Related Experiment Videos
Substitution of extracellular sodium ions blocks the voltage-dependent decrease of input conductance evoked by
Canadian Journal of Physiology and Pharmacology
|January 1, 1984
Summary
L-aspartic acid causes spinal cord neuron depolarization, but this effect and reduced conductance depend on external sodium ions. Removing sodium eliminates the voltage-dependent response, which quickly recovers when sodium is reintroduced.
Area of Science:
- Neuroscience
- Cellular Biology
Background:
- Spinal cord neurons exhibit complex responses to neurotransmitters.
- L-aspartic acid is an excitatory amino acid neurotransmitter.
Purpose of the Study:
- To investigate the role of external sodium ions in the response of cultured spinal cord neurons to L-aspartic acid.
- To elucidate the mechanism underlying L-aspartic acid-evoked neuronal depolarization and conductance changes.
Main Methods:
- Cultured spinal cord neurons were utilized.
- Superfusion techniques with solutions containing varying ion compositions (e.g., sodium substitution with choline or Tris) were employed.
- Electrophysiological recordings measured membrane potential and input conductance (Gm).
Main Results:
- L-aspartic acid induced membrane depolarization and a voltage-dependent decrease in input conductance (Gm) in spinal cord neurons.
- Substitution of external sodium (Na+) with choline or Tris significantly reduced or abolished these responses.
- Responses rapidly recovered upon reintroduction of sodium-containing solutions, indicating sodium dependency.
Conclusions:
- The voltage-dependent component of the response to L-aspartic acid in cultured spinal cord neurons is critically dependent on the presence of external sodium ions.
- External sodium plays a crucial role in mediating the excitatory effects of L-aspartic acid on these neurons.