Through iterative hypothesis testing, replication, and peer review that refine theories over time.

By relying on authority and tradition rather than empirical data.

By collecting anecdotes and forming beliefs without experiments.

Through single, definitive experiments that never require replication.

It integrates biology, psychology, chemistry, physics, computer science, and related social sciences to study the nervous system.

It excludes biology and focuses only on sociology.

It is purely philosophical and avoids empirical methods.

It studies only one brain region using a single discipline.

Thomas Willis

Santiago Ramón y Cajal

Camillo Golgi

Paul Broca

Phrenology links skull bumps to traits without scientific basis, whereas localization of function maps specific brain regions to specific functions using empirical evidence.

Both are modern, evidence-based neuroscientific theories.

Localization of function claims all brain areas perform the same task, unlike phrenology.

Phrenology is a valid clinical tool, whereas localization is pseudoscience.

The independent variable is manipulated; the dependent variable is measured outcome.

The dependent variable is manipulated; the independent variable is the outcome.

The control group receives the intervention; the experimental group does not.

Variables are unnecessary if random assignment is used.

Randomized controlled experiments with manipulation of an independent variable and appropriate controls.

Cross-sectional correlational surveys without manipulation.

Naturalistic observation without control groups.

Case studies of a single individual.

Golgi staining impregnates a small subset of neurons, revealing full morphology including dendrites and axons.

Nissl staining labels entire neurons, including axons and dendrites in detail.

Hematoxylin–eosin is specific for neurons only and shows complete processes.

Simple iodine stain reveals synaptic vesicles and action potentials.

A neuron is a specialized cell that transmits information; its four structural regions are dendrites, soma, axon, and axon terminals.

A neuron is any cell in the body; the four regions are nucleus, ribosomes, mitochondria, and cytosol.

A neuron is a glial cell; the four regions are astrocyte, microglia, oligodendrocyte, and ependyma.

A neuron is a hormone-secreting gland; the four regions are cortex, medulla, lobes, and sulci.

Dendrites receive input; soma integrates signals; axon conducts impulses; axon terminals release neurotransmitter onto target cells.

Dendrites generate action potentials; soma releases neurotransmitter; axon stores ions; terminals synthesize DNA.

Dendrites myelinate axons; soma forms myelin; axon digests debris; terminals create cerebrospinal fluid.

Dendrites secrete hormones; soma absorbs nutrients; axon digests proteins; terminals produce antibodies.

A synapse is a junction where a presynaptic terminal communicates with a postsynaptic membrane across a synaptic cleft.

A synapse is a gap in myelin between nodes of Ranvier only.

A synapse is any physical contact between two neurons’ somas.

A synapse is the space inside the nucleus where genes interact.

The central nervous system (brain and spinal cord) connects with the peripheral nervous system via afferent and efferent nerves.

Only the peripheral nervous system exists; the central system is part of the endocrine system.

The central nervous system is isolated and has no connection to peripheral nerves.

The autonomic nervous system operates independently of both CNS and PNS.

Oligodendrocytes myelinate CNS axons; astrocytes regulate environment and support synapses; microglia provide immune defense; ependymal cells produce and circulate cerebrospinal fluid.

Astrocytes generate action potentials; microglia form myelin; oligodendrocytes secrete hormones; ependymal cells digest neurotransmitters.

Ependymal cells myelinate PNS; astrocytes are neurons; microglia are endocrine cells; oligodendrocytes are muscle cells.

All glia have identical functions and are interchangeable.

Dendrites, soma, axon, and axon terminals are the principal parts to identify and label.

Myelin, skull, skin, and hair are the principal parts to label.

Cortex lobes only are neuron parts.

Nuclei of glial cells are the only parts of neurons.

CNS and PNS communicate through sensory (afferent) and motor (efferent) pathways.

Only CNS exists; PNS functions independently.

Somatic and autonomic systems are unconnected to CNS.

CNS signals travel only by hormones, not nerves.

Astrocytes regulate extracellular ions and neurotransmitters; oligodendrocytes provide myelin; microglia remove debris; ependymal cells line ventricles.

Neurons are unsupported by any glial cells.

Only microglia support neurons by generating action potentials.

Skin cells myelinate axons in the brain.

Dendrites, soma, axon, axon terminals

Nucleus, ribosomes, mitochondria, lysosome

Astrocyte, microglia, oligodendrocyte, ependyma

Frontal, parietal, occipital, temporal

Axon

Dendrites

Soma

Axon terminals

True

False

They increase postsynaptic contact area to receive synaptic inputs.

They produce myelin along axons.

They propagate action potentials without the axon hillock.

They secrete cerebrospinal fluid into ventricles.

