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14:37
Whole-cell Patch-clamp Recordings from Morphologically- and Neurochemically-identified Hippocampal Interneurons
Published on: September 30, 2014
Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia.
David A Lewis1, Allison A Curley, Jill R Glausier
1Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA 15213, USA. lewisda@upmc.edu
Trends in Neurosciences
|December 14, 2011
Summary
Schizophrenia impairs cognitive control through weakened parvalbumin-positive inhibitory neuron (PVBC) function, disrupting brain gamma oscillations. This suggests a compensatory model where reduced inhibition fails to restore necessary neural activity for cognitive function.
Area of Science:
- Neuroscience
- Psychiatry
- Cellular Biology
Background:
- Schizophrenia is characterized by cognitive control deficits, linked to impaired prefrontal gamma oscillations.
- Gamma oscillations depend on inhibitory inputs from parvalbumin-positive basket cells (PVBCs) to pyramidal neurons.
- Schizophrenia involves PVBC abnormalities that reduce their inhibitory efficacy.
Purpose of the Study:
- To propose a novel model for cortical dysfunction in schizophrenia.
- To explain how PVBC abnormalities contribute to cognitive deficits.
Main Methods:
- Review and synthesis of existing findings on PVBCs and schizophrenia.
- Theoretical modeling of cortical excitation-inhibition balance.
Main Results:
- Schizophrenia presents with pre- and postsynaptic PVBC abnormalities.
- These PVBC deficits weaken inhibitory control over pyramidal cells.
- A compensatory decrease in PVBC inhibition may occur in response to increased pyramidal cell excitation.
Conclusions:
- Reduced PVBC inhibition, while attempting to rebalance excitation-inhibition, is insufficient to restore gamma oscillation power.
- This imbalance underlies the cognitive control deficits observed in schizophrenia.
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