STUDENT NAME:____________________ TUTORIAL NUMBER/TA____

STUDENT NUMBER:_________
BIOLOGY 3P03
Test #2 Cell Physiology Dr. Alexander Little
Duration: 50 minutes Fall 2023
November 22, 2023

Special Instructions:
 This test contains 7 pages. Check both sides on all pages of this exam paper.
 Total Marks = /33

 Complete all answers by selecting the appropriate options on the provided OMR McMaster
SCANTRON examination answer sheet. It is your responsibility to ensure that the answer sheet is
properly completed. Your test result depends on proper attention to these instructions:

The scanner, which reads the sheets, senses the shaded areas by their non-reflection of light. A heavy
mark must be made, completely filling the circular bubble, with an HB pencil. Marks made with a pen
or felt-tip marker will NOT be sensed. Erasures must be thorough, or the scanner may still sense a mark.
Do NOT use correction fluid on the sheets. Do NOT put any unnecessary marks or writing on the sheet.

1. On side 1 (red side) of the form, in the top box, print in pen your student number, name, course
name, section number, instructor name and the date in the spaces provided. Then you MUST write your
signature.
2. In the second box, with a pencil, mark your student number, exam version number and course
section number in the space provided and fill in the corresponding bubbles underneath.
3. For answers, mark only ONE choice from the alternatives (1, 2, 3, 4, 5 or A, B, C, D, E)
provided for each question. If there is a True/False question, enter response of 1 (or A) as True, and 2
(or B) as False. The question number is to the left of the bubbles. Make sure that the number of the
question on the scan sheet is the same as the question number on the exam paper.
4. Pay particular attention to the Marking Directions on the form.
5. Begin answering questions using the first set of bubbles, marked “1”.
 For each of the following questions, please select the ONE BEST response for each question.

The figure below loosely relates to Questions 1 and 2. You may have to imagine other types of
synaptic connections that would occur but are not necessarily shown.

1. Which of the following is most likely?

A. The sensory neuron excites the extensor motor neuron but inhibits the inhibitory interneuron
B. The extensor motor neuron releases acetylcholine from its terminal
C. The inhibitory interneuron releases glutamate to the flexor motor neuron
D. When the inhibitory interneuron is excited, the hamstring muscle simply explodes

2. If the patellar hammer hits the tendon harder, the increased stretching of the quadriceps muscle
would pull harder on the muscle spindle and:
A. The sensory neuron would transmit a series of larger action potentials
B. The sensory neuron would transmit a series of more frequent action potentials
C. The sensory neuron would hyperpolarize more
D. The sensory neuron threshold of activation would increase

3. A skeletal muscle cell is voltage-clamped at a specific membrane potential in the presence of

acetylcholine but no net current is observed through its acetylcholine receptors. Which of the
following must be true?
A. This is expected because muscle cells do not have acetylcholine receptors
B. The membrane potential is clamped below the threshold potential
C. The membrane potential is clamped below the ENa
D. The membrane potential is clamped below the EK

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 4. In ionic terms, what are the main factors that contribute to the long-lasting plateau phase of the
cardiac action potential?
A. Inward flow of sodium and outward flow of calcium ions
B. Inward flow of potassium and outward flow of sodium ions.
C. Inward flow of sodium and outward flow of potassium ions.
D. Inward flow of calcium and outward flow of potassium ions.

5. During the absolute refractory period of a motor neuron action potential

A. Sodium channels are open.
B. All inactivation/H gates are closed.
C. Sodium channels are able to open with a stimulus in this period.
D. Sodium will influx into the cell and there will be a depolarization of the motor neuron.

6. The reversal potential for acetylcholine receptors on the sarcolemmal end plate is:
A. Above ENA
B. Below EK
C. Between ENA and EK

7. “The main role of potassium ions in a motor neuron during an action potential, is to help with
depolarization during an action potential.” Is this statement true or false?
A. True.
B. False.

