Synapses Between Neurons

Types of Synaptic Relationships

• Many-to-One Relationship: One neuron takes input from several neurons, creating multiple synaptic regions.

Location of Synaptic Connections

• Mainly on the cell body or dendritic membranes where ligand-gated channels are present.

Transmission of Action Potential

• Dendritic Synaptic Point: Action potential depolarizes the presynaptic membrane, releasing neurotransmitters (e.g., acetylcholine) into the synaptic cleft.
  • Neurotransmitter binds to receptors, opens channels, increasing Na+ and K+ conductance.
  • Sodium Influx dominates, depolarizing the postsynaptic membrane.
  • Depolarization thresholds: From -70mV to 0mV.
  • Threshold Potential: -10mV, triggering current flow toward the axon hillock.
• Axon Hillock: High density of voltage-gated sodium channels initiates action potentials.
  • Current flow increases membrane potential, causing Na+ channels to open, leading to Na+ influx and action potential initiation.

Influence of Synapse Distance

• Closer synapses to the axon hillock have a greater chance of generating an action potential.
• Summation: Multiple presynaptic cells' inputs determine if the postsynaptic cell will fire an action potential.

Excitatory and Inhibitory Postsynaptic Potentials

• Excitatory Postsynaptic Potential (EPSP):
  • Depolarization in the presynaptic membrane (e.g., release of glutamate).
  • Glutamate opens channels for Na+ and K+, leading to Na+ influx.
  • Depolarization: ~-60mV, closer to the threshold potential, increases excitability of the postsynaptic neuron.
  • Similar to the endplate potential at the neuromuscular junction.
  • Excitatory Neurotransmitters: Glutamate, acetylcholine, aspartate.
• Inhibitory Postsynaptic Potential (IPSP):
  • Depolarization releases inhibitory neurotransmitter (e.g., GABA).
  • GABA opens chloride channels, leading to Cl- influx.
  • Hyperpolarization: ~-85mV, away from threshold, decreases excitability.
  • Inhibitory Neurotransmitters: GABA, glycine.

Clinical Implications

• Decreased Neuronal Excitability

  • Signs: Weakness, ataxia, hyperreflexia, paralysis, sensory deficit.
  • Causes:
    1. Ion Disturbances: Hypokalemia, chronic hyperkalemia, hypercalcemia.
    2. Loss of Neurons / Demyelination: Guillain-Barre syndrome, amyotrophic lateral sclerosis (ALS), aging.
    3. Toxins and Drugs: Local anesthetics (e.g., cane drugs), tetrodotoxin, saxitoxin.
    4. Neuromuscular Junction Disorders: Lambert-Eaton syndrome, myasthenia gravis, botulinum toxin.

• Increased Neuronal Excitability

  • Signs: Hyperreflexia, spasms, muscle fasciculation, tremors, paresthesias, convulsions.
  • Causes:
    1. Ion Disturbances: Acute hyperkalemia, hypocalcemia.
    2. Loss of Neurons / Demyelination: Multiple sclerosis.
    3. Toxins: Sigma toxin, batrachotoxin.
    4. Neuromuscular Junction Disorders: Acetylcholine esterase inhibitors, lateral toxin.