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Jeffrey A. Gray - One of the best experts on this subject based on the ideXlab platform.
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GABA transmission in the ventral pallidum is not involved in the control of Latent Inhibition in the rat
Neuroscience, 2003Co-Authors: Natalia Lawrence, Jeffrey A. Gray, Trevor Sharp, S.p. Peters, Andrew M. J. YoungAbstract:Latent Inhibition describes a process of learning to ignore stimuli of no consequence, and is disrupted in acute, positive-symptomatic schizophrenia. Understanding the neural basis of Latent Inhibition in animals may help to elucidate the neural dysfunction underlying positive schizophrenic symptoms in man. Evidence suggests a crucial role for dopamine transmission in the nucleus accumbens in the control of Latent Inhibition. The present studies investigated the role of the GABA-ergic efferent from the nucleus accumbens to the ventral pallidum in Latent Inhibition. The GABA(A) agonist muscimol (4.56 ng/microl), and antagonist picrotoxin (0.2 microg/microl), were infused into the ventral pallidum, and effects on Latent Inhibition were assessed using a conditioned suppression procedure. Neither drug produced specific effects on Latent Inhibition when given alone and, in the case of muscimol, failed to reverse the disruption of Latent Inhibition induced by systemic amphetamine. In addition to significant non-specific drug effects, a positive control experiment revealed that intra-pallidal picrotoxin significantly enhanced locomotion, suggesting that our manipulations of ventral pallidal GABA function were behaviourally effective. We conclude that modulating ventral pallidal GABA transmission does not affect Latent Inhibition. The implications of this finding for theories of the neural circuitry mediating Latent Inhibition and for understanding the functional role of ventral pallidal GABA transmission are discussed.
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Nucleus accumbens, entorhinal cortex and Latent Inhibition: a neural network model.
Behavioural brain research, 2001Co-Authors: Nestor A. Schmajuk, Landon P. Cox, Jeffrey A. GrayAbstract:A neural network model of classical conditioning (Schmajuk, Lam, and Gray, J. Exp. Psychol.: Anim. Behav. Process, 22, 1996, 321-349) is applied to the description of the neural substrates of Latent Inhibition. Experimental data suggest that Latent Inhibition might be controlled by a circuit that involves the hippocampus, the entorhinal cortex, the nucleus accumbens, and the mesolimbic dopaminergic projection from the ventral tegmental area to the accumbens. By mapping different nodes and connections in the model onto this brain circuit, computer simulations demonstrate that, in most cases, the model provides a good quantitative description of: (1) the impairment of Latent Inhibition by lesions of the shell of the nucleus accumbens; (2) the restoration of Latent Inhibition by haloperidol following lesions of the shell; (3) the preservation of Latent Inhibition by lesions of the core of the nucleus accumbens; (4) the facilitation of Latent Inhibition by combined shell core lesions and by core lesions with extended conditioning; (5) the impairment of Latent Inhibition following lesions of the entorhinal cortex or the hippocampus; and (6) the restoration of Latent Inhibition by haloperidol following lesions of the entorhinal cortex and ventral subiculum. In addition, the model is able to describe neural activity in the nucleus accumbens.
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Modulation of Latent Inhibition in the rat by altered dopamine transmission in the nucleus accumbens at the time of conditioning
Neuroscience, 2000Co-Authors: M.h. Joseph, Andrew M. J. Young, Paula M. Moran, S.l. Peters, G.a. Grigoryan, Jeffrey A. GrayAbstract:Latent Inhibition describes a process by which pre-exposure of a stimulus without consequence retards the learning of subsequent conditioned associations with that stimulus. It is well established that Latent Inhibition in rats is impaired by increased dopamine function and potentiated by reduced dopamine function. Previous evidence has suggested that these effects are modulated via the meso-accumbens dopamine projections. We have now undertaken three experiments to examine this issue directly, especially in the light of one study in which Latent Inhibition was reported to be unaffected by direct injection of amphetamine into the accumbens. Latent Inhibition was studied using the effect of pre-exposure of a tone stimulus on the subsequent formation of a conditioned emotional response to the tone. 6-Hydroxydopamine-induced lesions of dopamine terminals in the nucleus accumbens resulted in potentiation of Latent Inhibition. Bilateral local injections of the dopamine antagonist haloperidol into the nucleus accumbens (0.5 microg/side) before conditioning also potentiated Latent Inhibition. Moreover, such injections were able to reverse the disruptive effect of systemic amphetamine (1mg/kg, i.p.) on Latent Inhibition. Bilateral local injection of amphetamine (5 microg/side) into the nucleus accumbens before conditioning was able to disrupt Latent Inhibition, provided that it was preceded by a systemic injection of amphetamine (1mg/kg) 24h earlier.We conclude that the attenuation of Latent Inhibition by increased dopamine function in the nucleus accumbens is brought about by impulse-dependent release of the neurotransmitter occurring at the time of conditioning. The previously reported failure to disrupt Latent Inhibition with intra-accumbens amphetamine is probably due to impulse-independent release of dopamine. The implications of these conclusions for theories linking disrupted Latent Inhibition to the attentional deficits in schizophrenia, and to the dopamine theory of this disorder, are discussed.
