BIOL 4220: EXAM 1
188 Cards in this Set
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Neurochemistry
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Study of neurochemicals and other drugs that influence neuron function
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neuropharmacology
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Chemicals' effect on the body
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Psychopharmocology
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Chemicals' affect on the mind
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Neurophysiology
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Study of the physiology of the nervous system
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Drug
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Chemical (molecule) that alters biological functions
-signaling mechanism for cells to turn on or off some cellular processes
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Exogenous
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Synthesized outside the body
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What is the difference btwn Drugs and Biochemicals
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Drugs are exogenous and biochemicals are endogenous
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Endogenous
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Synthesized inside the body
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D + R <--> DR* > biological effect
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Drug Receptor binding
When a drug binds with a receptor is creates a drug receptor complex
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Signal Transduction
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Conversion of a signal from outside the cell to a functional change inside the cell
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D + E <--> DE* > Biological Effect
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Drug enzyme binding
When a drug bonds with an enzyme it forms a drug enzyme complex
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Depolarized
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....
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Hyperpolarized
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Inhibits use of action potential
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Agonist
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Drug that mimicks the action of a naturally occurring substance
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Antagonist
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Drug that blocks a biological effect
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Receptors
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1) Float in lipid bilayer
2) Not anchored
3) Turnover
4) Span through membrane
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Ionotropic Receptor
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1) Has ion channel
2) Binding of ligand causes channel to open and ions to flow through
Ex. Glutamate receptor
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Metabotropic Receptor
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1) No ion channel
2) Contains a G protein
- Gs (stim)
- Gi (Inb)
3) Activates neighboring ionic channel
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Binding Site pulls molecules through
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Electrostatic force
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Ion channels open by
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Binding and electrostatic force
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Lock and key mechanism
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1) Due to electrostatic force
2) Depends on charge
3) Each atom is a different charge and size -- molecule has to compliment receptor
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Receptor Subtype
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Receptor Subtype
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Drug Effect
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Downstream effect
Ex. Getting high...so it's the effect of the action
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Drug Action
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Binding; molecular/biochemical action at binding site
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Therapeutic effect
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Desirable drug effect
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Side effect
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Undesirable drug effect
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Why we have side effects?
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Because we use same receptor for many things
-due to evolution
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Self-medication hypothesis
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1) Have a pre-existing condition so you seek out a medication to treat yourself
2) Have a pre-disposed factor
- Alcoholic has a deficiency in dopamine so they self medicate
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NMDA Receptor Requirements
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1) Bind with glutamate
2) Depolarization
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Describe what happens when the NMDA receptor is depolarized
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Expells Mg+ block and ions (Ca+) flow through
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What does the non-NMDA receptor do?
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It depolarizes the cell so the neighboring NMDA receptor can open its ion channels
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What is required for the non-NMDA receptor to depolarize the cell?
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Needs to bind with glutamate
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Exitotoxicity
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excessive stimulation of receptor by neurotransmitter that is toxic and kills the post synaptic cell
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Competitive Binding
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A and B compete for the same binding site
- presence of B can displace binding of A
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Noncompetitive binding
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A and B have different binding sites so they do not displace each other
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Affinity
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Attraction
Also indicator if it is reversible or not
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Reversibility
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Drug binding is temporary. It can bind and unbind.
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Selectivity (specificity)
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Selective to certain receptors
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Efficacy
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Effect or maximum response achievable from a drug
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Potency
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concentration of dosage
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Dose
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Amount of drug used
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Dosage
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Amount of drug per body weight
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Dose response curve
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Graph that plots the relationship btwn dosage and population response to that drug
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Effective dosage (ED50)
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Effective dosage in which 50% of the population experiences desirable effects
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Neurotransmitter
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released from a neuron to target cell (through synapse)
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Neurohormone
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Release chemicals into blood stream then carried to target cell
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Hormone
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Released from secondary cell to blood stream then to target cell
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Which is more selective drugs or neurotransmitters?
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Drugs
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Adenosine
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Has a feedback mechanism. The more a neuron fires the more adenosine is released
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What does Anandamine bind with
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Cannabinoid receptor
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Characteristics of Anandamine
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1) Natural neurotransmitter
2) Unstable (released on demand)
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Dopamine families have similar
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Genetic sequence
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What acts on the GABAa receptor?
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Alcohol
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What acts on the GABAb receptor?
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GHB (anti-epileptic drug; street: dape rape)
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Glycine
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Inhibitory neurotransmitter
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Glutamate
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1) Excitotoxicity
2) Glu blocker
-drug induced coma to prevent excitotoxicity
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Histamine
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more of a neuromodulator
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Norepinephrine
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1) Has alpha and beta receptors
2) similar to epinephrine
3) Beta blockers blick the exitability of norepenepherine and slows down the heart.
