Student-PDF-PSL300-Membrane-04

PSL300 Physiology - University of Toronto

Post-Synaptic Receptors

  • Types of Receptors:

    • Ionotropic Receptors: Open ion channels directly.

    • Metabotropic Receptors: Initiate metabolic cascades to activate enzymes.

  • Receptor Functionality: The receptor determines the effect, not the transmitter.

Spread of PSP (Post-Synaptic Potential)

  • PSP Generation: Created by binding of neurotransmitter to receptors on postsynaptic membrane.

PSP Summation

  • Types of PSP Summation:

    • Spatial Summation: Minimum of 10-30 EPSPs at different synapses.

    • Temporal Summation: Summation of EPSPs from few active synapses at high frequency.

Ionotropic Effects

  • Action Mechanism: Binding of neurotransmitter causes the ion channel to open, altering post-synaptic membrane potential (PSP).

  • PSP Duration: Approximately 20-40 ms, while neurotransmitters are present.

  • Ion Specificity:

    • EPSP: Cation channels (Na+, K+) cause depolarization.

    • IPSP: Channels for Cl- or K+ lead to hyperpolarization.

Metabotropic Effects

  • Mechanism:

    • Activates G-protein coupled enzyme leading to production/destruction of second messengers (e.g., cAMP, cGMP).

    • Second messengers modulate ion currents through phosphorylation of proteins.

  • Differences from Ionotropic: Metabotropic effects are slower, requiring enzyme activity for ion channel influence, resulting in slow EPSPs or IPSPs.

β-Adrenoreceptor Mechanism

  • Receptor Action: Binding of noradrenaline (NA) activates adenylyl cyclase, increasing cAMP levels.

  • Result: Activation of kinases leads to phosphorylation of Ca++ channels, increasing Ca++ influx important for cardiac muscle contractility.

  • Potential Therapeutics: Beta-blockers modulate this pathway.

Ligands for Receptors

  • Ionotropic Receptors: Common ligands include:

    • Acetylcholine (Ach)

    • Glutamate

    • GABA

    • Glycine

  • Metabotropic Receptors: Common ligands include:

    • Ach (Muscarinic)

    • Neuropeptides (e.g., substance P)

    • Catecholamines (e.g., noradrenaline)

    • Gases (e.g., NO, CO)

Mechanism of PSP Spread

  • Location of PSP Generation: PSPs occur in inexcitable membranes like dendrites and cell bodies, unable to initiate action potentials (APs).

  • Movement to Trigger Zone: PSPs need to passively conduct to the axon trigger zone for an AP to occur.

PSP Summation Roles

  • Biological implications:

    • Poor cable property of tissues results in current loss over distance.

    • Achieving action potentials requires effective summation of PSPs from multiple synapses.

Inhibitory Post-Synaptic Potential (IPSP)

  • Location and Function: IPSPs located on cell soma shunt depolarizing EPSP currents, preventing action potential generation when positioned strategically near the trigger zone.

  • Mechanism: IPSP involves Cl- channel opening, helping to 'clamp' resting membrane potential, preventing excitation.

Spike Train Generation

  • Concept: Sustained EPSPs above threshold lead to continuous firing of action potentials, forming a 'Spike Train'.

  • Overcoming Refractory Period: Requires hyperpolarization of the membrane after each spike to reset Na+ channels for the next AP.

After-Hyperpolarization

  • Role of K+ Channels: Voltage-gated K+ channels cause hyperpolarization after each spike, ensuring Na+ channels reset and can be reused for subsequent action potentials.

  • Effects on Repeated Firing: After-hyperpolarization facilitates the generation of multiple action potentials as long as EPSP remains sufficient.

Conclusion

  • Summary: Understanding the significance of post-synaptic receptors, PSP summations, and the mechanisms of action potentials is crucial for students of physiology.