BMS1052 Lesson 3 Notes: Neural Computation — Synapses and Dendrites (Key Points)

Electrical synapses

  • Structure: gap junctions with connexons; allow direct ionic current between neurons.

  • Function: fast, bidirectional signal transmission; very reliable in timing.

Chemical synapses

  • Structure: presynaptic terminal → cleft → postsynaptic membrane; neurotransmitter release triggers receptor response.

  • Receptors: ionotropic (fast, ligand-gated ion channels) and metabotropic (slow, G-protein-coupled).

  • Classification: typically excitatory or inhibitory based on the postsynaptic effect.

Synapses – Factors affecting synaptic strength

  • Release probability Pr: chance that an action potential triggers vesicle release. Pr < 1 in many synapses; varies by brain region.

  • Presynaptic factors: Ca^{2+} entry triggers vesicle fusion; modulation by presynaptic receptors can increase or decrease release.

  • Postsynaptic factors: receptor density/conductance changes determine the size of the postsynaptic response.

Dendrites and Post-synaptic potentials (PSPs)

  • EPSP size and soma impact: amplitude decays with distance from the soma due to cable properties; summation at the soma determines whether threshold is reached.

  • IPSP basics: Cl^{-} conductance can hyperpolarize or shunt; reversal potential near E_{Cl} governs effect.

  • Spatial vs. temporal summation: multiple PSPs from different locations (spatial) or at short intervals (temporal) can add up.

Dendrites – Factors affecting computation using PSPs

  • Cl^{-} channels: opening mediates inhibition; effect depends on Cl^{-} reversal potential and driving force.

  • Inhibition location: somatic (axo-somatic) inhibition can strongly veto incoming excitation via shunting.

  • Shunting inhibition: increased Cl^{-} conductance leaks charge, reducing PSP propagation to the soma without large hyperpolarization.

  • Mechanisms of Cl^{-} mediated inhibition and their impact on dendritic computation.

Modifying vesicle release: release probability (Pr)

  • Pr < 1 means not all vesicles released by first AP; modulation alters synaptic strength.

  • Reported Pr ranges: spinal motor neurons 0–1; cerebellar climbing fibers ~0.9; cortical pyramidal cells ~0.1–0.9; motor neurons typically ~1.

Presynaptic modulation of vesicle release

  • Action potentials open voltage-gated Ca^{2+} channels; Ca^{2+} entry triggers release.

  • Axo-axonal synapses regulate Ca^{2+} influx, modulating vesicle release.

  • Mechanisms: both ionotropic (fast) and metabotropic (slow).

  • States: inactive synapse → decreased Ca^{2+} influx and EPSP; active synapse → increased Ca^{2+} influx and EPSP.

Paired-pulse facilitation (short-term plasticity)

  • Two APs separated by short interval can produce larger release on the second spike due to residual Ca^{2+}.

  • Outcome depends on Pr:

    • If Pr is low, facilitation occurs (second EPSP larger).

    • If Pr is high, vesicles ready for release are depleted and the second response is smaller (depression).

  • Graphical note: this reflect Ca^{2+} dynamics and vesicle availability; it applies to EPSCs ( currents ) rather than EPSPs ( voltages ).

Paired-pulse timing and spacing

  • Greater inter-stimulus interval reduces facilitation; short intervals enhance facilitation if Pr is not saturated.

Autoreceptors and presynaptic receptors

  • Presynaptic metabotropic receptors monitor neurotransmitter release levels.

  • Negative feedback: inhibit neurotransmitter release and/or synthesis to limit transmission when levels are high.

Astrocytes and synaptic transmission

  • Astrocytes detect/respond to many neurotransmitters.

  • They regulate synaptic transmission (tripartite synapse) and can modulate neurotransmitter availability and uptake.

Circuits and reliability (example question)

  • If the rate of action potentials in node A increases, what happens to the rate at node B? Depends on:

    • synaptic reliability (Pr), short-term plasticity, and timing between A→B transmissions.

    • properties of the synapse (facilitation vs depression) and circuit wiring.

  • Key factors: release probability, synaptic depression/facilitation, and summation at the postsynaptic neuron.

Reading suggestion

  • Bear, Connors and Paradiso, Chapter 5

Important formulas

  • Chloride reversal potential (example):
    ECl=−65 mVE_{Cl} = -65 \text{ mV}

  • Resting membrane potential (example):
    Vrest≈−65 mVV_{rest} \approx -65 \text{ mV}

  • Opening Cl^{-} channels drives Vm toward EClE_{Cl}, producing possible shunting inhibition or hyperpolarization depending on the driving force.