth control pills, or erythromycin can potentiate (strengthen) sedative effects of benzodiazepines like Xanax ○ You might not expect it, b/c they’re such different kinds of drugs, but it happens. ● Antagonistic 1 drug canceling out the effectiveness of another drug ○ Smoking (tobacco or cannabis) can decrease the effectiveness of a wide range of medications b/c the liver is working harder ○ There’s an antidote drug you can give for someone who overdosed on a pain medication. This interaction can be live saving. ● Altered Side Effects taking alcohol & aspirin increases stomach upset Drug Names ● Chemical or structural name describes molecule ○ Usually super long. We won’t use those names. ○ Example: sodium 5ethyl5(1methylbutyl) barbiturate ● Generic name official, nonproprietary ○ No one owns it. It’s what we call the chemical compound. We’ll use these in class. ○ Example: sodium pentobarbital ● Brand or trade name owned by a company ○ Might be the way you know the drug. We’ll use these. ○ Example: Nembutal ● Street names ○ Users might use these names. Interesting, but vary a lot from place to place, & time to time, & aren’t very constant. We won’t really use these. ○ Example: bluebirds ● Generic v. Brand Name Drugs ○ Are generics as good? ■ By law, the active ingredients must be chemically & biologically equivalent. ● They have the be the same chemical & get into your system the same way. ■ We don’t know for sure if they’ll always be clinically equivalent… ● Would you notice the same effect if you take the generic v. the brand name? ○ Remember, placebo effect can come into play… ○ Will generic availability decrease drug development research? Are generic substitutions fair to brandname companies? States vary in their laws about substitution. ■ If drug companies don’t make enough money are they going to continue research & development on their drug? We need to have these drugs available to consumers… ■ Sometime when they’re trying to encourage drug development, they offer more control to the brand name companies. When we need drugs to be more reasonably priced, generics come into play. Nervous System Review for Understanding Psychoactive Drugs ● Central Nervous System (CNS) ○ Brain ○ Spinal Cord ● Peripheral Nervous System (PNS) all the nerves that are outside the brain & spinal cord. Virtually every drug will have some kind of effect on the peripheral nervous system ○ In 2 halves ■ Somatic: motor & sensory nerves (help us move & sense things). Not many drugs will affect those nerves, except cocaine being applied topically acts as an anesthetic. ■ Autonomic: involuntary or unconscious nerves, to regulate the functioning of organs (like, you don’t have to think about your heart beating for it to beat) ● In 2 halves ○ Sympathetic: “Fight or Flight” Nerves that turn on a lot of arousing body reactions so you can fight or flee. Prepares you for any situation where your body will be more active. ○ Parasympathetic: Most active when you’re just chillin’. Digesting, keeping mouth wet, mostly pretty calm maintenance functions. Keeps you sitting upright in your chair. Calming as opposed to arousing. ○ All day long we keep switching between sympathetic & parasympathetic activation of the PNS. ● Most drugs affect the autonomic nervous system. Like caffeine making your heart rate speed up. We call these the side effects often. ● Parts of the Brain Might be useful to print slide of labeled brain for studying & labeling. ○ Medulla: Lifesustaining & lifeprotecting reflexes. Overdose death usually due to drug action in the medulla, interfering with regulation of breathing or cardiovascular function. ■ Sustaining… ● Heart beating, breathing ■ Protecting… ● Vomiting, gagging ○ Cerebellum: Motor coordination & balance. Drug action on cerebellum may cause slurring, stumbling, loss of balance. ■ Alcohol is a classic example of a drug depressing the function of the cerebellum. ○ Hypothalamus: Drug action in hypothalamus affects appetite, hormone levels, sexual function, autonomic & instinctive emotional responses. ■ Some drugs affect sexual functioning, appetite, etc. ○ Reticular Formation: Arouses brain for normal waking & consciousness. Sometimes called reticular activating system. Sends messages to the upper parts of the brain. ■ Stimulants will increase wakefulness, depressants will make you sleepy or fully unconscious. ○ The Limbic System: Emotional Control System. Recognizing emotions, showing emotions, feeling emotions, & has an effect on memory. ■ Fornix ■ Thalamus ■ Hypothalamus ■ Amygdala ■ Mamillary Body ■ Hippocampus ○ Dopamine Pleasure/Reward System: Bundle of dopamine (DA) neurons from midbrain through hypothalamus & nucleus accumbens, then on to cortex & limbic system ■ It’s active when you do something “good for your survival” ■ We’ve found lots of drugs or substances that activate the reward system, so it makes you want to keep doing it. ■ Nucleus Accumbens: one of the key hubs of this system ○ Basal Ganglia or Extrapyramidal