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Extracellular calcium modulates persistent sodium current-dependent burst-firing in hippocampal pyramidal neurons
1Department of Physiology, Institute of Medical Sciences, The Hebrew University-Hadassah Faculty of Medicine, Jerusalem 91120, Israel.
Summary
Extracellular calcium concentration critically influences hippocampal CA1 pyramidal cell firing. Lowering calcium induces intrinsic bursting by augmenting persistent sodium currents (I(NaP)), a key mechanism in neuronal activation.
Area of Science:
- Neuroscience
- Cellular Electrophysiology
Background:
- Hippocampal CA1 pyramidal cells (PCs) exhibit complex spike bursts.
- These bursts are thought to be intrinsically generated by spike afterdepolarizations (ADPs).
Purpose of the Study:
- To investigate the role of extracellular calcium concentration ([Ca(2+)](o)) in regulating intrinsic burst-firing in CA1 PCs.
- To elucidate the ionic mechanisms underlying calcium-dependent bursting.
Main Methods:
- Intracellular recordings from adult rat hippocampal slices.
- Manipulation of extracellular calcium levels using Mn(2+) or Mg(2+) substitution.
- Pharmacological blockade of persistent sodium current (I(NaP)) and calcium-activated potassium currents.
Main Results:
- Decreased [Ca(2+)](o) induced intrinsic bursting in non-bursting CA1 PCs.
- Increased [Ca(2+)](o) suppressed bursting in native bursters.
- Low [Ca(2+)](o)-induced bursting and enlarged ADPs were blocked by I(NaP) inhibitors.
- Blockade of Ca(2+)-activated K(+) currents did not induce bursting.
Conclusions:
- Intrinsic burst-firing in CA1 PCs is highly dependent on [Ca(2+)](o).
- Reduced [Ca(2+)](o) likely induces bursting by augmenting I(NaP).
- This calcium-dependent mechanism may regulate neuronal firing modes during hippocampal activation.