Elementary neuronal dysfunctions in schizophrenia

Freedman, Robert; Waldo, Merilyne; Bickford, Paula C.; Nagamoto, Herbert T.

doi:10.1016/0920-9964(91)90035-p

Cited by 244 publications

(163 citation statements)

References 24 publications

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“…Using subdural strip electrodes, we identified auditory evoked responses with a 50ms latency from the surfaces of the medial and lateral temporal lobe. The P50 wave showed polarity reversal at the hippocampus, suggesting this site may be involved in generation of the wave (Freedman et al 1991). This finding was consistent with earlier reports showing auditory evoked responses in the hippocampus at a similar latency using depth electrodes (Goff et al 1980).…”

Section: Hippocampussupporting

confidence: 82%

“…In a rodent model of sensory gating, hippocampal activity is inhibited at the 500ms inter-stimulus interval, an inhibition which is dependent upon cholinergic activity from the medial septal fimbriafornix input (Miller and Freedman 1993). Studies recording intracranial evoked potentials from patients undergoing invasive presurgical evaluation for epilepsy have also implicated the hippocampus in sensory gating (Freedman et al 1991;Grunwald et al 2003;Boutros et al 2005). Involvement of the thalamus in sensory gating has also been proposed.…”

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

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130

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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: Hippocampussupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

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

Tregellas¹,

Davalos²,

Rojas³

et al. 2007

Schizophrenia Research

Self Cite

130

View full text Add to dashboard Cite

show abstract

“…Another measure in the ERP paradigm which appears to be altered among schizophrenia participants is the positive potential with a 50 ms latency (the P50) in response to a "test" click, which in normals is reduced when preceded by a "conditioning" click. This P50 conditioning:test ratio, which is larger in many schizophrenia participants (believed to reflect an impaired sensory "gating" response; see Freedman et al, 1991), was highly correlated with intracategory semantic priming effects under automatic priming conditions. A "defect in inhibitory pathways" was suggested to underlie both phenomena.…”

Section: Relationship Of Semantic Priming Effects To Electrophysiologmentioning

confidence: 99%

Semantic priming in schizophrenia: A review and synthesis

Minzenberg

Ober

Vinogradov

2002

J Int Neuropsychol Soc

132

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In this paper, we present a review of semantic priming experiments in schizophrenia. Semantic priming paradigms show utility in assessing the role of deficits in semantic memory network access in the pathology of schizophrenia. The studies are placed in the context of current models of information processing. In this review we include all English-language reports (from peer-reviewed journals) of single-word semantic priming studies involving participants with schizophrenia. The studies to date show schizophrenic patients to exhibit variable semantic priming effects under automatic processing conditions, and consistent impairments under controlled0attentional conditions. We also describe associations with other neurocognitive dysfunction, neurochemical and electrophysiological disturbances, and clinical manifestations (such as thought disorder).

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“…Because response attenuation depends on prior experience of a stimulus, habituation has been studied as a form of nonassociative learning in a variety of models (Hawkins 1988;Burrell and Sahley 1998;Rose and Rankin 2001;Deshmukh and Bhalla 2003;Ezzeddine and Glanzman 2003). Furthermore, since habituation may underlie selective attention (Groves and Thomson 1970;Freedman et al 1991;Gillberg 2003), its premature onset could impair adequate discrimination between novel and preexperienced stimuli. Habituation deficits have been associated with schizophrenia (Freedman et al 1991;Adler et al 1999;Gillberg 2003;Meincke et al 2004), learning disabilities (Gillberg 2003;Slaats-Willemse et al 2003), and migraines (Siniatchkin et al 2003), among other conditions.…”

mentioning

confidence: 99%

“…Furthermore, since habituation may underlie selective attention (Groves and Thomson 1970;Freedman et al 1991;Gillberg 2003), its premature onset could impair adequate discrimination between novel and preexperienced stimuli. Habituation deficits have been associated with schizophrenia (Freedman et al 1991;Adler et al 1999;Gillberg 2003;Meincke et al 2004), learning disabilities (Gillberg 2003;Slaats-Willemse et al 2003), and migraines (Siniatchkin et al 2003), among other conditions.…”

mentioning

confidence: 99%

Protection from premature habituation requires functional mushroom bodies in Drosophila

Acevedo¹,

Froudarakis²,

Kanellopoulos³

et al. 2007

Learn. Mem.

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Diminished responses to stimuli defined as habituation can serve as a gating mechanism for repetitive environmental cues with little predictive value and importance. We demonstrate that wild-type animals diminish their responses to electric shock stimuli with properties characteristic of short-and long-term habituation. We used spatially restricted abrogation of neurotransmission to identify brain areas involved in this behavioral response. We find that the mushroom bodies and, in particular, the ␣/␤ lobes appear to guard against habituating prematurely to repetitive electric shock stimuli. In addition to protection from premature habituation, the mushroom bodies are essential for spontaneous recovery and dishabituation. These results reveal a novel modulatory role of the mushroom bodies on responses to repetitive stimuli in agreement with and complementary to their established roles in olfactory learning and memory.

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Elementary neuronal dysfunctions in schizophrenia

Cited by 244 publications

References 24 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

Semantic priming in schizophrenia: A review and synthesis

Protection from premature habituation requires functional mushroom bodies in Drosophila

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