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Opiod
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Multiple functions (pain killer, activates pleasure, etc)
-endorphins
-endogenous opiod
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Serotonin
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1) One of the oldest neurotransmitters
2) Regulated with well being of animal
3) Estrogen modulates serotonin sensitivity (more=increases)
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Electrical synapse
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Only excitatory (depolarize)
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Chemical synapse
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Excitatory and inhibatory (hyperpolorize)
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MAOI
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1)monoamine oxidase inhibitor
2) Enzyme blocker (blocks enzymes from passing synapse
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Toxic Dosage
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Dosage that beings to have undesirable effects
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TD50
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50% of populations has undesirable effect
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Lethal dosage
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Dosage that kills
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LD50
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50% of population dies
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Therapeutic index
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Ratio of the dose that produces toxicity to the dose that produces a clinically desired effect in a pop of individuals
-measure of how safe a drug is with respect to the toxic dosage
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What is a safe TI?
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Greater than 1
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What is an unsafe TI?
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= or less than 1 (because that means there is overlap between the toxic and effective dosage)
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The wider the dose response curve the more...
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Variablility
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The slope in a dose response curve indicaties
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Variablity
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What does a shift of the dose response curve to the right indicate?
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Drug becomes less potent and it takes more of the drug to get the same effect
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What does a shift to the left indicate
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Drug is more potent
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Full agonist
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Maximum effect
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Partial agonist
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Has partial efficacy in relation to full agonist
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Inverse agonist
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Decreases effect; opposite effect of agonist
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Full antagonist
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Implies presence of another drug, completely blocked
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Partial Antagonist
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Partially blocks (looks like a partial agonist)
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Antagonist
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Renders original drug useless
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Example of Antagonist
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Morphine: blocks opiod receptor
Naloxone: block's morphine's affect
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Acupuncture
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Releases endorphines
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Endorphines
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Block pain; endogenous morphine
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How do you test acupunture?
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Use Naloxone
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Methadone
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Partial agonist opiod
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Dissociative anesthetics
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Block emotional pain (suffering), but physical pain is still felt
Used during post-op
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Suffering
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How much you can tolerate pain
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PCP: blocks NMDA receptor where
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PCP: blocks NMDA receptor where
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What is the disembodiment experience that PCP creates
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What is the disembodiment experience that PCP creates
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DXM (dextromethorphine)
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Partial agonist to PCP
In cough suppressants
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Depressant
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Decreases exitability
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Effects of CNS suppressant
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1) Normal
2) Relief from anxiety
3) Disihibition
4) Sedation
5) Hypnosis
6) General Anesthesia
7) Coma
8) Death
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Is MAO selective or non-selective
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Non-selective
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What is a side effect of MAO?
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Blocks tyramine, an enzyme of fermented cheese products which can be toxic if you eat any dairy products.
Cause an increase in blood pressure
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MAOI (inhibitor)
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Breaks down any monoamine
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SSRI
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Selective serotonin reuptake inhibitor
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What does the hypothalamic pituitary adrenal axis regulate?
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Stress, digestive and immune system
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In HPA axis what happens with CRF and NGF?
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CRF decreases NGF
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Cotical releasing factor
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Cotical releasing factor
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What does NGF stand for?
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Nerve growth factor
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Criteria for unconcious
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No response to stimulus
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Normal respiratory response when Oxygen level decreases
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Chemo receptors in the medulla (CSF) sense the drop in oxygen and pH receptors monitor CO2. Respiratory center in the medulla increases the breathing rhythm and oxygen increases.
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Respiratory response under CNS depressant
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Decrease firing of the neurons in the medulla
Decrease in respiratory rhythm
Decrease in O2
Greater decrease of neurons in medulla
Respiratory arrest
Stop breathing
GHB binds to GABA receptor and shuts down respiration
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Fate of drug
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Route of absorption
Absorption and distribution
Binding to the target site
Inactivation
Excretion
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Path of Oral administration
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Goes through GI tract via stomach and small intestine then absorbed in to blood stream
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What is the rate limiting step in Oral administration
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Gastric emptying
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How long is the delay of absorption on an empty stomach
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30 min
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How long is the delay of absorption on a full stomach
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2 hours
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What is the vomiting center?
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Medulla: If concentration of drug is too high, it triggers vomiting
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What senses the blood alcohol concentration in the medulla?
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Chemo receptors in the cerebro spinal fluid
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What is Vestibular ocular reflex?
