Elsevier

Brain Research

Volume 705, Issues 1–2, 24 December 1995, Pages 235-240
Brain Research

Restoration of sensory gating of auditory evoked response by nicotine in fimbria-fornix lesioned rats

https://doi.org/10.1016/0006-8993(95)01157-9Get rights and content

Abstract

Recordings of auditory evoked potentials in the CA3 region of the hippocampus reveal a decrement in the N40 wave after the presentation of the second of closely paired auditory stimuli (interstimulus interval of 500 ms), a phenomenon known as sensory gating. Previous experiments have suggested the involvement of nicotinic cholinergic systems in auditory sensory processing. The present study examined the effects of lesioning the fimbria-fornix on auditory sensory processing in the hippocampus. Fimbria-fornix lesions resulted in a failure to decrement the N40 wave in the auditory evoked response to the second tone. When nicotine was administered to rats with fimbria-fornix lesions the drug was able to reinstate the normal suppression of the second auditory evoked response. These data support the involvement of nicotinic cholinergic afferents in auditory sensory modulation in the hippocampus.

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    This region receives glutamatergic input from the entorhinal cortex and cholinergic input from the medial septum (Insausti et al., 1997; Cenquizca and Swanson, 2007). The rat N40-AEP has mainly been employed for studying mechanisms of sensory gating (De rojas et al., 2013; Okamoto et al., 2012; Chen et al., 2012; Swerdlow et al., 2012; Breier et al., 2010; Vohs et al., 2009; Zhou et al., 2008; Keedy et al., 2007; Hashimoto et al., 2005; Zheng et al., 2005; Siegel et al., 2005; Miyazato et al., 1999; Boutros et al., 1997; Boutros and Kwan1998; Johnson et al., 1998: Stevens et al., 1998; Flach et al., 1996; Shinba et al., 1996; Bickford and Wear, 1995; Campbell et al., 1995; Bickford and Wear, 1995; Luntz-Leybman et al., 1992). Sensory gating can be defined as the ability of the brain to attenuate incoming irrelevant sensory stimuli (Freedman et al., 1987).

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    Several neurophysiological studies found that low α7 receptor expression or function abnormalities might be one of the mechanisms of sensory gating defect (Luntz-Leybman et al., 1992; Freedman, et al., 1994; Leonard et al., 1996; Stevens et al., 1996). Pharmacology studies found that nicotine could instantly improve P50 suppression defects of schizophrenia patients and their first-degree relatives (Bickford and Wear, 1995; Adler et al., 1992, 1993; Stevens et al., 1995). Patients with schizophrenia have high rates of smoking compared with normal subjects, even compared with patients with other mental illnesses (Hamera et al., 1995); this nicotine dependence reflects a self-treatment with sensory gating defects (Goff et al., 1992).

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