Empty words in schizophrenia. Semantic satiation as the mechanism of formal language disorders

The aim of the research was to explain the cognitive mechanisms responsible for formal language disorders in schizophrenia by relating them to the semantic satiation effect.The semantic satiation is the subjective and temporary experience of loss of meaning of words which are repeatedly and rapidly pronounced. Saying it aloud or fixating it the person ceases to understand the word's meaning still being able to recognizing its formal features. The loss of access to the meaning of words and building the utterances on the basis of formal aspects of words is a common feature of schizophrenic language. Therefore it could be assumed that schizophrenic patients would be prone to satiation effect more than healthy subjects.Semantic satiation was determined for patients suffering from schizophrenia and for healthy controls. Participants task was to compare the meanings of two words presented on a computer screen and decide if they are semantically related. Negative, positive and emotionally neutral words were used as the first element for each pair and they were satiated by the prolonged presentation. It was expected that the loss of meaning of satiated word would delay participants’ lexical decision and that this effect should be stronger for the schizophrenic than for control group.The results confirmed that people suffering from schizophrenia are more susceptible for semantic satiation effect. Also it was observed that in this group the satiation effect depends on valence of words. Emotionally positive and negative words were satiated faster than neutral ones.

Revisiting Satiation: Evidence for an Equalization Response Strategy

This reply revisits the topic of syntactic satiation as first discussed in Snyder 2000. I argue that the satiation effect reported in Snyder 2000 is the result of a response strategy in which participants attempt to equalize the number of yes and no responses, a strategy enabled by the design features of Snyder's original experiment. Four predictions differentiate the response strategy from a true satiation effect. Nine experiments are presented to test these predictions. The results are discussed with respect to the nature of satiation, the stability of acceptability judgments, and the consequences for linguistic methodology.

Interaction of apolipoprotein AIV with cholecystokinin on the control of food intake

Apolipoprotein AIV (apo AIV) and cholecystokinin (CCK) are peptides that act both peripherally and centrally to reduce food intake by decreasing meal size. The present study examined the effects of intraperitoneally administered bolus doses of recombinant apo AIV, CCK-8, and a combination of subthreshold doses of apo AIV and CCK on 4-h food intake in rats that were fasted overnight. Apo AIV at 100 μg/kg reduced food intake significantly relative to the saline control for 1 h, as did doses of CCK-8 at or above 0.125 μg/kg. Doses of apo AIV (50 μg/kg) or CCK (0.06 μg/kg) alone had no effect on food intake. However, when these subthreshold doses of apo AIV and CCK were administered together, the combination produced a significant inhibition of food intake relative to saline controls ( P < 0.001), and the duration of the effect was longer than that caused by the administration of either apo AIV or CCK alone. The satiation effect produced by CCK-8 + apo AIV was attenuated by lorglumide, a CCK1 receptor antagonist. We conclude that, whereas the intraperitoneal administration of doses of either recombinant apo AIV or CCK at or above threshold levels reduces food intake, the coadministration of subthreshold doses of the two peptides is highly satiating and works via CCK1 receptor.

Leptin and CCK selectively activate vagal afferent neurons innervating the stomach and duodenum

The hormone leptin and the gut peptide CCK synergistically interact to enhance the process of satiation. Although this interaction may occur at several levels of the neuroaxis, our previous results indicate that leptin can specifically enhance the satiation effect of CCK by acting on subdiaphragmatic vagal afferent neurons. Because of this localized action, we hypothesized that a high proportion of vagal afferent neurons innervating the stomach or duodenum would be responsive to leptin and/or CCK. To test this hypothesis, we measured changes in cytosolic calcium levels induced by leptin and CCK in cultured nodose ganglion neurons labeled with a retrograde neuronal tracer injected into either the stomach or the duodenum. In the neurons labeled from the stomach, CCK activated 74% (39 of 53) compared with only 35% (34 of 97) of nonlableled cells. Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive. Leptin activated 42% (22 of 53) of the stomach innervating neurons compared with 26% of nonlabeled neurons. All of the leptin-sensitive neurons labeled from the stomach also responded to CCK. In the neurons labeled from the duodenum, CCK activated 71% (20 of 28). Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive. Leptin activated 46% (13 of 28) of these duodenal innervating neurons, of which 89% (8 of 9) were capsaicin-sensitive. Among neurons labeled from the duodenum 43% (12 of 28) were responsive to both leptin and CCK, compared with only 15% (15 of 97) of unlabeled neurons. Our results support the hypothesis that vagal afferent sensitivity to CCK and leptin is concentrated in neurons that innervate the stomach and duodenum. These specific visceral afferent populations are likely to comprise a substrate through which acute leptin/CCK interactions enhance satiation.