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Reduced prepulse inhibition in rats with entorhinal cortex lesions
Kyoko Goto1, Akinori Ueki, Hiroyuki Iso
1Department of Neuropsychiatry, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. npsy@hyo-med.ac.jp
Behavioural Brain Research
|August 23, 2002
Summary
Damage to the entorhinal cortex impairs sensorimotor gating (prepulse inhibition). Dopamine pathways, modulated by haloperidol, partially restore this function, suggesting a link between the entorhinal cortex, dopamine, and gating.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Psychopharmacology
Background:
- Prepulse inhibition (PPI) is a measure of sensorimotor gating, reduced in neuropsychiatric disorders and dopamine-dysregulated states.
- The entorhinal cortex, crucial for hippocampal input, is implicated in cognitive functions potentially affected in disorders like schizophrenia.
Purpose of the Study:
- To investigate the relationship between the entorhinal cortex and prepulse inhibition (PPI).
- To examine the role of dopaminergic systems in mediating the entorhinal cortex's influence on sensorimotor gating.
Main Methods:
- Bilateral entorhinal cortex lesions were induced using ibotenic acid in rats.
- Acoustic startle experiments were conducted, assessing PPI during treatment with haloperidol (a dopamine antagonist) or saline.
- Startle movement amplitude was measured to control for non-specific effects.
Main Results:
- Bilateral entorhinal cortex lesions significantly reduced PPI.
- Haloperidol treatment partially restored PPI in lesioned rats.
- Neither ibotenic acid injection nor haloperidol affected the startle movement amplitude.
Conclusions:
- The entorhinal cortex is involved in sensorimotor gating, potentially through dopaminergic circuits.
- Dopaminergic modulation, possibly via the nucleus accumbens, may mediate the entorhinal cortex's effect on PPI.
- Entorhinal cortex dysfunction could contribute to cognitive deficits in disorders like schizophrenia due to its role in hippocampal function.