Surface auditory evoked potentials in the unrestrained rat: component definition

Knight, Robert T.; Brailowsky, Simón; Scabini, Donatella; Simpson, Gregory V.

doi:10.1016/0013-4694(85)91035-1

Cited by 77 publications

(30 citation statements)

References 44 publications

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“…The inability to attend appropriately to sensory stimuli suggests that neuronal mechanisms responsible for Þltering or gating sensory input to higher brain centers may be deÞcient. Central Þltering mechanisms have been experimentally demonstrated in both humans and laboratory animals (Davis et al 1966;Knight et al 1985;Bourbon et al 1987). While paradigms and analysis are still in reÞnement, several studies have demonstrated that these mechanisms are aberrant in schizophrenic humans (Roth et al 1980;Adler et al 1982;Freedman et al 1987;Bra¤ and Geyer 1990; but see Kathman and Engle 1990) and in certain strains of inbred mice (Stevens et al 1996.…”

Section: Introductionmentioning

confidence: 97%

Selective α 7 -nicotinic agonists normalize inhibition of auditory response in DBA mice

et al. 1998

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Abnormal sensory inhibition is a measurable indicator of a sensory processing deficit which is observed in schizophrenia, and other disorders, and which may be heritable. This deficit has also been observed in certain inbred mouse strains where the intensity of the deficit has been correlated with reduction in the number of hippocampal alpha-bungarotoxin-sensitive nicotinic receptors. Nicotine and certain nicotinic agonists produce brief periods of normal sensory inhibition in these mice. Similarly, nicotine also transiently normalizes sensory inhibition in schizophrenics. The present study assessed the effects of a novel nicotinic partial agonist (GTS-21), selective for the alpha-bungarotoxin site, on sensory inhibition in DBA mice, a strain with no sensory inhibition under routine experimental conditions. GTS-21 produced a dose-dependent normalization of sensory inhibition which was blocked by alpha-bungarotoxin but not mecamylamine. In contrast to other nicotinic agonists, normalization of sensory inhibition by GTS-21 and two related anabaseine compounds, DMAB-anabaseine and DMAC-anabaseine, was observed when administered a second time to the animal, after a 40-min delay. Our results indicated that the anabaseine compounds increase sensory inhibition through alpha7 nicotinic receptors, and that their ability to act repeatedly on these receptors may be less affected by desensitization.

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Section: Introductionmentioning

confidence: 97%

Selective α 7 -nicotinic agonists normalize inhibition of auditory response in DBA mice

et al. 1998

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“…The N40 waveform of the auditory evoked potential (AEP) in the rat was first described by Knight et al (1985). The rat N40-AEP is a negative component that is recorded from the cortex 40 to 60 msec following auditory stimulation (Adler et al, 1986;Boutros et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Histological correlates of N40 auditory evoked potentials in adult rats after neonatal ventral hippocampal lesion: animal model of schizophrenia

Romero-Pimentel

Vázquez-Roque

Camacho-Ábrego

et al. 2014

Schizophrenia Research

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“…Cross-species similarities in the topography and response properties of AEPs has allowed for the use of rodent models to assess the potential effects of physiologic, pharmacologic, and genetic alterations on human AEPs (Adler et al, 1986;Knight et al, 1985). In such models, AEPs represent neuronal activity in response to controlled stimuli.…”

Section: Introductionmentioning

confidence: 99%

Corticosterone Modulates Auditory Gating in Mouse

Maxwell

Ehrlichman

Liang

et al. 2005

Neuropsychopharmacol

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Previous studies suggest that circulating glucocorticoids may influence the encoding and processing of sensory stimuli. The current study investigated this hypothesis by measuring the generation (amplitude), gating (recovery cycle), and sensitivity (intensity function) of auditory evoked responses in C57BL/6 mice treated with chronic corticosterone (0, 1, 5, 15, or 30 mg/kg/day for 14 days). We found that low-dose corticosterone (5 but not 1 mg/kg/day) enhanced the amplitude and improved gating of evoked potentials without affecting the intensity function. In comparison, higher doses (15 and 30 mg/kg/day) decreased the amplitude and impaired gating of evoked potentials, also without altering the stimulus intensity function. At all doses, lower amplitudes of evoked potentials were significantly correlated with higher circulating corticosterone levels. These data highlight the need to consider serum glucocorticoid levels when assessing human disease states associated with aberrations of information processing such as schizophrenia and depression.

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Surface auditory evoked potentials in the unrestrained rat: component definition

Cited by 77 publications

References 44 publications

Selective α 7 -nicotinic agonists normalize inhibition of auditory response in DBA mice

Selective α 7 -nicotinic agonists normalize inhibition of auditory response in DBA mice

Histological correlates of N40 auditory evoked potentials in adult rats after neonatal ventral hippocampal lesion: animal model of schizophrenia

Corticosterone Modulates Auditory Gating in Mouse

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