What are the key structural components of a typical neuron and what function does each serve?
A: Soma (metabolic centre, contains nucleus), dendrites (receive synaptic input), axon (conducts action potentials away from soma), axon terminals/synaptic boutons (release neurotransmitters onto target cells); the axon hillock is where the action potential is initiated
B: Soma (initiates action potentials electrically), axon (metabolic centre, contains nucleus), dendrites (output fibres), myelin sheath (functions as a sensory receptor)
C: Nucleus (electrical signalling), axon hillock (protein synthesis), dendrites (inhibitory input only), soma (excitatory input only)
D: Soma (primary output site), axon (sensory input), dendrites (motor output), myelin (inhibitory regulation)
Correct: Soma (metabolic centre, contains nucleus), dendrites (receive synaptic input), axon (conducts action potentials away from soma), axon terminals/synaptic boutons (release neurotransmitters onto target cells); the axon hillock is where the action potential is initiated
A typical neuron has four morphologically distinct regions with specialised functions. The soma (cell body) contains the nucleus and most of the cell's biosynthetic machinery; it synthesises proteins, maintains metabolic viability, and integrates some synaptic inputs. Dendrites are branching processes that receive synaptic inputs from thousands of other neurons; their total surface area (often greatly expanded by dendritic spines) determines the cell's integrative capacity. The axon is a single, elongated process that conducts action potentials away from the soma — it may extend from millimetres to over a metre, and is often myelinated for faster conduction. Axon terminals (synaptic boutons) are the presynaptic elements at which the cell signals to target neurons or effector cells by releasing neurotransmitters. The axon hillock is the critical integration zone where the soma meets the axon — it has the lowest threshold for action potential initiation because of its high density of voltage-gated Na+ channels.
Neurons are classified into three major functional types. What are they and what proportion of CNS neurons does each represent?
A: Motor neurons, interneurons, and glial cells — roughly equal proportions
B: Sensory (afferent) neurons — detect stimuli and carry signals toward the CNS; motor (efferent) neurons — carry commands from CNS to effectors; interneurons — connect sensory and motor neurons and mediate all complex processing; interneurons constitute ~99% of all CNS neurons
C: Myelinated neurons, unmyelinated neurons, and glial neurons — distributed ~50/40/10%
D: Excitatory neurons, inhibitory neurons, and modulatory neurons — each constituting roughly one-third of CNS neurons
Correct: Sensory (afferent) neurons — detect stimuli and carry signals toward the CNS; motor (efferent) neurons — carry commands from CNS to effectors; interneurons — connect sensory and motor neurons and mediate all complex processing; interneurons constitute ~99% of all CNS neurons
Neurons are functionally classified as: (1) Sensory (afferent) neurons detect stimuli in the internal or external environment (touch, temperature, pain, light, sound, chemical signals) and transmit this information toward the CNS. Their cell bodies are typically located in dorsal root ganglia (spinal sensory) or cranial nerve ganglia. (2) Motor (efferent) neurons carry commands from the CNS to effector organs — skeletal muscle (somatic) or smooth muscle, cardiac muscle, and glands (autonomic). (3) Interneurons are by far the most numerous type — they constitute approximately 99% of all neurons in the CNS. They connect sensory and motor pathways, integrate information across circuits, and mediate all complex cognitive processing. The enormous number of interneurons and their dense interconnections are what give the CNS its extraordinary computational power. The remaining 1% (sensory + motor neurons) simply links the brain to the body's periphery.
Glial cells are often more numerous than neurons in the CNS. What are the major types and their functions?
A: Astrocytes (synthesise myelin in CNS), Schwann cells (myelin in PNS), microglia (release neurotransmitters), oligodendrocytes (regulate blood flow)
B: Astrocytes (maintain BBB, regulate synaptic environment, metabolic support), oligodendrocytes (myelinate CNS axons), Schwann cells (myelinate PNS axons), microglia (resident immune cells of the CNS), ependymal cells (line ventricles, produce and circulate CSF)
C: Glial cells are a uniform support network with no specialised subtypes or distinct functions
D: Oligodendrocytes myelinate PNS axons; Schwann cells myelinate CNS axons; astrocytes fire action potentials
Correct: Astrocytes (maintain BBB, regulate synaptic environment, metabolic support), oligodendrocytes (myelinate CNS axons), Schwann cells (myelinate PNS axons), microglia (resident immune cells of the CNS), ependymal cells (line ventricles, produce and circulate CSF)
Glial cells (glia = "glue") are essential, non-neuronal cells of the nervous system. Astrocytes are the most abundant CNS glial type; they maintain the blood-brain barrier by signalling cerebral endothelial cells, buffer extracellular K+ and take up glutamate and GABA after synaptic release (keeping concentrations low), provide lactate as fuel for neurons, and modulate synaptic transmission — forming "tripartite synapses" (presynaptic terminal, postsynaptic membrane, astrocyte process). Oligodendrocytes myelinate multiple CNS axons (one cell can wrap segments of up to 50 axons); their loss causes demyelinating diseases such as multiple sclerosis. Schwann cells myelinate individual PNS axons and also support peripheral nerve regeneration after injury. Microglia are the CNS's resident immune cells — derived from macrophage lineage, they survey the brain, phagocytose debris and dead cells, and initiate neuroinflammatory responses. Ependymal cells line the ventricular system and the central canal of the spinal cord; specialised ependymal cells (choroid plexus) produce CSF.