The description below, relates to Questions 8 and 9.

An extracellular chemical ligand is thought to modulate muscle contraction via the elevation of a
diffusible second messenger. In addition, the extracellular ligand causes activation of protein kinase C
(PKC), leading to muscle contraction in this cell.

8. What receptor type do you expect would be activated by this extracellular chemical ligand
A. a RTK.
B. a GPCR.
C. a nicotinic acetylcholine receptor.

9. What second messenger would you expect to be directly produced?

A. calcium
B. IP3
C. cAMP
D. cGMP

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10. During the patellar reflex, the stretching of the quadriceps muscle pulls on the muscle spindle,
signaling the muscle to
A. contract
B. relax

11. Multiple sclerosis (MS) is an autoimmune disease that leads to the destruction of myelin
sheaths. Which of the following would be true of this pathology?
A. Neural dysfunctional because action potentials are now bidirectional
B. More eletrotonic decay
C. Higher conduction velocities
D. Lower thresholds of activation

12. Which of the following determines the threshold of an action potential?

A. The diameter of the axon
B. The voltage sensitivity of ion channels
C. The size of the stimulus applied
D. The speed of conduction in the axon

13. Why does the refractory period of a neuron prevent backward propagation of an action
potential?
A. The absolute refractory period ensures all voltage-gated Na⁺ channels are open.
B. Voltage-gated Na⁺ channels are inactivated, preventing depolarization.
C. Potassium channels are blocked, allowing only forward propagation.
D. The action potential resets itself along the axon after each firing.

14. What triggers the release of acetylcholine at the neuromuscular junction?

A. Opening of ligand-gated ion channels
B. Action potential in the motor neuron
C. Binding of glycine to the synaptic terminal
D. Direct depolarization of the postsynaptic membrane

15. Which type of acetylcholine receptor is found at the vertebrate neuromuscular junction?
A. Muscarinic acetylcholine receptor
B. Nicotinic acetylcholine receptor
C. Dopamine receptor
D. AMPA receptor

16. What is the primary effect of acetylcholine binding to nicotinic receptors?

A. Increases potassium efflux
B. Decreases sodium influx
C. Opens non-selective cation channels
D. Inhibits action potential generation

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17. Why does the end plate potential (EPP) at the neuromuscular junction lead to an action potential
in the muscle cell?
A. It causes hyperpolarization of the muscle membrane.
C. It depolarizes the muscle membrane sufficiently to open voltage-gated sodium channels.
D. It activates inhibitory interneurons that propagate the signal.

18. What type of synapse involves an axon connecting to the cell body of another neuron?
A. Axodendritic
B. Axosomatic
C. Axo-axonic
D. Dendrosomatic

19. What occurs during temporal summation at a synapse? Keep in mind that IPSPs are inhibitory
postsynaptic potentials and EPSPs are excitatory postsynaptic potentials.
A. EPSPs from multiple neurons sum simultaneously.
B. Multiple EPSPs from one neuron sum over time.
C. IPSPs and EPSPs sum to cancel out.
D. Only IPSPs are summed at the axon hillock.

20. How does the axon hillock determine whether an action potential will occur?
A. By detecting the balance between sodium and chloride ion fluxes.
B. By integrating EPSPs and IPSPs and reaching a voltage threshold.
C. By summing neurotransmitter concentrations in the synaptic cleft.
D. By opening all ion channels simultaneously.

21. Which neurotransmitter is the major inhibitory transmitter in the spinal cord?
A. Glutamate
B. Acetylcholine
C. Glycine
D. Dopamine

22. What is a key structural feature of synapses?

A. Presynaptic active zones are regions involved in neurotransmitter release.
B. Postsynaptic membranes contain no receptors.
C. Synaptic vesicles are found on the postsynaptic side.
D. Synaptic clefts are absent in inhibitory synapses.