Depolarization occurs when voltage-gated Na+ channels open and Na+ (positive) ions rush into the neuron.

Depolarization occurs when Cl− enters and makes the membrane more negative.

Depolarization is caused by K+ leaving the neuron first.

Depolarization does not involve any ion movement.

The Na+/K+ ATPase uses energy from ATP to move 3 Na+ out and 2 K+ in, maintaining gradients that power ion flow during action potentials.

The Na+/K+ pump requires no energy and moves ions down their gradients.

The Ca2+ pump moves Na+ into the cell and K+ out using no ATP.

Ion pumps operate only during resting potential and shut off during action potentials.

The rapid rising phase corresponds to depolarization due to opening of voltage-gated Na+ channels.

The rapid rising phase is hyperpolarization due to K+ efflux.

The rapid rising phase is the absolute refractory period only.

The rapid rising phase occurs when all channels are closed.

Na+ influx commonly produces EPSPs.

Ca2+ influx can contribute to EPSPs.

Cl− influx commonly produces IPSPs.

K+ efflux can contribute to IPSPs.

A ligand-gated ion channel opens rapidly, allowing specific ions to flow and producing a fast postsynaptic potential.

A G-protein dissociates to alter gene transcription over hours.

The receptor internalizes and permanently blocks ion flow.

Nothing happens until action potentials cease.

They open an ion channel directly and cause immediate depolarization

They activate a G protein that triggers second‑messenger cascades to modulate ion channels and gene expression

They internalize the ligand and prevent any signaling

They release neurotransmitter into the synaptic cleft

Demonstrated chemical neurotransmission with the vagusstoff frog heart experiment

Invented magnetic resonance imaging for brain imaging

Mapped the motor homunculus by stimulating the cortex during surgery

Discovered the ionic basis of the action potential in squid axon

Ionotropic receptors are G‑protein coupled and slower; metabotropic receptors are ligand‑gated ion channels and faster

Ionotropic receptors are ligand‑gated ion channels that act rapidly; metabotropic receptors are G‑protein coupled and produce slower modulatory effects

Both are voltage‑gated channels that open during action potentials

Only metabotropic receptors bind neurotransmitters; ionotropic receptors do not

Agonists bind and activate receptors; antagonists bind but block receptor activation

Agonists block receptors; antagonists activate receptors

Agonists and antagonists both increase receptor signaling

Antagonists remove receptors from the membrane while agonists insert more receptors

Dopamine synthesized from L‑DOPA via DOPA decarboxylase

Acetylcholine synthesized from choline and acetyl‑CoA via choline acetyltransferase

Serotonin synthesized from tyrosine via tyrosine hydroxylase

GABA synthesized from glutamate via glutamic acid decarboxylase

Blocking the serotonin transporter (SERT) with an SSRI increases serotonin levels in the synaptic cleft

Blocking voltage‑gated Na+ channels increases neurotransmitter release

Inhibiting vesicular transporters increases postsynaptic receptor activation

Enhancing monoamine oxidase activity raises synaptic monoamine concentrations

Benzodiazepines enhance GABA_A receptor function by increasing chloride channel opening frequency, reducing anxiety

Antipsychotics primarily enhance dopamine D2 receptor signaling

SSRIs decrease serotonin levels in the synaptic cleft

Lithium blocks all glutamate receptors

Fertilization → neurulation → cleavage → gastrulation

Fertilization → cleavage → blastula → gastrulation → neurulation

Cleavage → fertilization → gastrulation → neurulation

Fertilization → gastrulation → cleavage → neurulation

Gastrulation forms the ectoderm, mesoderm, and endoderm germ layers

Neurulation forms the heart, lungs, and kidneys directly

Cleavage forms the neural tube from the notochord

Blastula stage creates only ectoderm and mesoderm

Neural plate formation is induced by the notochord signaling to overlying ectoderm to fold into a neural tube

Gastrulation is driven by apoptosis of all ectodermal cells

Cleavage is driven by synaptogenesis between blastomeres

Neurulation occurs only after birth

Neurogenesis, cell migration, differentiation, synaptogenesis, programmed cell death, synapse rearrangement

Neurogenesis, glycolysis, differentiation, angiogenesis, apoptosis, mitosis

Cell migration, mitosis, transcription, translation, maturation, vision

Fertilization, cleavage, blastula, gastrulation, neurulation, birth

In humans, neural tube closure begins near the cervical region and proceeds both rostrally and caudally