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compensatory eye movement in rotation
If you rotate to the left, eyes will rotate right to fix the gaze
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Sublingual administration
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Drug is dissolved through the mucous membranes in the mouth and absorbed into the blood stream
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Topical Application
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Topical Application
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Subcutaneous injection
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Injection under the skin
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IV: intravenous injection
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Injection into the vein
It's fast but susceptible to aspectic condition (infection)
Rate dependant on rate of injection
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Intramuscular (IM)
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Injection into the muscle
Can cause Vasodilation (which increases absorption) and vasoconstrictioin (which decreases absorption)
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Intraperitoneal (IP)
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Injection of a substance into the peritoneal (body cavity)
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Inhalation - Through the lungs
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Goes to the lungs and absorbed through the alvealor sacs
Faster than and IV because it goes from the lung staight to the aorta
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Atomize
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Make into smaller particles through vaporizing so you can inhale it
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Inhalation through mucous membrane
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Snorting
Vasoconstrictor: will make you lose cartilage in nose
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pH of Gastric juice
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2-3
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pH of small intestine
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5-6.6
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pH of blood
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7.4
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pH of urine
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4.5-7
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less lipid soluable and less absorption
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less lipid soluable and less absorption
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Asprin in water is
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More ionized b/c it has to ionize itself to dissociate more, so it's less soluble and absorbs less
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Asprin in acid
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Is less ionized b/c the acid steals the electrons so it doesn't have to ionize itself, it's more soluble and absorbs easier
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Half life
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The amount of time it takes to decrease the initial concentration by half
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Steady state therapeutic level
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Amount of drug going in is the same as the amount of drug getting taken out
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Steady state therapeutic level
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Factors that influence drug (absorption, distribution, metabolism, elimination)
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Pharmacokinetics
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Factors that influence drug (absorption, distribution, metabolism, elimination)
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Pharmacodynamics
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Drug-receptor interactions
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Drug metabolism
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Drug-molecule modification.
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2 types of drug metabolism
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Synthetic and non synthetic
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Type of synthetic rxn
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Conjugation: coupling of drug molecules
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COOH
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COOH
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Hydroxyl
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OH
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Amino
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NH2
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Sulfhydryl
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SH
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Non-synthetic rxn
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Biotransformation: transform drug molecule into diff drug molecule
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Types of biotransformation
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oxidation, reduction, hydrolysis
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Therapeutic drug monitoring
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How you find out the concentration that is affected
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Depot binding
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binding with silent receptors that soak up drug as a buffer
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Disadvantage of Depot binding
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Diminishes concentration at target site
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Advantage of depot binding
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releases drug from silent receptors long after drug was administered
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Drug tolerance (types)
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Bx tolerance and pharmocological tolerance
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Types of pharmocological tolerance
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Metabolic and cellular
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Metabolic tolerance
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There's an increased number of enzymes with chronic exposure to a drug
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Metabolic reverse tolerance
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liver starts to fail. There is a decrease in enzymes and a decrease in metabolism. Chronically drunk.
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cellular adaptation pharmocodynamic tolerance
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when the receptor adapts to continuous presence of drug, the cell responds by increasing or decreasing the number of receptors
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Up regulation
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Increase number of receptors
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Down regulation
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decrease number of receptors
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Sensitization
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Up regulation
increased effects of drug
reverse tolerance
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Tolerance
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Down regulation
decrease effects of drug
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Cross tol
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...
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cross interaction
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Build tolerance to drugs that act on same receptor
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Bx tolerence
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Learned association btwn the effects of the drug an the environment
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Drug taking bx processes
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Set: mindset and Setting: environment
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State dependent learning
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Learn differently in different states and environments
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Adaptation: sensitization
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Become sensitized if stimulus is noxious
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Adaptation: desensitization
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Tolerance/habituation if stimulus is non-noxious
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How many stimuli does adaptation require
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1
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How many stimuli does conditioning require
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2
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US
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Unconditioned stimulus: food
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CS
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Conditioned stimlus: bell
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UR
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Unconditioned response: salivate to food
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CR
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Conditioned response: salivate to bell
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Substituted reinforcer
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Nucleus acumbus
Ventral tegmental area
Pre frontal cortex
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Nuclus Acumbus
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Reward center
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Ventral tegmental area
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Motivation
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Nucleus acumbus
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Decisions
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Excrete drugs through
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Kidneys, skin, sweat, lungs, etc.
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Long term potentiation
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Strengthen synapse
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Long term depression
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Weaken synapse
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Extinction
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Stop reinforcing and bx stops
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Timing dependent synapse plasticity
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Secondary trauma stress disorder
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Witness the trauma, feel empathy
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Operant conditioning
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Self learning w/out a teacher
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Classical conditioning
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Supervised learning with a teacher
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Learned helplessness
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stop avoiding shock
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In group vs. out group
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ppl will do anything to protect the in-group if you're in the outgroup they don't care to protect you.
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Moral dilemma
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Conflict: Have to choose between two things that oppose each other and are both unwanted
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Scheduled reinforcement
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FR
FI
VR
VI
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Fixed ratio
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Reward every 10 times
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Fixed interval
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Reward every 10 seconds
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Variable ratio
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Reward every 10 times on average
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Variable interval
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Reward every 10 seconds on average
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Differential Reinforcement of Low-rate of Responding schedule (DRL)
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You train animal to wait certain time in bar press test and add another condition. If animal presses early time starts over. Time exceeded=reinforced
Monitors ability to tell time elapsed and know that no action is allowed b4 timer expires.
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BIOL 4220: EXAM 2