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Test Bank for Lippincott Illustrated Reviews: Neuroscience, 2nd Edition (Krebs, Weinberg, Akesson & Dilli) | All Chapters (1–22) |

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Complete test bank for Lippincott Illustrated Reviews: Neuroscience, 2nd Edition, covering chapters 1–22 for medical and health science courses.

Institution
Neuroscience
Course
Neuroscience













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Institution
Neuroscience
Course
Neuroscience

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Uploaded on
January 15, 2026
Number of pages
198
Written in
2025/2026
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, CHAPTER LIST

Chapter 1: Introduction to the Nervous System and Basic Neurophysiology

Chapter 2: Overview of the Central Nervous System

Chapter 3: Overview of the Peripheral Nervous System

Chapter 4: Overview of the Visceral Nervous System

Chapter 5: The Spinal Cord

Chapter 6: Overview and Organization of the Brainstem

Chapter 7: Ascending Sensory Tracts

Chapter 8: Descending Motor Tracts

Chapter 9: Control of Eye Movements

Chapter 10: Sensory and Motor Innervation of the Head and Neck

Chapter 11: Hearing and Balance

Chapter 12: Brainstem Systems and Review

Chapter 13: The Cerebral Cortex

Chapter 14: The Thalamus

Chapter 15: The Visual System

Chapter 16: The Basal Ganglia

Chapter 17: The Cerebellum

Chapter 18: The Integration of Motor Control

Chapter 19: The Hypothalamus

Chapter 20: The Limbic System

Chapter 21: Smell and Taste

Chapter 22: Pain

,Chapter 1 Test Bank — Introduction to the Nervous
System & Basic Neurophysiology


1) Resting membrane potential and selective permeability

A researcher replaces extracellular Na⁺ with an impermeant cation of equal osmolarity
while keeping extracellular K⁺ constant. Neuronal resting membrane potential changes
minimally. Which explanation best accounts for this observation?

A. Resting potential is determined primarily by Na⁺ permeability through ligand-gated
channels
B. Resting potential is determined primarily by K⁺ permeability through leak channels
C. Resting potential is determined primarily by Ca²⁺ influx through voltage-gated
channels
D. Resting potential is determined primarily by Cl⁻ efflux through transporter reversal

Answer: B

Rationale:
At rest, the neuronal membrane is far more permeable to K⁺ than to Na⁺ because K⁺
leak channels are open and abundant. Therefore, the resting membrane potential
(RMP) lies near the K⁺ equilibrium potential (E_K), not E_Na. If extracellular Na⁺ is
replaced with an impermeant cation, E_Na changes dramatically, but because the
membrane’s Na⁺ permeability at rest is low, the weighted contribution of Na⁺ to the
Goldman-Hodgkin-Katz (GHK) equation is small—so RMP shifts only slightly. In
contrast, changing extracellular K⁺ would significantly alter E_K and therefore RMP.
The key principle is permeability-weighting, not simply concentration gradients.

Key words: resting membrane potential, GHK equation, K⁺ leak channels,
permeability weighting, E_K



2) Nernst logic applied to hyperkalemia

A patient with severe hyperkalemia develops generalized weakness. In motor neurons,
the initial electrophysiologic change most directly caused by increased extracellular K⁺
is:

A. More negative E_K, hyperpolarizing the membrane
B. Less negative E_K, depolarizing the resting membrane potential
C. Reduced Na⁺ conductance, hyperpolarizing the membrane
D. Increased Cl⁻ influx, depolarizing the membrane

Answer: B

,Rationale:
E_K depends on the ratio of intracellular to extracellular K⁺. Increasing extracellular K⁺
reduces this ratio, making E_K less negative. Because RMP is close to E_K, the
membrane depolarizes. Clinically, early depolarization can increase excitability, but
sustained depolarization inactivates voltage-gated Na⁺ channels (h-gates close),
reducing action potential upstroke and conduction—leading to weakness. The “initial”
change is depolarization (less negative RMP), with downstream sodium channel
inactivation causing functional failure.

Key words: hyperkalemia, Nernst equation, E_K less negative, depolarization, Na⁺
channel inactivation



3) Action potential threshold as a balance of currents

Which change most directly raises the threshold for firing an action potential in an
axon initial segment?

A. Increased density of voltage-gated Na⁺ channels
B. Increased extracellular Ca²⁺ screening surface charge and shifting Na⁺ activation to
more positive voltages
C. Increased intracellular Na⁺ concentration
D. Increased membrane resistance (R_m) at rest

Answer: B

Rationale:
Threshold is reached when inward Na⁺ current exceeds outward/leak currents,
generating positive feedback. Extracellular Ca²⁺ affects surface charge near Na⁺
channels; higher Ca²⁺ stabilizes the membrane and shifts Na⁺ channel activation to
more depolarized potentials, effectively raising threshold (harder to open Na⁺
channels). Increased Na⁺ channel density (A) lowers threshold. Increased R_m (D)
increases voltage response to a given synaptic current (V = IR), making threshold
easier to reach. Intracellular Na⁺ (C) modestly changes E_Na but does not typically
dominate threshold compared with gating shifts.

