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Inhibitory effect of mouse neocortex layer I on the underlying cellular network
Dan Shlosberg1, Saundra L Patrick, Yossi Buskila
1Department of Physiology and Zlotowski Center for Neuroscience, Box 653, Faculty of Health Sciences, Ben-Gurion University, Beer-Sheva, Israel 84105.
The European Journal of Neuroscience
|December 6, 2003
Summary
Layer I inhibition in the mammalian cortex significantly impacts neural network activity. Blocking this inhibition increases cortical excitability but does not induce epileptic phenomena.
Area of Science:
- Neuroscience
- Cellular Neuroscience
- Cortical Circuitry
Background:
- Mammalian cortical layer I integrates sub- and intracortical inputs and pyramidal neuron dendrites.
- Layer I features a dense plexus of inhibitory axons from stellate cells, whose role in cortical network activity is unclear.
Purpose of the Study:
- To investigate the influence of inhibitory inputs in layer I on the activity of the underlying cellular network.
- To determine the extent to which layer I inhibition modulates cortical excitability and epileptiform activity.
Main Methods:
- Field potentials (FPs) were recorded in layer II/III.
- Inhibition was manipulated via focal application of the GABAA blocker picrotoxin in layer I or by layer I removal.
- Immunocytochemistry was used to identify inhibitory interneuron subtypes (somatostatin- and calretinin- immunoreactive axons).
Main Results:
- Blocking GABAA inhibition in layer I or removing layer I increased field potential amplitudes.
- Partial blockade of inhibition followed by layer I removal reduced the stimulus threshold for epileptiform events and increased their propagation velocity.
- Layer I inhibition is predominantly somatostatin-immunoreactive (SM-ir), constituting about one-third of cortical SM-ir axons.
Conclusions:
- Layer I exerts a significant inhibitory influence on the cortical cellular network.
- This inhibition provides a moderate restraining effect, and its absence enhances cortical circuit excitability.
- While layer I removal increases excitability, it is insufficient to trigger epileptic phenomena on its own.