02_Membrane Potential_Q and A_Jonathan Flashcards Preview

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Flashcards in 02_Membrane Potential_Q and A_Jonathan Deck (15):

Note: These questions are not complete because the lecture was mostly review. Please see the notes for additional info.

Note: These questions are not complete because the lecture was mostly review. Please see the notes for additional info.


V = IR

V = IR


Capacitor is the lipid bilayer. It stores charge.

Capacitor is the lipid bilayer. It stores charge.


What are the Nernst Equations?

Eion = RT/ZF ln [ion]out/[ion]in

Eion = 61 log [ion]out/[ion]in (for monovalent ions at 37 degrees C)


What are leak channels? What do they do?

• Tandem-pore domain K-selective channels that are constitutively open at rest and are not gated by voltage or ligands
• Primarily esponsible for generating resting membrane potential in neurons


How much does the conductance of chloride (Gcl) contribute to the resting potential of neurons? What about muscle cells?

• in neurons the conductance is very low and can be ignored
• in muscle cells, the conductance of Cl is significant and can contribute to channelopathies (eg myotonia congenital)


How much does Na conductance contribute to resting membrane potential in neurons and muscle cells? When does Na become significant?

• There are some Na leak channels that cause the cell to depolarize slightly thereby causing the resting potential to become less negative than if reliant on K leak channels alone
• Also, because Na is involved in so many other ion pumps (co- and anti-porters), small perturbations of Na can cause channelopathies due to other ions. (eg hyperkalemic periodic paralysis)


What percentage of ATP is dedicated to the Na/K channel in the brain? What about in active nerve cells?

• 24%
• 70%


What are cardiac glycosides?

• inhibit the Na/K pump by competitive binding to the K binding site on the outside of the cells


What is Ouabain? How does it work?

• a poisonous cardiac glycoside
• formerly used as an ionotropic agent
• blocks the Na/K channel ==> Na builds up in cell ==> stimulates the Na/Ca channel to reverse (usually Na/Ca pumps Na into cell and Ca out of cell) ==> Ca gets pumped INTO the cell ==> cardiac myocytes contract more forcefully (ionotropic)


What is a Dystonia?

• Dystonia is a neurological movement disorder, in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures.


What is Rapid-Onset Dystonia-Parkinsonism (RDP)?

• hereditary
• loss of function in the alpha3 subunit of the Na/K channel
• disrupt neuronal function in the cerebellum ==> thalamus ==> basal ganglia
• Parkinson-like symptoms
• Rapid onset (age 15 to 45 and up to 58) symptoms stabilize and remain constant 4 weeks after onset


What is Myotonia?

• Myotonia is a symptom of neuromuscular disorders characterized by the slow relaxation of the muscles after voluntary contraction or electrical stimulation.
• repeated effort is needed to relax the muscles, and the condition improves after the muscles have warmed up.
• prolonged, rigorous exercise may also trigger the condition.
• may have trouble releasing their grip on objects or may have difficulty rising from a sitting position and a stiff, awkward gait.


What is myotonia congenita?
What channel is involved?
What are the mechanisms involved?

• Remember, Cl channels effect muscle Vm
• Mutation in the Cl channel subunit (CLCN1)
• Reduced Cl conductance (Cl works to hyperpolarize the cell), so Vm is not restored as fast as it should be
• (normally, high K in the T-tubules is balanced by the high resting Cl conductance (Gcl)

• K accumulates in the T-tubules ==> muscle cells remain depolarized and contracted
• Mutated Cl channels only activate at very positive membrane potentials following the multiple action potentials
• Bouts of myotonia can be triggered by cold, exercise, or fatigue


What is Hyperkalemic periodic paralysis (HYPP)?

• In muscle cells
• mutation in voltage-dependent Na channel ==> high serum K from exercise
• The mutation in Na channel opens and stays open (becomes voltage-independent) ==> promotes K efflux and further depolarization
• Loss of resting potential causes inability to respond to nerve signals ==> paralysis