Midlatency auditory evoked responses in schizophrenia

Erwin, Roland J.; Mawhinney-Hee, Maureen; Gur, Ruben C.; Gur, Raquel E.

doi:10.1016/0006-3223(91)90304-5

Cited by 106 publications

(49 citation statements)

References 23 publications

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“…Inhibitory gating in a train of clicks separated by 500ms is nearly identical to gating in a paired click paradigm, in that responses to the second and subsequent clicks are diminished, compared to the first click (Rosburg et al 2004). Patients with schizophrenia also show deficits in gating with click trains (Adler et al 1985;Erwin et al 1991).…”

Section: Fmri Paradigmmentioning

confidence: 94%

“…Animal studies and a limited number of human intracranial recording and lesion studies point to the involvement of several brain regions, including the hippocampus, thalamus and prefrontal cortex (Miller and Freedman 1995;Erwin et al 1991;Knight et al 1989;Grunwald et al 2003). The most often studied region is the hippocampus.…”

Section: Introductionmentioning

confidence: 99%

“…Early studies of depth recordings of midlatency auditory potentials in cats suggested a generator system involving the thalamus (Hinman and Buchwald 1983). Correspondence of cat to human midlatency responses led investigators to propose the thalamus as a P50 source generator (Erwin and Buchwald 1987). Reports of thalamic dysfunction in schizophrenia led to the hypothesis that this region may be involved in sensory gating deficits in the disease (Erwin et al 1991).…”

Section: Introductionmentioning

confidence: 99%

“…Correspondence of cat to human midlatency responses led investigators to propose the thalamus as a P50 source generator (Erwin and Buchwald 1987). Reports of thalamic dysfunction in schizophrenia led to the hypothesis that this region may be involved in sensory gating deficits in the disease (Erwin et al 1991). Finally, both surface and intracranial recordings support the involvement of the dorsolateral prefrontal cortex in sensory gating (Knight et al 1989;Grunwald et al 2003).…”

Section: Introductionmentioning

confidence: 99%

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Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Tregellas¹,

Davalos²,

Rojas³

et al. 2007

Schizophrenia Research

129

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Objective-Deficits in sensory gating are a common feature of schizophrenia. Failure of inhibitory gating mechanisms, shown by poor suppression of evoked responses to repeated auditory stimuli, have been previously studied using EEG methods. These methods yield information about the temporal characteristics of sensory gating deficits, but do not identify brain regions involved in the process. Hence, the neuroanatomical substrates of poor sensory gating in schizophrenia remain largely unknown. This study used functional magnetic resonance imaging (fMRI) to investigate the functional neuroanatomy of sensory gating deficits in schizophrenia.Methods-Twelve patients with schizophrenia and 12 healthy comparison subjects were scanned at 3 Tesla while performing a sensory gating task developed for fMRI. P50 EEG evoked potential recordings from a paired-stimulus conditioning-test paradigm were obtained from the same subjects.Results-Compared to healthy comparison subjects, patients with schizophrenia exhibited greater activation in the hippocampus, thalamus, and dorsolateral prefrontal cortex (DLPFC) during the fMRI sensory gating task. No group difference was observed in the superior temporal gyrus. Schizophrenia subjects also showed decreased P50 suppression as measured with EEG. Hemodynamic response in the fMRI measure was positively correlated with test/conditioning ratios from the EEG sensory gating measure.Conclusions-Poor sensory gating in schizophrenia is associated with dysfunction of an apparent network of brain regions, including the hippocampus, thalamus and DLPFC. Greater activation of these regions is consistent with evidence for diminished inhibitory function in schizophrenia.

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Section: Fmri Paradigmmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Tregellas¹,

Davalos²,

Rojas³

et al. 2007

Schizophrenia Research

129

View full text Add to dashboard Cite

show abstract

“…For instance, schizophrenia patients and their first-degree relatives exhibit a smaller reduction in the startle response or, in other words, show reduced PPI (Cadenhead et al, 2000;Geyer and Braff, 1987;Swerdlow et al, 1994;Swerdlow and Geyer, 1998). In addition, investigators have also developed protocols to assess auditory gating directly in the brain by using surface electrodes or, in animals, intracranial electrodes, and have found similar results (Adler et al, 1982;Boutros et al, 1991;Clementz et al, 1997;Connolly et al, 2003;Erwin et al, 1991;Freedman et al, 1996;Judd et al, 1992;Stevens et al, 1996).…”

Section: Introductionmentioning

confidence: 96%

Sensorimotor Gating Deficits in Transgenic Mice Expressing a Constitutively Active Form of Gsα

Gould

Bizily

Tokarczyk

et al. 2003

Neuropsychopharmacol

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Schizophrenia is a complex disorder characterized by wide-ranging cognitive impairments, including deficits in learning as well as sensory gating. The causes of schizophrenia are unknown, but alterations in intracellular G-protein signaling pathways are among the molecular changes documented in patients with schizophrenia. Using the CaMKIIα promoter to drive expression in neurons within the forebrain, we have developed transgenic mice that express a constitutively active form of G s α (G s α*), the G protein that couples receptors such as the D 1 and D 5 dopamine receptors to adenylyl cyclase. We have also generated mice in which the CaMKIIα promoter drives expression of a dominant-negative form of protein kinase A, R(AB). Here, we examine startle responses and prepulse inhibition of the startle reflex (PPI) in these G s α* and R(AB) transgenic mice. G s α* transgenic mice exhibited selective deficits in PPI, without exhibiting alterations in the startle response, whereas no deficit in startle or PPI was found in the R(AB) transgenic mice. Thus, overstimulation of the cAMP/PKA pathway disrupts PPI, but the cAMP/ PKA pathway may not be essential for sensorimotor gating. G s α* transgenic mice may provide an animal model of certain endophenotypes of schizophrenia, because of the similarities between them and patients with schizophrenia in G-protein function, hippocampus-dependent learning, and sensorimotor gating.

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Central Auditory Maturation and Babbling Development in Infants With Cochlear Implants

Sharma

Tobey

Dorman

et al. 2004

Arch Otolaryngol Head Neck Surg

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Midlatency auditory evoked responses in schizophrenia

Cited by 106 publications

References 23 publications

Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex during abnormal sensory gating in schizophrenia

Sensorimotor Gating Deficits in Transgenic Mice Expressing a Constitutively Active Form of Gsα

Central Auditory Maturation and Babbling Development in Infants With Cochlear Implants

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