Motor System: initiating voluntary movements & keeping undesired movements in check. Involved in initiating voluntary action & controlling unwanted movements that might interfere with what we want to do. ○ Cortex: the site of all of our higher functions. Drug action here affects judgment & reasoning, selfcontrol, sensation/perception, contact with reality. ■ Frontal, Parietal, Temporal, & Occipital Lobes ○ Neuron: sends, processes, & receives messages in the brain ■ Nucleus ■ Dendrite: message receiving part of a neuron ■ Cell Body: integrates all those individual messages coming into dendrites. Sometimes called soma. ■ Terminal Buttons: Tips of the axon branch. Takes you to the synapse ■ Axon: single outgoing branch. Message sending part. ■ Myelin Sheath ■ Synapse: the gap between terminal buttons & the next dendrites. ● Presynaptic terminal (terminal button): the terminal that’s sending the message ● Synaptic vesicle containing neurotransmitter (message) ● Transmitter is released from vesicles & diffuses across the synapse ● Postsynaptic Terminal: the neuron receiving the message ○ Transmitters will only fit into the receptors made to receive them. ■ Eliminating the Neurotransmitter… ● Transmitter must be removed from synapse after its release (to prepare for the next messag). ● Most common way… Most neurotransmitters are recycled through a process called “reuptake” transported back into axon ending (so the molecules can used again later). ● Less common way… An enzyme in the synapse breaks down transmitter into inactive components. ■ Postsynaptic Receptor Specificity ● Each transmitter binds only to its receptors, but there are multiple types of receptors for each. ○ This is complicated, b/c some drugs only affect certain types of receptors… ● Drugs may increase or decrease the synaptic function of neurotransmitters. ● The “Big Seven” (see Table 3.1) (Best Known Neurotransmitters) Need to know ○ Acetylcholine (ACh) ■ Neurons using ACh = cholinergic neurons ■ Found in ● Nerves to skeletal muscles ○ You would be totally paralyzed without them ● Parasympathetic NS ● Learning & memory areas of brain ■ Some drugs increase ACh ■ Others (anticholinergics) block its action ○ Norepinephrine (NE) ■ Found in ● Sympathetic NS ● Brain areas involved in appetite, arousal, mood ■ Some drugs activate NE receptors (sympathomimetics) ■ Others block NE receptors ■ Very close chemical relative to DA. ○ Dopamine (DA) ○ Serotonin or 5Hydroxytryptamine (5HT) ■ Found in ● Sleep & pain suppression areas of brain ● In limbic system (mood) ● In sensory processing areas (vision, hearing, touch, etc) ■ Several Drugs increase 5HT (antidepressants) ■ 5HT blockers are used to decrease nausea (like for chemo) ○ GABA ■ Best known inhibitory transmitter (when it crosses the synapse, it tells the next neuron to stop firing, or to diminish firing) ■ If you are born with not enough GABA, you may suffer from seizures, anxiety, etc. b/c of excessive neuronal activity. ■ Widely known in the CNS ■ It’s an amino acid type transmitter. ○ Endorphin ■ Family of transmitters which decrease pain perception & elevate mood. ■ Narcotic analgesic drugs (like our pain killers) act on endorphin receptors ○ Glutamate (newest addition): amino acid ■ Amino acid which acts as an excitatory transmitter almost everywhere in the CNS (kind of like the opposite of GABA. It excites the next neuron instead of calming it down). ■ PCP blocks some glutamate receptors. Thursday, September 8, 2016 Some notes from today integrated into notes from Tuesday, above, then continued from above. ○ Ways drugs may affect neurons (Part of Drug Action) ■ Drugs may affect any of the normal neuron processes ● Production of transmitter ● Storage of the transmitter in vesicles ● Release of transmitter ● Binding & action of transmitter at receptor sites ● Elimination of transmitter by reuptake or enzymatic breakdown ■ Two Broad Categories ● AGONIST: a drug that triggers or increases the usual synaptic effects of a transmitter ○ Example: a drug which fits postsynaptic receptor sites & MIMICS action of transmitter ● ANTAGONIST: a drug prevents or decreases the usual synaptic effects of a transmitter ○ Example: A drug which fits receptor site by doesn’t trigger a response. This drug is a blocker. ● Drug Actions ○ AGONIST examples: ■ Narcotic pain relievers fit & activate opiate receptors mimicking the action of normal endorphins. ■ Nicotine fits into & stimulates ACh receptor sites, arousing the cortex like ACh. ○ ANTAGONIST examples: ■ Haldol blocks DA receptors in schizophrenic people. ■ Naloxone blocks opiate receptors (it’s the antidote for a narcotic overdose). Your own endorphin effects are also blocked while it’s in your system. *Some lines of notes copied directly from slides in order to maintain testing accuracy. Most is of the lecture & discussion, not found on slides. Likely on Exam! it was asked in class as an extra credit quiz question Vocab
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