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• W2097439999 endingPage "92" @default.
• W2097439999 startingPage "83" @default.
• W2097439999 abstract "Dark Agouti rats were lesioned by intra-ventricular injection of 5,7-dihydroxytryptamine (DHT) and, 2 weeks later, learning was tested in a conditioned suppression of drinking procedure. Lesioned and vehicle-injected control rats were conditioned with a discrete stimulus (tone or light conditioned stimulus, CS) twice paired with footshock (unconditioned stimulus), with or without a 30-s trace interval between theseevents to produce strong and weak learning conditions (a trace conditioning effect). During this conditioning session, the alternate stimulus (light or tone) was presented continuously in the background. Since the 5,7-DHT lesion also reduced the baseline licking response in the experimental chambers, we used drinkingc during the first minute, when this non-specific effect was minimal, as the dependent variable. We tested conditioning to target CS and to the alternative experimental background stimulus in exactly the same way in the same rats. We found that a level of serotonergic depletion without any intrinsic action on the trace conditioning effect nevertheless increased conditioning to the alternative background stimulus, irrespective of trace interval or stimulus modality. Thus, for both light and tone stimuli, the effect of serotonergic depletion depended only on the discrete target versus diffuse background role of the stimulus in use. These findings have implications for the modification of human cognition by serotonergic drugs." @default.
• W2097439999 created "2016-06-24" @default.
• W2097439999 creator A5057849647 @default.
• W2097439999 creator A5066735641 @default.
• W2097439999 creator A5078107927 @default.
• W2097439999 date "2001-03-01" @default.
• W2097439999 modified "2023-10-14" @default.
• W2097439999 title "Serotonergic depletion increases conditioned suppression to background stimuli in the rat" @default.
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• W2097439999 doi "https://doi.org/10.1177/026988110101500204" @default.
• W2097439999 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11448092" @default.
• W2097439999 hasPublicationYear "2001" @default.
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