Key words: threshold, Na⁺ activation curve, extracellular Ca²⁺, surface charge
screening, axon initial segment



4) Absolute vs relative refractory period

A neuron is stimulated twice: the second stimulus occurs 2 ms after the first action
potential peak. A second action potential cannot be triggered regardless of stimulus
strength. This failure is primarily due to:

,A. Inactivation of voltage-gated Na⁺ channels
B. Closure of voltage-gated K⁺ channels
C. Depletion of intracellular Na⁺
D. Failure of neurotransmitter release

Answer: A

Rationale:
The absolute refractory period occurs when most voltage-gated Na⁺ channels are
inactivated (h-gates closed) and cannot reopen until the membrane repolarizes
sufficiently. During this window, no stimulus—no matter how strong—can trigger
another AP. K⁺ channel opening contributes to repolarization and the relative
refractory period (needing stronger stimulus due to hyperpolarization), but “cannot be
triggered regardless of strength” points directly to Na⁺ channel inactivation.

Key words: absolute refractory period, Na⁺ channel inactivation, h-gate, excitability,
repolarization



5) Conduction velocity: myelin vs axon diameter

Two axons have identical diameters. Axon 1 is heavily myelinated; Axon 2 is
unmyelinated. Compared with Axon 2, Axon 1 primarily achieves faster conduction by:

A. Increasing membrane capacitance and increasing charge storage
B. Decreasing membrane resistance to promote ionic flow across internodes
C. Increasing length constant and enabling saltatory conduction between nodes
D. Decreasing axial resistance by widening the axon

Answer: C

Rationale:
Myelin increases membrane resistance (R_m) and decreases membrane
capacitance (C_m) across internodes. Higher R_m reduces current leak; lower C_m
reduces the amount of charge needed to change membrane voltage. Together these
increase the length constant (λ) and reduce the time constant (τ = R_m·C_m) for
charging at nodes, allowing depolarizing current to travel farther and faster to the next
node of Ranvier, producing saltatory conduction. A is wrong because myelin
decreases capacitance. B is reversed—myelin increases resistance. D is diameter-
related, but diameter is held constant.

Key words: myelin, saltatory conduction, length constant, membrane capacitance,
nodes of Ranvier



6) Demyelination and “conduction block” mechanism

, In multiple sclerosis, demyelination in an axonal segment most directly predisposes to
conduction block because:

A. Na⁺ channel density becomes excessively high at internodes, preventing
depolarization
B. Membrane capacitance decreases, preventing current spread
C. Membrane resistance decreases and current leaks before reaching the next node
D. Axial resistance increases due to oligodendrocyte loss

Answer: C

Rationale:
Demyelination removes the insulating wrap that normally prevents transmembrane
current leak. Without myelin, R_m decreases, so current dissipates across the
membrane instead of traveling longitudinally to depolarize the next node. Even if Na⁺
channels redistribute over time, acutely the internode lacks sufficient nodal-like
channel clustering and the depolarizing wave can fail—conduction block.
Capacitance actually increases when myelin is lost (opposite of B). Axial resistance
depends mainly on axoplasm and diameter, not myelin (D).

Key words: demyelination, conduction block, membrane resistance, current leak, MS



7) EPSP vs IPSP: conductance logic

A postsynaptic neuron has E_Cl ≈ −70 mV and resting potential −65 mV. Activation of
GABA_A receptors will most likely:

A. Depolarize the neuron toward threshold (excitatory)
B. Hyperpolarize strongly because Cl⁻ always exits the cell
C. Clamp the membrane near E_Cl and reduce excitability via shunting inhibition
D. Produce a slow IPSP through G-protein activation

Answer: C

Rationale:
GABA_A receptors are ligand-gated Cl⁻ channels. Whether the membrane
hyperpolarizes depends on driving force: at −65 mV (more positive than E_Cl −70 mV),
opening Cl⁻ channels tends to move Vm toward −70 mV, causing a small
hyperpolarization. But the crucial effect is increased conductance, lowering
membrane resistance so that concurrent excitatory currents produce smaller voltage
changes (shunting inhibition). Option D describes GABA_B (metabotropic) causing
slow IPSPs via K⁺ channels.

Key words: GABA_A, chloride reversal potential, shunting inhibition, conductance,
driving force

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