The resting membrane potential of most neurons is approximately −70 mV. What primarily determines this value?
A: The equilibrium potential for Na+ — the resting membrane is primarily permeable to Na+, which flows in to create the negative interior
B: The selective permeability of the membrane to K+ via leak channels (K+ diffuses out down its concentration gradient, leaving behind negative charge) combined with the Na+/K+ ATPase, which actively maintains the K+ (high inside) and Na+ (high outside) concentration gradients that make this possible
C: The negative charge of proteins in the extracellular fluid, which electrostatically repels K+ into the cell
D: The equilibrium potential for Cl− — the resting membrane is predominantly permeable to Cl−, which is pumped in, creating a negative interior
Correct: The selective permeability of the membrane to K+ via leak channels (K+ diffuses out down its concentration gradient, leaving behind negative charge) combined with the Na+/K+ ATPase, which actively maintains the K+ (high inside) and Na+ (high outside) concentration gradients that make this possible
The resting membrane potential arises from two interacting mechanisms. First, concentration gradients maintained by the Na+/K+ ATPase (sodium-potassium pump): this active transporter moves 3 Na+ out and 2 K+ in per ATP hydrolysed, creating high [K+] inside (~140 mM) and high [Na+] outside (~145 mM). Second, selective resting membrane permeability: at rest, the membrane is most permeable to K+ through inwardly rectifying K+ leak channels. K+ diffuses out down its concentration gradient, but each departing K+ leaves behind a net negative charge inside, building an electrical gradient (inside negative) that opposes further K+ efflux. The membrane potential at which these two forces balance is the K+ equilibrium potential (EK ≈ −90 mV, calculated by the Nernst equation). The actual resting potential is approximately −70 mV because the membrane also has a small but non-zero Na+ permeability (Na+ leaks in, partially depolarising the membrane). The Na+/K+ ATPase continuously works to maintain the ion gradients that underlie this potential.
What triggers an action potential and what sequence of ionic events underlies it? Include the refractory periods.
A: When membrane potential reaches threshold (~−55 mV): voltage-gated Na+ channels open → rapid Na+ influx → depolarisation to ~+40 mV (rising phase); Na+ channel inactivation gates close AND voltage-gated K+ channels open → K+ efflux → repolarisation; K+ channels close slowly → brief afterhyperpolarisation. Absolute refractory period (Na+ channels inactivated): no AP possible. Relative refractory period (afterhyperpolarisation): requires suprathreshold stimulus
B: When membrane potential reaches threshold: Ca2+ channels open → Ca2+ influx drives depolarisation; Ca2+ channels inactivate → Na+ efflux repolarises membrane; no refractory period exists because ion channels reset immediately
C: Action potentials are graded (proportional to stimulus strength) and arise from K+ influx during depolarisation and Na+ efflux during repolarisation
D: Cl− influx triggers depolarisation; K+ influx then repolarises the membrane; a hyperexcitable refractory period follows in which any stimulus generates an action potential
Correct: When membrane potential reaches threshold (~−55 mV): voltage-gated Na+ channels open → rapid Na+ influx → depolarisation to ~+40 mV (rising phase); Na+ channel inactivation gates close AND voltage-gated K+ channels open → K+ efflux → repolarisation; K+ channels close slowly → brief afterhyperpolarisation. Absolute refractory period (Na+ channels inactivated): no AP possible. Relative refractory period (afterhyperpolarisation): requires suprathreshold stimulus
The action potential is an all-or-none electrical event — its amplitude is fixed regardless of stimulus strength above threshold. Sequence: (1) When summated EPSPs depolarise the axon hillock to threshold (~−55 mV), a positive feedback cascade begins. (2) Voltage-gated Na+ channels open (activation gate opens, inactivation gate still open): Na+ rushes in down both concentration and electrical gradients, rapidly depolarising the membrane to approximately +40 mV — the rising phase (depolarisation). (3) Within ~0.5 ms, Na+ channel inactivation gates close — the Na+ channels are now inactivated and cannot reopen regardless of membrane potential — producing the absolute refractory period. Simultaneously, voltage-gated K+ channels (which are slower to open) open: K+ flows out, rapidly repolarising the membrane. (4) K+ channels close slowly, causing brief overshoot below resting potential — the afterhyperpolarisation — which constitutes the relative refractory period (a suprathreshold stimulus is required during this phase). (5) The Na+/K+ ATPase restores ion gradients over subsequent milliseconds. The whole event lasts ~1–2 ms in most neurons.