Neural tube closure starts only at the frontal pole and moves caudally

The neural plate arises from mesoderm rather than ectoderm

Neural tube closure is completed before gastrulation

Differentiation typically follows cell migration in the developmental sequence

Synaptogenesis precedes neurogenesis

Apoptosis occurs before any synapses are formed

Cell migration is the final stage

C. elegans synaptic wiring is largely genetically specified with minimal pruning; mammals show extensive activity‑dependent synaptogenesis and pruning; zebrafish are intermediate

All three species rely exclusively on adult experience for forming synapses

Mammals have fixed synaptic wiring with no pruning; C. elegans shows large activity‑dependent remodeling

Zebrafish lack synaptogenesis

Genotype is an organism’s genetic makeup; phenotype is the observable traits influenced by both genotype and environment

Phenotype describes DNA sequence; genotype describes observed behavior only

Genotype changes with environment while phenotype never does

Phenotype is independent of genotype

Caused by deficiency of phenylalanine hydroxylase leading to toxic accumulation of phenylalanine

Caused by excess dopamine synthesis in the basal ganglia

An infectious prion disease

Treated by high‑phenylalanine diet

DNA methylation of the glucocorticoid receptor promoter generally reduces receptor gene expression

DNA methylation universally increases glucocorticoid receptor expression

Histone acetylation decreases receptor transcription

Methylation causes immediate opening of the receptor’s ion channel

Alzheimer’s disease is a neurodegenerative dementia characterized by beta‑amyloid plaques and neurofibrillary tangles with progressive memory decline

Dementia refers only to vascular lesions and never includes Alzheimer’s disease

Alzheimer’s disease is an acute reversible confusion state

Alzheimer’s disease is defined by increased dopamine in the striatum

Advanced age

APOE ε4 genotype

Family history

High vitamin C intake

Acetylcholinesterase inhibitors (e.g., donepezil) provide symptomatic benefit in mild to moderate Alzheimer’s disease

High‑dose dopamine agonists reverse Alzheimer’s pathology

Broad‑spectrum antibiotics are first‑line therapy

Complete cure is achieved with vitamin supplements

Stimulus intensity is often represented by increased firing rate and recruitment of more afferent neurons (population coding)

Only the identity of the neuron matters; firing rate carries no information

All sensory modalities use chemical synapses without action potentials

The brain decodes signals solely by random chance

A receptor whose ion channel opens with membrane stretch; the conversion of physical energy to neural signals is transduction

A receptor activated only by neurotransmitter diffusion; the conversion is translation

A voltage‑gated receptor; the conversion is transformation

A photopigment receptor; the conversion is replication

Phasic receptors adapt rapidly and signal changes; tonic receptors adapt slowly and signal sustained stimuli

Phasic receptors are slow‑adapting; tonic receptors are fast‑adapting

Phasic receptors exist only in the visual system

Tonic receptors never fire action potentials

Penfield mapped somatosensory and motor cortices via direct stimulation; Merzenich demonstrated cortical plasticity and its reorganization with training

Penfield discovered DNA methylation; Merzenich developed MRI

Penfield proved chemical neurotransmission; Merzenich discovered sodium channels

Penfield mapped the hippocampus exclusively; Merzenich studied only spinal reflexes

A‑delta fibers are myelinated and convey fast, sharp pain; C fibers are unmyelinated and convey slow, dull pain

A‑delta fibers are unmyelinated and slow; C fibers are myelinated and fast

Both fibers are motor efferents only

Neither fiber transmits nociception

Mirror therapy can reduce phantom limb pain by providing congruent visual feedback

Cutting all remaining nerves reliably cures phantom limb pain

Phantom limb pain is caused solely by inflammation at the stump

Treatment requires only opioid medication

Pain and temperature ascend primarily through the spinothalamic tract

Fine touch ascends via the spinocerebellar tract only

Motor commands descend through the dorsal column pathway

All sensory signals ascend through the corticospinal tract

Sound is a mechanical pressure wave measured in decibels (dB) for intensity

Sound is electromagnetic radiation measured in lumens

Sound is chemical energy measured in molarity

Sound is thermal energy measured in joules

On a waveform or spectrogram, pitch corresponds to frequency (higher pitch = higher frequency) and loudness corresponds to amplitude (greater loudness = larger amplitude)

Pitch is determined by amplitude; loudness is determined by wavelength

Pitch and loudness cannot be represented visually

Higher loudness always lowers frequency

The stapes of the middle ear transmits vibrations to the oval window of the cochlea to initiate fluid motion

The tympanic membrane is part of the inner ear

The cochlea is in the middle ear and contains the ossicles

The malleus contacts the round window

Inner and outer hair cells with mechanically gated tip‑link channels on stereocilia

Spiral ganglion neurons with voltage‑gated sodium channels that open to sound pressure

