Synaptic Transmission and Neural Integration

Synapses

  • Functional association of a neuron with another neuron or effector organs (muscle, gland).
  • Two types: Electrical and Chemical.

Electrical Synapses

  • Direct transfer of Action Potential (AP).
  • Neurons linked by gap junctions.
  • Functions:
    • Rapid communication.
    • Synchronous activity.
    • Bidirectional communication.
    • Both excitation or inhibition at the same synapse.
  • Identified in retina, cortex, brainstem, hypothalamus.

Chemical Synapses

  • Functional Anatomy: Presynaptic neuron, synaptic cleft (30-50
    \text{ nm} wide), postsynaptic neuron.
  • Unidirectional communication.
  • Locations: Axodendritic, Axosomatic, Axoaxonic, Dendrodendritic.
  • Presynaptic Axon Terminal: Neurotransmitter-containing vesicles, voltage-gated Ca^{2+} channels, reuptake molecules.
  • Postsynaptic Neuron: Receptors, enzymes.

Synaptic Communication Steps (Chemical)

  1. Action potential arrives at presynaptic terminal.
  2. Voltage-gated Ca^{2+} channels open.
  3. Ca^{2+} entry triggers vesicle docking and neurotransmitter secretion via exocytosis.
  4. Neurotransmitter diffuses across synaptic cleft and binds to receptors on postsynaptic membrane.
  5. Response in postsynaptic cell (e.g., change in membrane potential).
  6. Neurotransmitter removed from cleft by: enzymatic degradation, reuptake into presynaptic terminal (degraded or recycled), or diffusion out of cleft.

Synaptic Delay

  • 0.5-5 \text{ msec} delay between AP arrival and postsynaptic V_m change.
  • Caused by: Ca^{2+} entry, vesicle docking, and neurotransmitter release.

Signal Transduction at Chemical Synapses

  • Channel-linked (Ionotropic) Receptors:
    • Ligand-gated ion channels.
    • Fast change in postsynaptic V_m (Postsynaptic Potential - PSP).
    • Channel closes quickly as neurotransmitter dissociates.
  • G protein-coupled (Metabotropic) Receptors:
    • Slow acting.
    • Involve direct coupling or second messenger pathways.

Postsynaptic Potentials (PSPs)

  • Graded potential in postsynaptic cell due to receptor-neurotransmitter binding.
  • Excitatory Postsynaptic Potential (EPSP): Causes depolarization.
  • Inhibitory Postsynaptic Potential (IPSP): Causes hyperpolarization or membrane stabilization.

Excitatory Postsynaptic Potential (EPSP)

  • Fast Response:
    • Cation channels (e.g., Na^{+} and K^{+}) open.
    • At resting Vm = -70 \text{ mV}, Na^{+} has a higher electrochemical gradient (relative to E{Na} = +60 \text{ mV} and E_K = -94 \text{ mV}).
    • Short duration, few to hundreds of msec.
  • Slow Response:
    • Activation of metabotropic receptor with G protein and cAMP second messenger.
    • K^{+} channels close, reducing K^{+} leak out.
    • Na^{+} still leaks in, leads to depolarization.
    • Longer duration, seconds to hours.

Inhibitory Postsynaptic Potential (IPSP)

  • Neurotransmitter binds, opening channels for K^{+} or Cl^{-}.
  • If K^{+} channels open: K^{+} moves out, causing hyperpolarization.
  • If Cl^{-} channels open:
    • Cl^{-} moves in, causing hyperpolarization (in cells with Cl^{-} ATPase pump which maintains an inward Cl^{-} gradient).
    • Cl^{-} stabilizes membrane potential (in cells with Cl^{-} leak channels and no Cl^{-} ATPase pump, where Cl^{-} is at equilibrium).
    • Can also stabilize membrane if both Cl^{-} and excitatory (cation) channels open, balancing ion movements.
  • IPSPs are graded potentials: Higher AP frequency \rightarrow more neurotransmitter \rightarrow greater ion permeability change \rightarrow greater hyperpolarization.