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Altered visual processing in a rodent model of Attention-Deficit Hyperactivity Disorder
L R Brace1, I Kraev1, C L Rostron1
1Department of Life, Health and Chemical Sciences, The Open University, Milton Keynes MK7 6AA, UK.
Neuroscience
|July 14, 2015
Summary
Attention-Deficit Hyperactivity Disorder (ADHD) may involve a hyper-responsive superior colliculus (SC). This study found altered SC structure and function in a rat model of ADHD, suggesting SC dysfunction contributes to ADHD symptoms like distractibility.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Animal Models of Disease
Background:
- Attention-Deficit Hyperactivity Disorder (ADHD) is characterized by distractibility, potentially linked to the superior colliculus (SC).
- Evidence suggests altered SC functioning in ADHD, with a hyper-responsive SC proposed to mediate core symptoms.
Purpose of the Study:
- To systematically characterize the superior colliculus (SC) in spontaneously hypertensive rats (SHR), a validated animal model for ADHD.
- To investigate collicular-dependent behavior, neural activity, and morphology in SHRs compared to control strains.
Main Methods:
- Assessed collicular-dependent orienting behavior in SHRs and control strains (Wistar Kyoto and Wistar).
- Recorded local field potential (LFP) and multiunit activity in response to visual stimuli in anesthetized rats.
- Examined morphological measures including SC volume, neuron and glia densities, and glia:neuron ratio.
Main Results:
- SHRs exhibited prolonged responsiveness and longer response duration to repeated visual stimuli compared to controls.
- SHRs displayed hyper-responsive LFP and multiunit activity in the superficial SC layers, not attributable to retinocollicular pathway changes.
- SHRs showed a reduced glia:neuron ratio in the SC compared to WKY rats, potentially explaining heightened responsiveness.
Conclusions:
- This study reveals strain-specific alterations in SC function and structure in SHRs.
- Findings provide convergent evidence supporting a role for SC dysfunction in ADHD pathophysiology.