Cochlear supporting cells with chemically gated chloride channels

Auditory cortex pyramidal neurons with ligand‑gated potassium channels

Conductive hearing loss

Sensorineural hearing loss

Mixed hearing loss

Central visual field loss

Vestibular hypofunction

By using an electrotactile tongue display to provide head‑motion signals for balance

By implanting a cochlear device to amplify environmental sounds

By prescribing prism glasses to shift the visual field

By delivering deep brain stimulation to the thalamus

Cornea: major refractive surface that initially focuses incoming light

Iris: phototransduction of photons into neural signals

Lens: regulates intraocular pressure by draining aqueous humor

Retina: controls pupil diameter to modulate light entry

Photoreceptors (rods and cones)

Bipolar cells

Ganglion cells

Horizontal cells

Amacrine cells

Light causes photoreceptors to hyperpolarize and reduce glutamate release

Light depolarizes photoreceptors, increasing glutamate release

Light triggers action potentials in rods and cones that increase GABA release

Light closes cGMP‑gated channels leading to increased neurotransmitter release

Suprachiasmatic nucleus (SCN)

Lateral geniculate nucleus (LGN)

Superior colliculus

Primary visual cortex (V1)

Visual acuity testing (e.g., Snellen chart)

Perimetry to assess visual fields

Color vision testing (e.g., Ishihara plates)

Pupillary light reflex assessment

Bone conduction testing for the cochlea

Photoreceptors → bipolar cells → ganglion cells

Horizontal cells → amacrine cells → ganglion cells

Photoreceptors → amacrine cells → optic nerve

Bipolar cells → photoreceptors → ganglion cells

Horizontal and amacrine cells

Photoreceptors and ganglion cells

Bipolar and ganglion cells

Microglia and Müller glia

Rods exhibit greater convergence onto bipolar and ganglion cells, enhancing sensitivity at the cost of acuity

Cones exhibit greater convergence, maximizing sensitivity and reducing spatial resolution

Both rods and cones have minimal convergence, yielding uniformly high acuity

Rods have minimal convergence, optimizing fine detail at the fovea

A small pit with highest visual acuity due to high cone density, minimal convergence, and displaced inner layers

The optic disc where ganglion cell axons exit the eye and no photoreceptors are present

A peripheral region enriched in rods specialized for scotopic vision

A vascularized area with dense capillaries that enhances photon capture

Signals are graded rather than transmitted by action potentials

Ribbon synapses support continuous neurotransmitter release

Glutamate release is highest in darkness and decreases with light

Transmission relies exclusively on electrical synapses with gap junctions

Postsynaptic responses are mediated only by inhibitory receptors

Cones dominate the fovea for high‑acuity, color vision, whereas rods dominate the periphery for sensitivity in low light

Rods dominate the fovea for high‑acuity vision, whereas cones dominate the periphery for color

Horizontal cells convey the eye’s output to the brain via the optic nerve

Ganglion cells are photoreceptors that convert photons directly into action potentials

Optic nerve → optic chiasm → optic tract → LGN → optic radiations → V1

Optic nerve → LGN → optic chiasm → optic tract → V1

Optic tract → optic chiasm → optic nerve → V1 → LGN

Optic nerve → superior colliculus → optic radiations → V1

Yes; axons from the nasal retina cross at the optic chiasm, carrying the temporal visual field contralaterally

Yes; axons from the temporal retina cross at the optic chiasm, carrying the nasal visual field contralaterally

No; all retinal fibers remain ipsilateral throughout the pathway

Only macular fibers cross in the LGN

Cones are densest at the fovea and support photopic, high‑acuity color vision; rods peak parafoveally and mediate scotopic sensitivity

Rods are densest at the fovea and mediate color vision; cones peak in the periphery and support scotopic sensitivity

Rods and cones are uniformly distributed across the retina

Rods and cones function only in bright light

Light‑dependent modulation of cGMP‑gated channels adjusts sensitivity (adaptation)

Horizontal‑cell‑mediated lateral inhibition shapes center‑surround receptive fields

Rod pathways saturate in bright light whereas cone pathways sustain photopic signaling

Receptive fields are determined solely by ganglion cell axon diameter

Adaptation is produced exclusively by the iris changing pupil size

Dorsal stream (parietal, “where/how”) supports spatial processing; lesions cause optic ataxia. Ventral stream (temporal, “what”) supports object recognition; lesions cause visual agnosia

Ventral stream (parietal, “where”) supports spatial processing; lesions cause optic ataxia. Dorsal stream (temporal, “what”) supports object recognition; lesions cause visual agnosia

Dorsal and ventral streams both originate in the LGN and bypass V1

Damage to either stream produces hemianopia without higher‑order deficits