A Preliminary Report on Alpha 7 Nicotinic Acetylcholine Receptor Expression in the Hippocampus of Patients with Schizophrenia
Shruti Varshney1, Minjal Patel1, Ananya Nethikunta1, Mary Kosciuk3, Randel Swanson4, Venkat Venkataraman2, Robert Nagele3, Eric Goldwaser5, Nimish Acharya3
1Rowan-Virtua School of Osteopathic Medicine, 2Department of Cell Biology & Neuroscience, Rowan-Virtua School of Osteopathic Medicine, 3Department of Geriatrics and Gerontology, New Jersey Institute for Successful Aging (NJISA), Rowan-Virtua School of Osteopathic Medicine, 4Department of Physical Medicine and Rehabilitation, University of Pennsylvania Perelman School of Medicine, 5Weill Cornell Medicine, New York-Presbyterian
Objective:
We compared the expression profiles of alpha 7 nicotinic acetylcholine receptors (α7nAChR) in the hippocampus and surrounding cortex between patients with schizophrenia (SCZ) and age-matched controls (CTRL).
Background:
SCZ is a psychiatric condition characterized by disruptions in cognition, social activity, affect, and perception, and it has a poorly understood pathophysiology. Previous studies have shown that the α7nAChR in the hippocampus can be associated with auditory sensory gating and cognitive function. Variations in these processes have been linked to auditory hallucinations experienced by patients with SCZ. We have identified a need to directly measure α7nAChR expression in the hippocampus and surrounding cortex of patients with SCZ as there have been very few recent reports on this subject. Notably, earlier reports were based on indirect methods and/or failed to provide conclusive data.
Design/Methods:
We used an immunohistochemistry (IHC) technique to assess α7nAChR expression directly. Formalin-fixed paraffin-embedded postmortem brain sections from the hippocampus and surrounding cortex from patients with SCZ (n=19) and CTRL (n=24) were probed with anti-α7nAChR antibodies. The stained sections were scanned on an Aperio Slide Scanner at 20X (Leica BIOSYSTEMS), and the area of the sections demonstrating immunoreactivity over the entire section, Percent Total Positive (PTP) immunoreactivity, was determined for each section and used for comparison.
Results:
Neurons and neuropil in the hippocampus and cortex demonstrated selective α7nAChR expression in both SCZ and CTRL. However, when we compared α7nAChR immunoreactivity, PTP, between the SCZ and CTRL, the SCZ group showed significantly increased α7nAChR expression (p=0.0406).
Conclusions:
Elevated α7nAChR expression in patients with SCZ could be a part of the damage response initiated by the pathophysiological changes related to SCZ. Since our results contradict some earlier reports, future studies comprising a larger sample size are proposed for conclusively determining the α7nAChR expression profile in the context of SCZ pathogenesis.
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