Synaptic Transmission and Neurotransmitter Function

Synaptic Transmission

• Synaptic Transmission: The process of communication between neurons involves the transmission of signals via synapses.

Gap Junctions

• Definition: A type of electrical synapse.
• Structure:
  • Composed of connexons forming channels between cells.
  • Allow intercellular communication by permitting ions and small molecules to pass.
• Application: Critical in cardiac muscle structure (e.g., intercalated disks).

Otto Loewi Experiment (1920)

• Significance: First demonstration of chemical transmission in synapses.
• Process:
  1. Stimulated vagus nerve of heart 1.
  2. Transferred solution to heart 2.
  3. Observed inhibitory effects on heart rate in heart 2 (vagal stimulation).

Types of Synapses

• Neuronal Synapses: Characterized by their presynaptic and postsynaptic components.

Exocytosis in Synaptic Transmission

• Process:
  • Release of neurotransmitters occurs through exocytosis at the presynaptic membrane.
  • Involves synaptic vesicles filled with neurotransmitters and voltage-gated calcium channels.
  • Neurotransmitters cross the synaptic cleft to bind to postsynaptic receptors.

Receptors in the Postsynaptic Neuron

• Types of Receptors:
  • Ionotropic Receptors: Fast and direct, formed as ion channels.
  • Metabotropic Receptors (G-protein-coupled): Slower, long-lasting effects due to second messengers that amplify signaling.

G-protein-coupled Receptors

• Structure: Smaller than ionotropic receptors, involves guanine nucleotide-binding complex.
• Function: Utilize second messengers like cAMP to enhance signaling effects.

Comparison of Receptor Types

• Ionotropic Receptors:

  • Fast acting (less than 0.1 seconds).
  • More localized effects.

• Metabotropic Receptors:

  • Slower (minutes to hours) but can have widespread effects.

Post-Synaptic Potentials (PSPs)

• Types:
  • Excitatory Post-Synaptic Potential (EPSP): Caused by Na+ channel opening.
  • Inhibitory Post-Synaptic Potential (IPSP): Caused by K+ or Cl- channel opening.
• Travel: Decremental nature; they get smaller as they move toward the axon hillock.

Summation of PSPs

• Requirement for Action Potential (AP):
  • One EPSP alone typically cannot cause a neuron to fire; summation of EPSPs and IPSPs is needed.
  • Threshold for AP is about -55 to -50 mV at the axon hillock.

Types of Summation

• Temporal Summation: Integration of multiple EPSPs or IPSPs occurring in rapid succession.
• Spatial Summation: Integration of simultaneous EPSPs or IPSPs from multiple synapses.

Neurotransmitter Inactivation

• Mechanisms to Turn Off Activity:
  1. Reuptake: Recycling neurotransmitter back into the presynaptic neuron.
  2. Enzymatic degradation: Breakdown of neurotransmitters by enzymes.

Neurotransmitter Criteria**

• Definition: Must be produced by a neuron, released at the axon terminal, mimic natural effects when applied externally, and have a mechanism for deactivation.

Types of Neurotransmitters**

• Small Molecule Neurotransmitters: Synthesized in the terminal button, packed in vesicles. Include amino acids (e.g., Glutamate, GABA) and monoamines (e.g., Dopamine).
• Neuropeptides: Larger molecules affecting multiple areas, e.g., endorphins for pain relief, oxytocin for social bonding.

Pharmacology of Synaptic Transmission

• Drugs can Alter Neurotransmitter Activity:
  • Agonists: Enhance or facilitate neurotransmitter activity.
  • Antagonists: Inhibit or reduce neurotransmitter activity.

Examples of Agonists**

• Cocaine: Prevents reuptake of catecholamines.
• Benzodiazepines: Facilitate GABA receptor function.

Examples of Antagonists**

• Picrotoxin: Blocks GABA receptors.
• Botulinum Toxin: Inhibits neurotransmitter release by acting on synaptic vesicles.

Mechanisms of Drug Action**

• Agonistic Effects: Increase synthesis or release of neurotransmitter molecules, prevent breakdown, or enhance receptor effects.
• Antagonistic Effects: Inhibit synthesis or release, block receptor sites, promote receptor action to inhibit neurotransmitter release.