Why does myelination dramatically increase conduction velocity, and what is "saltatory conduction"?
A: Myelin adds extra Na+ channels to the axon surface, enabling faster Na+ influx and therefore faster action potentials at every point
B: Myelin reduces membrane capacitance and increases axial resistance, so the action potential "jumps" between unmyelinated gaps called nodes of Ranvier (saltatory conduction) rather than being continuously regenerated along the entire membrane — dramatically increasing speed (up to 120 m/s) compared to unmyelinated fibres (0.5–2 m/s)
C: Saltatory conduction occurs because myelinated axons have more Na+/K+ ATPase pumps that restore ion gradients faster, allowing higher firing rates
D: Myelin makes the axon membrane permeable to K+ along its entire length, speeding repolarisation and reducing the duration of each action potential
Correct: Myelin reduces membrane capacitance and increases axial resistance, so the action potential "jumps" between unmyelinated gaps called nodes of Ranvier (saltatory conduction) rather than being continuously regenerated along the entire membrane — dramatically increasing speed (up to 120 m/s) compared to unmyelinated fibres (0.5–2 m/s)
Myelin is a lipid-rich insulating sheath wrapped in concentric layers around axons by oligodendrocytes (CNS) or Schwann cells (PNS). Its key biophysical effects: it dramatically reduces membrane capacitance (the membrane stores less charge per unit area) and increases electrical resistance of the internode (less current leaks out laterally). The combined effect is that depolarisation current generated at one node of Ranvier (a short unmyelinated gap of ~1 µm every ~1 mm, where Na+ channels are densely concentrated) flows rapidly and efficiently along the axon interior to the next node, where it regenerates the action potential. The action potential thus "jumps" from node to node — saltatory conduction (from Latin saltare: to jump) — rather than propagating through continuous membrane. This confers two advantages: speed (myelinated Aα fibres: 70–120 m/s; unmyelinated C fibres: 0.5–2 m/s) and metabolic efficiency (Na+/K+ ATPase operates only at nodes, not along the whole axon). Demyelinating diseases (multiple sclerosis, Guillain-Barré syndrome) disrupt this, causing slowed or blocked conduction and diverse neurological symptoms.
Describe the complete sequence of events in chemical synaptic transmission from action potential arrival to postsynaptic response.
A: AP arrives at presynaptic terminal → voltage-gated Ca2+ channels open → Ca2+ influx → synaptic vesicles dock and fuse with presynaptic membrane (exocytosis, triggered by Ca2+ binding to synaptotagmin) → neurotransmitter released into synaptic cleft → NT diffuses across cleft → NT binds to postsynaptic receptors → ionotropic receptors open ion channels directly (fast EPSP/IPSP); metabotropic receptors activate G-protein cascades (slow, modulatory)
B: AP arrives → Na+ influx at terminal triggers vesicle fusion → NT released → NT binds presynaptic autoreceptors → electrical induction in postsynaptic membrane generates potential
C: AP causes postsynaptic membrane to depolarise directly via gap junctions → NT then released as a secondary amplification signal
D: AP arrives at postsynaptic terminal → postsynaptic receptors activate → Ca2+ flows retrogradely into presynaptic terminal → vesicles form, fill with NT, and fuse with presynaptic membrane
Correct: AP arrives at presynaptic terminal → voltage-gated Ca2+ channels open → Ca2+ influx → synaptic vesicles dock and fuse with presynaptic membrane (exocytosis, triggered by Ca2+ binding to synaptotagmin) → neurotransmitter released into synaptic cleft → NT diffuses across cleft → NT binds to postsynaptic receptors → ionotropic receptors open ion channels directly (fast EPSP/IPSP); metabotropic receptors activate G-protein cascades (slow, modulatory)
Chemical synaptic transmission proceeds in a precisely coordinated sequence. (1) An action potential invades the presynaptic terminal bouton. (2) Membrane depolarisation opens voltage-gated Ca2+ channels (primarily P/Q-type at fast synapses). (3) Ca2+ flows in down its steep electrochemical gradient — Ca2+ is the essential trigger for vesicle fusion; blocking Ca2+ entry abolishes neurotransmitter release. (4) Ca2+ binds to synaptotagmin on docked synaptic vesicles, which triggers rapid SNARE protein complex assembly (VAMP/synaptobrevin on vesicle; SNAP-25 and syntaxin on plasma membrane), pulling vesicle and plasma membranes together — exocytosis releases NT into the cleft (~0.5 ms). (5) NT diffuses across the ~20 nm synaptic cleft (virtually instantaneous at this scale). (6) NT binds to postsynaptic receptors. Ionotropic (ligand-gated ion channel) receptors respond within milliseconds: Na+/Ca2+ influx (excitatory) or Cl−/K+ flux (inhibitory). Metabotropic (G-protein-coupled) receptors act over hundreds of milliseconds to seconds via second messenger cascades, modulating channel conductance, gene expression, or intracellular signalling.