23. Which ion is involved in generating an IPSP via glycine receptors?

A. Sodium (Na⁺)
B. Calcium (Ca²⁺)
C. Potassium (K⁺)
D. Chloride (Cl⁻)

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24. What is the primary role of second messengers in a cell?
A. To directly bind DNA and modify transcription.
B. To activate signal cascades after receptor activation.
C. To act as the main signaling molecules outside the cell.
D. To store ions in the endoplasmic reticulum.

25. How does phospholipase C contribute to the production of second messengers?

A. By converting ATP into cyclic AMP.
B. By cleaving PIP₂ into DAG and IP₃, which activate separate signaling pathways.
C. By opening calcium channels directly on the membrane.
D. By phosphorylating GPCRs.

26. What is the primary difference between fast and slow chemical synaptic transmission?
A. Fast transmission involves the activation of G-protein coupled receptors, while slow
transmission involves ionotropic receptors.
B. Fast transmission directly opens ligand-gated ion channels, while slow transmission activates
intracellular signaling molecules that eventually open ion channels.
C. Fast transmission occurs at axo-axonic synapses, while slow transmission occurs at
axodendritic synapses.
D. Fast transmission is always excitatory, while slow transmission is always inhibitory.

27. How does norepinephrine increase the frequency of pacemaker action potentials in the heart?
A. By decreasing potassium efflux through muscarinic receptors
B. By activating β-adrenergic receptors and increasing cAMP levels, which enhance sodium
and calcium influx
C. By opening NMDA receptors on pacemaker cells
D. By directly binding to voltage-gated sodium channels

28. What is the primary mechanism by which IP₃ and DAG are generated during G-protein
signaling?
A. Gαs subunits activate adenylyl cyclase to produce IP₃ and DAG from cAMP.
B. Phospholipase C catalyzes the breakdown of phosphatidylinositol 4,5-bisphosphate (PIP₂)
into IP₃ and DAG.
C. GPCR activation causes direct opening of calcium channels, leading to IP₃ production.
D. DAG is generated in the cytosol, while IP₃ is formed in the nucleus.

29. What role do inhibitory interneurons play in the knee-jerk reflex?

A. They increase the action potential frequency in the quadriceps motor neuron.
B. They hyperpolarize the hamstring motor neuron to prevent contraction of the antagonistic
muscle.
C. They depolarize the sensory neuron to enhance signal transmission to the spinal cord.
D. They inhibit the release of acetylcholine at the neuromuscular junction of the quadriceps.

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30. What happens to the end plate potential (EPP) if the postsynaptic muscle cell is clamped at a
membrane potential more negative than resting?
A. The EPP becomes smaller due to reduced sodium influx.
B. The EPP becomes larger due to increased sodium influx.
C. The EPP reverses polarity due to potassium efflux.
D. The EPP remains unchanged because it is not dependent on membrane potential.

31. How does acetylcholine binding to muscarinic receptors affect cardiac pacemaker cells?
A. It increases sodium conductance, leading to faster depolarization.
B. It decreases calcium conductance and increases potassium conductance, slowing the
pacemaker potential.
C. It directly blocks voltage-gated sodium channels.
D. It stimulates Gs proteins, increasing cAMP levels in pacemaker cells.

32. What determines the reversal potential (ERR) of nicotinic acetylcholine receptor (nAChR)
channels at the neuromuscular junction?
A. The concentration gradient of sodium ions across the membrane
B. The equilibrium potential for potassium ions
C. The balance of sodium and potassium ion fluxes through the channel
D. The presence of chloride ions in the extracellular environment

33. How do inhibitory postsynaptic potentials (IPSPs) decrease the likelihood of action potential
generation in the postsynaptic neuron?
A. By increasing sodium ion influx, leading to depolarization below threshold
B. By opening anion channels, leading to hyperpolarization of the membrane
C. By reducing the time constant for depolarization in the postsynaptic neuron
D. By directly blocking voltage-gated calcium channels in the presynaptic neuron