Long Answer Qs Exam 1 Flashcards
Define the terms drug potency and drug efficacy. How does increasing efficacy or potency change the dose response curve?
Note: the exam question also asks a typical curve be drawn
Drug efficacy is the maximum effect that a drug can have regardless of how high the dose. Drug potency is how much of the drug you need to get any effect
Increasing potency shifts the curve to the left as you need less of a drug, whereas decreasing potency does the opposite
Increasing efficacy makes the curve taller, whereas decreasing efficacy does the reverse
Define LD50 and ED50. How do you calculate the therapeutic index? What is the therapeutic window?
The ED50 is the effective dose -> how much you need to produce an effect in 50% of subjects tested
LD50 is the lethal dose -> how much you need to have lethal consequences in 50% of subjects tested
The LD50 divided by the ED50 = Therapeutic index
the therapeutic window is the dosage range where you get the desired clinical effect, with minimal adverse effects
With respect to human participants, name and briefly describe a test for i) short term memory, ii) executive function, and iii) motor performance
[i can’t really make an answer card for this since it has a few options]
name and describe three schedule of reinforcement
(fixed ratio, progressive ratio, variable ratio, fixed interval, variable ratio)
Briefly describe the results of Siegels study on heroin overdose in vehicle- vs. drug-associated contexts and how can they be explained in terms of opponent process theory and classical conditioning? How are the A and/or B processes different during first few administrations vs. after many administrations of heroin?
All rats were given the same lethal dose of heroin (15mg/kg). The rats that were given this in the same environment as where there they had been receiving the drug in the conditioning phase had lower mortality rates than those who received the overdose injection in a different environment (and those in the control who had never received heroin)
This is due to opponent process theory and conditional tolerance as the rats had learned to associate that environment with heroin injection. The body thus initiated the b process (preparation) in advance of the drug in order to combat the a process (the effect of the drug) and keep the body in homeostasis.
The A process stays the same between first and repeated administrations, but the B process starts sooner and gets stronger with continued use
Define metabolic tolerance and physiological tolerance. Briefly describe
the results from Barrett and Smith experiment and what they tell us about the nature of withdrawal
metabolic tolerance occurs when fewer drug molecules reach their site of action due to the body’s increased rate/ability to metabolise a drug, usually because of enzyme induction (an increase of enzyme levels)
physiological tolerance has a similar basis to opponent process theory. with repeated use, the body makes adjustments to compensate for the effects caused by the drug in order to keep homeostasis
in barrett and smith’s experiment, rats initially responded with the lever associated with CDP (which reduced anxiety) but then later started responding with the one associated with PTZ (which increased anxiety). eventually they responded equally on both levers. the pattern suggests that while they were calm for a while, a compensatory response started building in the body causing feelings of agitation and an increase in hitting the PTZ lever. gradually that compensatory response faded until the rats were hitting both levers around equal amounts
- when it comes to withdrawal, it tells us that after drug use, the body begins to counteract the effects in order to get back to homeostasis. eventually, the drug effects wear off and what is left is the body’s b process effects. this period is the hangover and withdrawal phase (i hope i understood this right sob)
Briefly describe the terms EPSP and IPSP with respect to changes of the membrane poten-
tial . Briefly describe what is meant by spatial summation and temporal
summation. Briefly describe what happens during depolarization-induced
suppression of inhibition.
EPSP = excitatory postsynaptic potential occurs when sodium ions enter the cell, making it less negatively charged (aka depolarisation)
IPSP = inhibitory postsynaptic potential. occurs when potassium ions exit the cell, OR when chlorine enters the cell, making it more negatively charged (aka hyperpolarisation)
temporal summation = a neuron experiences multiple postsynaptic potentials closely in time, thus accumulating
Spatial summation = two or more postsynaptic potentials occur in close proximity on a neuron. a neuron may have Na entering in some places, Cl entering some, or K exiting and these local changes may cancel each other out or summate together
depolarisation induced suppression of inhibition occurs when the level of stimulation is changed through neurotransmitter synthesis and release by the presynaptic neuron, specifically where activity at the synapse is inhibitory (if it were excitatory it would be depolarisation induced suppression of excitation. unless i got the orders mixed up?…)
Name, and describe, two methods by which a neurotransmitter may be removed from the
synapse. Briefly describe the difference between an ionotropic vs. a metabotropic receptor (2 points)
reuptake (uses transporter protein molecules. presynaptic cell reabsorbs the intact transmitter and it gets repackaged into vesicles are further use), enzymatic degradation (synapse contains an enzyme that breaks neurotransmitter into it’s precursors. these can also be taken back into presynaptic cell to be remanufactured for future release)
ionotropic receptors is when receptor proteins have binding sites directly connected to a gated ion channel. neurotransmitter binding activates the receptor and reconfiguration of the protein which makes the ion channel open or close
metabotropic receptors are located on the extracellular portion of a long signal protein. the intracellular part is connected to g protein and when the receptor is bound to, this makes the g protein break away and interact with other downstream cellular components
What are the major excitatory and the major inhibitory neurotransmitter systems in the
brain? Name two brain structures in which dopamine is synthesized and two functions served by dopamine transmission in the brain
major excitatory system = glutamate, major inhibitory system = GABA
The substantia nigra (SN), which projects to the dorsal striatum and the ventral tegmental area (VTA) which projects to the ventral striatum
dopamine is associated with learning, by way of enhancing attention, motivation, and memory consolidation (this is mostly relevant with the VTA projection). it is also involved with the motor loop and general motor function (SN). this is why the SN is involved in parkinsons and the VTA in schizophrenia
Briefly describe the incentive sensitization and hedonic dysregulation and adaptation theories of drug addiction. For each theory, provide one type of experimental evidence that lends support to the theory
Incentive sensitisation = your motivation system gets more excitable with extended use. aka wanting gets sensitised. explains craving without withdrawal, impulsivity, and cue associated relapse
Hedonic Dysregulation and adaptation = opponent process theory essentially. you seek pleasure, and the body regulates against that. then, by taking more drug during the hangover phase, you start at a lower point and your allostatic points get lower and lower as you cannot prevent a hangover, only postpone it. explains psychological withdrawal, compulsivity, and stress related relapse