What is the difference between an EPSP and an IPSP, and how do neurons integrate thousands of simultaneous inputs to decide whether to fire?
A: EPSPs are produced by Ca2+ influx and are always inhibitory; IPSPs are produced by Na+ influx and are always excitatory; each is processed independently at the axon hillock
B: An EPSP (excitatory postsynaptic potential) is a graded depolarisation that moves the membrane toward threshold; an IPSP (inhibitory postsynaptic potential) is a graded hyperpolarisation or conductance increase that moves it away from threshold. Neurons integrate these via spatial summation (simultaneous inputs from multiple synapses) and temporal summation (rapid successive inputs from one synapse) at the axon hillock — an AP fires if net depolarisation exceeds threshold
C: EPSPs are produced at glutamatergic synapses and are inhibitory; IPSPs are produced at GABAergic synapses and are excitatory
D: The terms are synonymous — both refer to the same depolarisation event; the excitatory/inhibitory distinction is determined solely by which presynaptic neuron fires
Correct: An EPSP (excitatory postsynaptic potential) is a graded depolarisation that moves the membrane toward threshold; an IPSP (inhibitory postsynaptic potential) is a graded hyperpolarisation or conductance increase that moves it away from threshold. Neurons integrate these via spatial summation (simultaneous inputs from multiple synapses) and temporal summation (rapid successive inputs from one synapse) at the axon hillock — an AP fires if net depolarisation exceeds threshold
EPSPs are graded (not all-or-none), short-lasting depolarisations that bring the membrane potential closer to threshold. Typically produced by glutamate acting on AMPA receptors (causing Na+ — and some Ca2+ — influx) or by acetylcholine on nicotinic receptors. IPSPs are graded hyperpolarisations or shunts that move the membrane away from threshold or stabilise it. Typically produced by GABA on GABA-A receptors (opening Cl− channels — Cl− flows in since EClˉ ≈ −75 mV, hyperpolarising the cell) or by glycine (same mechanism). Neurons are continuously integrating thousands of simultaneous inputs. Temporal summation: EPSPs from the same synapse in rapid succession overlap and summate (each EPSP decays slowly, so successive ones add). Spatial summation: simultaneous EPSPs from many different synapses on different dendritic branches spread to the axon hillock and add there. The axon hillock is the decision point — it integrates all incoming graded potentials: if the algebraic sum (ΣEPSPs − ΣIPSPs) reaches threshold, a full action potential fires. Otherwise, the membrane potential simply fluctuates below threshold.
What are the major neurotransmitter systems in the CNS and periphery, and what are their primary functions?
