Pharmacology 2060A/B Lecture Notes - Lecture 7: Gaba Receptor, Macromolecule, Titration

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3 Mar 2016

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Module 7 pharmacodynamics dose response. Pharmacodynamics what the drug does to the body. Biochemical + physiological effects of drugs and mechanisms by which drugs produce effects. Pharmacodynamcics increasing dose increases response of drug (monotonic) Dose response curves are not linear therefore, look at it as a semi- logarithmic plot. Phases of the semi- logarithmic dose- response curve. Phase 1 doses are too low to elicit a clinically relevant response. Phase 2 the response is graded and nearly linear. Phase 3 larger dose do not lead to greater response. Larger dose may cause toxicity. Efficacy measure of how effective a drug is at a given dose. Maximal efficiacy max effect that a drug is capable of achieving. We choose the drug and dose that are therapeutically effective with the fewest side effects. Health care professionals often titrate the dose of a drug.

Related Questions

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewiâs classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

receptor	Agonist	antagonist


a1	Norephinephrine	Phenylephrine
a2	Phenoxybenzamine	Prazosin
B1	Clonidine	Yohimbine
	Norephinephrine	Propranolol
	Epinephrine	Metoprolol
	Isoproterenol
	Dobutamine
B2	Epinephrine	Proranolol
	Norepinephrine	Butoxamine
	Isoproterenol
	Albuterol


Nicotinic	Ach	Curare
	Nicotine
		Hexamethonium
Muscarinic	Ach	Atropine

Assume all the chemicals in the table are available to you.

You are given a piece of smooth muscle tissue, you stimulate it with Norepinephrine and find the muscle responds with contractions. Your hypothesis is that the muscle contraction is caused by the activation of Î±1 adrenergic receptors. Now you need to design an experiment protocol to test your hypothesis.

Background knowledge: The figure below is an experiment setup, the red tissue in the organ bath is the smooth muscle tissues. In this kind of experiment smooth muscle tissue is minimally stretched vertically by two hooks or clips in the organ bath filled with physiological saline solution (PSS). Agonist is added to the PSS to challenge the muscle tissue, muscle contraction is sensed by a force transducer at the top and force is recorded by a computer. Adding antagonist before adding agonist blocks agonist action. PSS may or may not be changed, it depends on your purposes, e.g. if you want to block a type receptors, then you do not want change PSS after you add antagonist to the PSS. Your correct step is that you add antagonist to PSS, wait some time, and add agonist, you keep both antagonist and agonist in the PSS so that you can judge if the receptor blockage by antagonist abolish the agonist action.

The key to this assignment is that you eliminate possible cross-activities of agonists. Cross-activity means an agonist activate more than one types of receptors, you need block each type of the receptor in order to see what type of the receptor is activate to cause contraction. This muscle tissue can have both Î± and Î² receptor types and their subtypes, you need to demonstrate convincingly that you only stimulate Î±1 receptors.

Write an experimental protocol to demonstrate your work, for each step in the protocol you write the chemical(s) you add, why you add, what result you are expecting to see e.g. contract, relax, no response. If the step is to wash the tissue with fresh PSS, then you do not need to indicate the responses.

Here is an example of the answer.

step	chemical added	response
1.	epinephrine, activate alpha and beta receptors,	blood vessel ring contract slightly.
2.	wash with PSS
3.	alpha receptor antagonist and norepinerphine, block NE activating alpha receptor.	blood vessel ring should not contract.
4.	wash with PSS
5.	â¦	â¦
6.	â¦	â¦

Discuss your protocol to show the relation between activation of Î±1 receptors and the vascular smooth muscle contraction.Design the experiemnt and its conclusion/ results.

Find compounds (drugs and toxicants) that target each of the following: A receptor tyrosine kinase pathway.

- The name of the receptor involved

- The type of ligand that the drug or toxicant presents: Agonist, antagonist. Are there natural ligands that interact with the receptor? If so explain the interaction.

Provide a brief explanation of the mechanism of the cellular response upon ligand binding to the receptor (i.e what signal transduction mechanisms occur).

How does the cellular response translate into a physiological response? What are the intended target tissue(s)? Are there any reported examples for the drug/toxicant acting on an off-target site?

Have there been any toxicology studies that assessed the dose response relationship of the compound? Provide data on TD50, LD50 and TI if you were able to find it. If not available, please note that.

Pharmacology 2060A/B Lecture Notes - Lecture 7: Gaba Receptor, Macromolecule, Titration

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