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BACKGROUND - Learning and memory are impaired in schizophrenia. Some theories have proposed that one form of memory, habituation, is particularly impaired. Preliminary evidence suggests that memory impairment is associated with failed hippocampal habituation in patients with chronic schizophrenia. We studied how abnormal habituation of the hippocampus is related to relational memory deficits in the early stage of psychosis.
METHODS - We measured hippocampal activity in 62 patients with early psychosis and 70 healthy individuals using functional magnetic resonance imaging. Habituation was defined as the slope of functional magnetic resonance imaging signal change to repeated presentations of faces and objects. Relational memory ability was measured as the slope of preferential viewing during a face-scene pair eye movement task outside the scanner.
RESULTS - Patients with early psychosis showed impaired relational memory (p < .001) and less hippocampal habituation to objects (p = .01) than healthy control subjects. In the healthy control group, better relational memory was associated with faster anterior hippocampal habituation (faces, r = -.28, p = .03). In contrast, patients with early psychosis showed no brain-behavior relationship (r = .12, p = .40).
CONCLUSIONS - We found evidence for disrupted hippocampal habituation in the early stage of psychosis along with an altered association between hippocampal habituation and relational memory ability. These results suggest that neural habituation may provide a novel target for early cognitive interventions in psychosis.
Copyright © 2019 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
BACKGROUND - Neural habituation, the decrease in brain response to repeated stimulation, is a basic form of learning. There is strong evidence for behavioral and physiological habituation deficits in schizophrenia, and one previous study found reduced neural habituation within the hippocampus. However, it is unknown whether neural habituation deficits are specific to faces and limited to the hippocampus. Here we studied habituation of several brain regions in schizophrenia, using both face and object stimuli. Post-scan memory measures were administered to test for a link between hippocampal habituation and memory performance.
METHODS - During an fMRI scan, 23 patients with schizophrenia and 21 control subjects viewed blocks of a repeated neutral face or neutral object, and blocks of different neutral faces and neutral objects. Habituation in the hippocampus, primary visual cortex and fusiform face area (FFA) was compared between groups. Memory for faces, words, and word pairs was assessed after the scan.
RESULTS - Patients showed reduced habituation to faces in the hippocampus and primary visual cortex, but not the FFA. Healthy control subjects exhibited a pattern of hippocampal discrimination that distinguished between repeated and different images for both faces and objects, and schizophrenia patients did not. Hippocampal discrimination was positively correlated with memory for word pairs.
CONCLUSION - Patients with schizophrenia showed reduced habituation of the hippocampus and visual cortex, and a lack of neural discrimination between old and new images in the hippocampus. Hippocampal discrimination correlated with memory performance, suggesting reduced habituation may contribute to the memory deficits commonly observed in schizophrenia.
© 2013 Elsevier B.V. All rights reserved.
The cost of attending to a visual event can be the failure to consciously detect other events. This processing limitation is well illustrated by the attentional blink paradigm, in which searching for and attending to a target presented in a rapid serial visual presentation stream of distractors can impair one's ability to detect a second target presented soon thereafter. The attentional blink critically depends on 'top-down' attentional settings, for it does not occur if participants are asked to ignore the first target. Here we show that 'bottom-up' attention can also lead to a profound but ephemeral deficit in conscious perception: Presentation of a novel, unexpected, and task-irrelevant stimulus virtually abolishes conscious detection of a target presented within half a second after the 'Surprise' stimulus, but only for its earliest occurrences (generally 1 to 2 presentations). This powerful but short-lived deficit contrasts with a milder but more enduring form of attentional capture that accompanies singleton presentations in rapid serial visual presentations. We conclude that the capture of stimulus-driven attention alone can limit explicit perception.
The global obesity epidemic has heightened the need for an improved understanding of how body weight is controlled, and research using mouse models is critical to this effort. In this perspective, we provide a conceptual framework for investigation of feeding behavior in this species, with an emphasis on factors that influence study design, data interpretation, and relevance to feeding behavior in humans. Although we focus on the mouse, the principles presented can be applied to most other animal models. This document represents the current consensus view of investigators from the National Institutes of Health (NIH)-funded Mouse Metabolic Phenotyping Centers (MMPCs).
Copyright 2010 Elsevier Inc. All rights reserved.
Peptide YY(3-36) (PYY(3-36)), a peptide released postprandially by the gut, has been demonstrated to inhibit food intake. Little is known about the mechanism by which PYY(3-36) inhibits food intake, although the peptide has been shown to increase hypothalamic proopiomelanocortin (POMC) mRNA in vivo and to activate POMC neurons in an electrophysiological slice preparation. Understanding the physiology of PYY(3-36) is further complicated by the fact that some laboratories have had difficulty demonstrating inhibition of feeding by the peptide in rodents. We demonstrate here that, like cholecystokinin, PYY(3-36) dose-dependently inhibits food intake by approximately 20-45% over a 3- to 4-h period post ip administration, with no effect on 12-h food intake. This short-lived satiety effect is not seen in animals that are not thoroughly acclimated to handling and ip injection, thus potentially explaining the difficulty in reproducing the effect. Surprisingly, PYY(3-36) was equally efficacious in inducing satiety in wild-type and melanocortin-4 receptor (MC4-R)-deficient mice and thus does not appear to be dependent on MC4-R signaling. The expression of c-Fos, an indirect marker of neuronal activation, was also examined in forebrain and brainstem neurons after ip treatment with a dose of PYY(3-36) shown to induce satiety. The peptide induced no significant neuronal activation in the brainstem by this assay, and only modest activation of hypothalamic POMC neurons. Thus, unlike cholecystokinin, PYY(3-36)-induced satiety is atypical, because it does not produce detectable activation of brainstem satiety centers and is not dependent on MC4-R signaling.
According to modular models of cortical organization, many areas of the extrastriate cortex are dedicated to object categories. These models often assume an early processing stage for the detection of category membership. Can functional imaging isolate areas responsible for detection of members of a category, such as faces or letters? We consider whether responses in three different areas (two selective for faces and one selective for letters) support category detection. Activity in these areas habituates to the repeated presentation of one exemplar more than to the presentation of different exemplars of the same category, but only for the category for which the area is selective. Thus, these areas appear to play computational roles more complex than detection, processing stimuli at the individual level. Drawing from prior work, we suggest that face-selective areas may be involved in the perception of faces at the individual level, whereas letter-selective regions may be tuning themselves to font information in order to recognize letters more efficiently.