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Resting Membrane Potential
Resting neurons have an internal voltage of approximately −70 mV relative to outside. This is maintained by: Na⁺/K⁺-ATPase (3Na⁺ out, 2K⁺ in per ATP — generates net negative charge inside); K⁺ leak channels (K⁺ diffuses out down its concentration gradient, leaving negative charge behind); and low resting Na⁺ permeability (Na⁺ is high outside but cannot freely enter). K⁺ Nernst potential: E_K = −90 mV; Na⁺ Nernst potential: E_Na = +62 mV; resting potential (~−70 mV) reflects weighted average.
Action Potential
Triggered when membrane reaches threshold (~−55 mV). Phases: (1) Depolarization — voltage-gated Na⁺ channels open; Na⁺ rushes in → membrane rises to ~+40 mV. (2) Repolarization — Na⁺ channels inactivate; voltage-gated K⁺ channels open; K⁺ flows out → voltage falls. (3) After-hyperpolarization — K⁺ channels slow to close; membrane briefly more negative than rest. Refractory period: absolute (cannot fire); relative (only strong stimulus can fire). Propagates down axon via local circuit depolarization; saltatory conduction in myelinated axons (jumps between nodes of Ranvier) is faster.
Synaptic Transmission
Chemical synapse: action potential reaches presynaptic terminal → Ca²⁺ channels open → Ca²⁺ influx → neurotransmitter vesicles fuse with membrane (exocytosis) → neurotransmitter diffuses across synaptic cleft → binds postsynaptic receptors → EPSP (depolarization) or IPSP (hyperpolarization). Neurotransmitters: glutamate (main excitatory), GABA (main inhibitory), acetylcholine, dopamine, serotonin, norepinephrine.
Glossary
Frequently Asked Questions
The resting membrane potential of a typical neuron is approximately −70 mV (inside negative relative to outside). It is maintained by: (1) Na⁺/K⁺-ATPase actively pumping 3 Na⁺ out and 2 K⁺ in per ATP — creating high [K⁺] inside and high [Na⁺] outside; (2) K⁺ leak channels allowing K⁺ to diffuse out down its concentration gradient, leaving negative charge behind; (3) very low resting Na⁺ permeability. The resting potential reflects the balance between K⁺ diffusion (tending toward −90 mV Nernst) and Na⁺ diffusion (tending toward +62 mV Nernst), weighted by their relative permeabilities.
An action potential is a brief, rapid, all-or-none change in membrane potential triggered when depolarization reaches threshold (~−55 mV). Sequence: depolarization (voltage-gated Na⁺ channels open → Na⁺ rushes in → membrane reaches ~+40 mV); repolarization (Na⁺ channels inactivate → voltage-gated K⁺ channels open → K⁺ flows out → voltage falls); after-hyperpolarization (K⁺ channels close slowly → brief overshoot below −70 mV). Propagation: local depolarization activates adjacent Na⁺ channels. In myelinated axons, saltatory conduction jumps between nodes of Ranvier, dramatically increasing speed (up to 120 m/s vs. ~1 m/s unmyelinated).
At a chemical synapse: (1) Action potential arrives at presynaptic terminal. (2) Voltage-gated Ca²⁺ channels open; Ca²⁺ flows in. (3) Ca²⁺ triggers SNARE protein-mediated fusion of synaptic vesicles with the presynaptic membrane → neurotransmitter release into the synaptic cleft (exocytosis). (4) Neurotransmitter diffuses across the ~20 nm cleft. (5) Binds postsynaptic ionotropic receptors (directly opens ion channels → fast) or metabotropic receptors (activate G proteins → slow signaling). (6) Neurotransmitter is removed by reuptake (DAT, SERT), enzymatic degradation (acetylcholinesterase), or diffusion.
Major neurotransmitters: Glutamate — the primary excitatory neurotransmitter in the CNS; activates AMPA, NMDA, and kainate receptors; essential for learning and memory. GABA (γ-aminobutyric acid) — the primary inhibitory neurotransmitter; opens Cl⁻ channels (GABA_A) or K⁺ channels (GABA_B); benzodiazepines and alcohol enhance GABA activity. Dopamine — reward, motor control, motivation; depletion causes Parkinson's disease; excess activity implicated in schizophrenia. Serotonin — mood, sleep, appetite; SSRIs block its reuptake to treat depression. Acetylcholine — neuromuscular junction, autonomic nervous system, memory (Alzheimer's involves cholinergic neuron loss).