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Acetylcholine binds to a G-coupled protein receptor on the heart muscle to make the heart beat more slowly. It does so by stimulating the opening of K+ channels in the plasma membrane, which makes it more difficult to initiate and action potential. Describe the following on contraction of the heart.
A.) Addition of a drug that inhibits the GTPase activity of the Ga subunit.

B.) Mutations in the K+ channel that keep it closed all the tiem.

C.) A mutation that decreases the affinity of the (Beta gamma) complex of the G protein for the K+ channel.

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Tod Thiel
Tod ThielLv2
28 Sep 2019

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Related questions

Acetylcholine binds to a GPCR on heart muscle, making the heart beat more slowly. Remember, the activated receptor stimulates a G protein, which opens a K+ channel in the plasma membrane. Which of the following would enhance this effect of the acetylcholine?

(a) addition of a high concentration of a non-hydrolyzable analog of GTP

(b) addition of a drug that prevents the α subunit from exchanging GDP for GTP

(c) mutations in the acetylcholine receptor that weaken the interaction between the receptor and acetylcholine

(d) mutations in the acetylcholine receptor that weaken the interaction between the receptor and the G protein

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 Loewi’s 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

3. a) The neurotransmitter that is responsible for “communication” at the neuromuscular junction between motor nerve cells and skeletal muscle fibers is acetylcholine (ACh). The ACh receptor protein is a channel that opens when ACh binds. Upon the opening of this channel, the membrane at the motor end plate region of the muscle cell becomes depolarized, resulting in the generation of an action potential in the muscle fiber membrane. The ACh receptor channel is equally permeable to both Na+ and K+ ions. Explain how opening a channel that allows both potassium and sodium to cross the membrane results in membrane depolarization. (2 points)

b) In normal individuals, a single end-plate potential (EPP) is always sufficient to elicit an action potential (and hence contraction) in a skeletal-muscle fiber. This is not the case in individuals suffering from myasthenia gravis (MG). MG is an autoimmune disorder in which antibodies are produced that attack the AChRs at skeletal-muscle endplates reducing their number. Patients suffering from the disease present with significant muscle weakness. Explain why patients with MG would exhibit muscle weakness. (2 points)

c) Treatment strategies for myasthenia gravis include thymectomy (removing the source of the antibody producing cells) or immunosuppressant drug therapy (inhibiting the synthesis and release of the antibodies). In addition, the drug neostigmine administered at carefully monitored doses is highly effective in treating myasthenia gravis. Investigate the actions of neostigmine, and discuss in detail why it may be an effective treatment. (2 points)

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