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Physiology 3% exam weight

Blood

Part of the INI CET (AIIMS PG) study roadmap. Physiology topic physio-002 of Physiology.

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Nerve Conduction and Synaptic Transmission covers nerve conduction and synaptic transmission for INI CET (AIIMS PG).

Neuron Structure and Function:

  • Soma (cell body): Contains nucleus, organelles (Nissl bodies — RER for protein synthesis)
  • Dendrites: Receive input signals (receptive field)
  • Axon hillock: Site of action potential initiation (most excitable region — highest density of voltage-gated Na⁺ channels)
  • Axon: Conducts action potentials; myelinated axons conduct much faster (saltatory conduction)
  • Axon terminal: Synaptic vesicles containing neurotransmitter

Resting Membrane Potential (RMP):

  • Typically –70 mV (inside negative relative to outside)
  • Causes:
    1. Na⁺/K⁺-ATPase: Pumps 3Na⁺ out, 2K⁺ in (creates concentration gradients: [Na⁺]i < [Na⁺]o; [K⁺]i > [K⁺]o)
    2. K⁺ leak channels (most important): High permeability to K⁺ → K⁺ flows out (down gradient) → inside becomes negative
    3. Na⁺ leak channels: Small inward leak → partially offsets K⁺ efflux
    4. Ion distribution: Intracellular proteins (organic anions) are non-diffusible, contributing to negative intracellular charge
  • Goldman equation (constant field equation): E_m = 61 log [(P_K[K⁺]_o + P_Na[Na⁺]_o + P_Cl[Cl⁻]_i) / (P_K[K⁺]_i + P_Na[Na⁺]_i + P_Cl[Cl⁻]_o)]

Action Potential (AP):

  • Phases:
    • Resting: –70 mV; Na⁺ channels closed; K⁺ channels open
    • Depolarization (phase 0): Rapid upstroke to +30 mV — voltage-gated Na⁺ channels open (fast, transient)
    • Overshoot: Membrane potential briefly positive (+30 mV)
    • Repolarization (phase 1): Initial rapid fall — voltage-gated Na⁺ channels inactivate; transient K⁺ efflux (I_to)
    • Plateau (phase 2) — cardiac muscle only: Ca²⁺ channels sustain depolarization → long refractory period
    • Repolarization (phase 3): K⁺ efflux through delayed rectifier K⁺ channels → returns to –70 mV
    • Resting (phase 4) — neurons: Full restoration of ion gradients

Conduction Velocity:

  • Myelinated fibers: Saltatory conduction (AP “jumps” between Nodes of Ranvier) — up to 120 m/s
  • Unmyelinated fibers: Continuous conduction — 0.5–2 m/s
  • Factors increasing conduction velocity: Larger diameter, myelination, temperature (↑T° → ↑CV; local anesthetics block Na⁺ channels → block AP)

Synaptic Transmission:

  1. Presynaptic terminal: AP arrives → voltage-gated Ca²⁺ channels open → Ca²⁺ influx → vesicles fuse with presynaptic membrane (SNARE proteins) → neurotransmitter release
  2. Synaptic cleft: ~20–40 nm gap
  3. Postsynaptic receptor: Neurotransmitter binds → postsynaptic potential (EPSP or IPSP)
  4. Termination: Reuptake (NET, DAT, SERT), enzymatic degradation (AChE for ACh; MAO, COMT for catecholamines)

EPSP vs IPSP:

  • EPSP (Excitatory): Na⁺/K⁺ permeability ↑; depolarizing; brings membrane toward threshold
  • IPSP (Inhibitory): Cl⁻ influx (GABA-A) or K⁺ efflux; hyperpolarizing; takes membrane away from threshold
  • Spatial and temporal summation: Multiple PSPs combine algebraically; critical for neural integration

⚡ Exam Tip for INI CET (AIIMS PG): Curare (d-tubocurarine) blocks nicotinic Nm receptors at the NMJ → competitive antagonism → can be reversed by AChE inhibitors (neostigmine) → ACh accumulates → competes with curare. Succinylcholine (depolarizing blocker) → binds Nm receptor → causes sustained depolarization → phase I block (flaccid paralysis); prolonged use → phase II block (desensitization).