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Related Experiment Video

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Assessment of Stress Effects on Cognitive Flexibility using an Operant Strategy Shifting Paradigm

Assessment of Stress Effects on Cognitive Flexibility using an Operant Strategy Shifting Paradigm

Published on: May 4, 2020

More is less: a disinhibited prefrontal cortex impairs cognitive flexibility.

Aaron J Gruber¹, Gwendolyn G Calhoon, Igor Shusterman

¹Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|December 17, 2010

Summary

Neonatal ventral hippocampal lesions in rats cause prefrontal cortex (PFC) disinhibition, impairing decision-making and cognitive flexibility. Treatment with a specific glutamate agonist improved flexibility in these rats, suggesting a therapeutic target for PFC dysfunction.

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Operant Procedures for Assessing Behavioral Flexibility in Rats

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Area of Science:

Neuroscience
Cognitive Science
Neuropsychiatry

Background:

The prefrontal cortex (PFC) is crucial for decision-making and is often dysfunctional in neuropsychiatric disorders.
Studies suggest a loss of inhibitory interneuron function in the PFC in conditions like schizophrenia.
Neonatal ventral hippocampal lesion (NVHL) in rats models PFC interneuron dysfunction and dopamine (DA) modulation deficits.

Purpose of the Study:

To determine if NVHL rats exhibit PFC disinhibition and altered decision-making.
To investigate the neural processing and cognitive flexibility deficits in NVHL rats.
To explore potential therapeutic interventions for PFC disinhibition.

Main Methods:

Recorded medial PFC neural activity in NVHL rats during a reward-discounting choice task.
Assessed cognitive flexibility using reward outcome reversals and response bias.
Administered LY379268 (a mGluR2/3 agonist) and eticlopride (a D2 antagonist) to evaluate treatment effects.

Main Results:

NVHL rats showed PFC pyramidal neuron hyperactivity and reduced oscillations, indicating disorganized processing.
NVHL rats exhibited impaired cognitive flexibility and made more errors during reward reversals.
LY379268 improved behavioral flexibility in NVHL rats, while eticlopride impaired it in control rats.

Conclusions:

NVHL in rats leads to PFC disinhibition, impacting neural processing and behavioral responses.
Dopamine D2 receptors play a role in cognitive flexibility within the PFC.
Targeting cortical excitability may offer a therapeutic strategy for PFC-related cognitive deficits.