A: Glutamate (primary excitatory NT in CNS; AMPA, NMDA receptors), GABA (primary inhibitory NT in CNS; GABA-A, GABA-B receptors), dopamine (reward, motor control, executive function), serotonin (mood, sleep, appetite), acetylcholine (neuromuscular junction, autonomic ganglia, memory/attention), noradrenaline (arousal, stress, attention)
B: GABA (primary excitatory NT), glutamate (primary inhibitory NT), serotonin (motor control), dopamine (sleep regulation only), acetylcholine (reward circuits)
C: Glutamate and GABA are the same molecule at different concentrations; dopamine and serotonin differ only in molecular weight and are functionally identical
D: Serotonin is the primary excitatory NT; GABA mediates reward; noradrenaline is the primary inhibitory NT; dopamine regulates pain sensation only
Correct: Glutamate (primary excitatory NT in CNS; AMPA, NMDA receptors), GABA (primary inhibitory NT in CNS; GABA-A, GABA-B receptors), dopamine (reward, motor control, executive function), serotonin (mood, sleep, appetite), acetylcholine (neuromuscular junction, autonomic ganglia, memory/attention), noradrenaline (arousal, stress, attention)
The major neurotransmitters: Glutamate is the principal excitatory NT in the CNS, active at the large majority of fast excitatory synapses. It acts on AMPA receptors (fast Na+ influx), NMDA receptors (Ca2+ influx; critical for synaptic plasticity and LTP), and kainate receptors. GABA (gamma-aminobutyric acid) is the principal inhibitory NT in the CNS; GABA-A (ionotropic, opens Cl− channels — target of benzodiazepines and barbiturates) and GABA-B (metabotropic). Dopamine: four major projections — mesolimbic/mesocortical (reward, motivation, psychosis), nigrostriatal (motor control; depleted in Parkinson's disease), tuberoinfundibular (prolactin regulation). Serotonin (5-HT): raphe nuclei projections throughout brain; mood, sleep-wake cycles, appetite, social behaviour; SSRIs target SERT. Acetylcholine (ACh): neuromuscular junction (nicotinic nAChR), all autonomic ganglia (nicotinic), parasympathetic postganglionic (muscarinic), basal forebrain cholinergic system (memory, attention; depleted in Alzheimer's disease). Noradrenaline: locus coeruleus projections; arousal, attention, fight-or-flight, mood.
How is neurotransmitter action terminated at the synapse, and how do major drug classes exploit these mechanisms?
A: Reuptake transporters remove NT molecules from the cleft back into the presynaptic terminal; enzymatic degradation in the cleft (e.g., acetylcholinesterase for ACh) or intracellularly after reuptake (MAO, COMT for monoamines); and diffusion away from the cleft. SSRIs block SERT; cocaine blocks DAT; acetylcholinesterase inhibitors (e.g., donepezil) block ACh degradation
B: NT molecules are destroyed by postsynaptic receptors after binding; the cleft is then passively refilled by the presynaptic terminal
C: The action potential in the presynaptic terminal simply reverses, pulling NT molecules electrostatically back into the vesicles
D: NT action is exclusively terminated by the presynaptic membrane reabsorbing complete vesicles via endocytosis; no degradation occurs in the cleft
Correct: Reuptake transporters remove NT molecules from the cleft back into the presynaptic terminal; enzymatic degradation in the cleft (e.g., acetylcholinesterase for ACh) or intracellularly after reuptake (MAO, COMT for monoamines); and diffusion away from the cleft. SSRIs block SERT; cocaine blocks DAT; acetylcholinesterase inhibitors (e.g., donepezil) block ACh degradation
Three mechanisms terminate neurotransmitter signalling: (1) Reuptake: specific transporter proteins in the presynaptic membrane (and sometimes glial membranes) actively transport NT molecules from the cleft back into the presynaptic terminal, where they can be repackaged into vesicles. This is the primary mechanism for monoamines (SERT for serotonin, DAT for dopamine, NET for noradrenaline), GABA (GAT transporters), and glutamate (EAATs, predominantly on astrocytes). (2) Enzymatic degradation: acetylcholinesterase (AChE) rapidly cleaves ACh into choline + acetate directly in the cleft — choline is then taken up by the presynaptic terminal and re-acetylated. Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) degrade monoamines intracellularly. (3) Diffusion: NT molecules diffuse away from the cleft, reducing their concentration. Drug implications: SSRIs (fluoxetine, sertraline) block SERT, increasing synaptic serotonin; SNRIs block SERT and NET; cocaine and amphetamines block DAT (and others); acetylcholinesterase inhibitors (donepezil, rivastigmine) prolong ACh action — used in Alzheimer's disease; organophosphate nerve agents also inhibit AChE.
Neural Communication: Neurons & Synaptic Transmission
What are the key structural components of a typical neuron and what function does each serve?
About this quiz
All psychological processes — from perception to memory to emotion — depend on electrical and chemical signalling between neurons. This quiz covers the fundamental mechanisms: neuron structure and types, the roles of glial cells, how the resting membrane potential is maintained, the action potential mechanism, myelination and saltatory conduction, the sequence of synaptic transmission, excitation and inhibition (EPSPs and IPSPs), the major neurotransmitter systems, and how neurotransmitter action is terminated.
Key sources include Kandel et al. (2013) Principles of Neural Science and Bear, Connors & Paradiso (2016) Neuroscience: Exploring the Brain.