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Latent Inhibition of conditioned dopamine release in rat nucleus accumbens
Neuroscience, 1993Co-Authors: Andrew M. J. Young, M.h. Joseph, Jeffrey A. GrayAbstract:Classical conditioning both to rewarding and to aversive stimuli is sensitive to drugs which act on the dopaminergic system: amphetamine enhances conditioning and neuroteptics attenuate it.3,25 Many lines of evidence point to the nucleus accumbens as being part of an anatomical substrate for reward.8,34 We have examined the release of dopamine in the nucleus accumbens during classical aversive conditioning using microdialysis in the unrestrained rat. Two mild footshocks caused a release of dopamine, which was potentiated when each footshock was immediately preceded by a novel tone or light stimulus. Presentation of either of these stimuli after conditioning elicited an increase in dopamine, only to that stimulus which had been conditioned; presentation of either stimulus after footshock alone without conditioning produced no dopamine response. Latent Inhibition is a process whereby pre-exposure to a stimulus without consequence impairs learning about that stimulus at subsequent conditioning.20,21 This process too is believed to be under the control of dopaminergic systems,30 particularly in nucleus accumbens.28 Pre-exposure to the tone stimulus both markedly attenuated the potentiation of dopamine release at conditioning and abolished the conditioned release of dopamine at subsequent tone presentation. This is the first report of direct measurement of potentiated dopamine release during conditioning, and may provide a neurochemical basis for the effects of dopaminergic drugs on conditioning and Latent Inhibition. The results also support the hypothesis that disrupted Latent Inhibition in schizophrenia reflects increased mesolimbic dopamine function.
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5,7-Dihydroxytryptamine lesions in the fornix—fimbria attenuate Latent Inhibition
Behavioral and neural biology, 1993Co-Authors: Helen J. Cassaday, Jonathan H. Williams, Stephen N. Mitchell, Jeffrey A. GrayAbstract:When animals are preexposed to a stimulus without consequence they are subsequently slower to associate this stimulus with an important event, such as footshock. This retarding effect of stimulus preexposure is called Latent Inhibition and can be demonstrated in a variety of classical and instrumental paradigms and in a wide range of species, including man. Latent Inhibition is disrupted in acute schizophrenics and by amphetamine treatment in both rat and man. The present study investigated the role of hippocampal 5HT terminals in Latent Inhibition using a conditioned suppression procedure with male Sprague-Dawley rats. Microinjections of 5,7-dihydroxytryptamine in the fornix-fimbria significantly reduced hippocampal indoleamine levels and attenuated Latent Inhibition of conditioned suppression. This finding supports the hypothesis that the destruction of mesolimbic 5-hydroxytryptamine terminals reduces Latent Inhibition. This result is discussed in terms of the possible involvement of reduced serotonergic function in schizophrenic attentional disorder. In addition to the predicted lesion effect, biochemical analyses indicated that experimental treatments in the Latent Inhibition procedure altered neurotransmitter turnover: utilization ratios for 5-hydroxytryptamine and/or dopamine were increased in preexposed relative to nonpreexposed animals in four of the six brain regions sampled.
Andrew M. J. Young - One of the best experts on this subject based on the ideXlab platform.
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Disruption of Latent Inhibition by subchronic phencyclidine pretreatment in rats.
Behavioural brain research, 2019Co-Authors: Asmaa M. Al-ali, Andrew M. J. YoungAbstract:Abstract Repeated subchronic treatment with the NMDA-receptor antagonist, phencyclidine, causes behavioural changes in rats, which resemble cognitive and negative symptoms of schizophrenia. However, its effects on behaviours modelling positive symptoms are less clear. This study investigated whether subchronic phencyclidine pretreatment affected Latent Inhibition: impaired conditioning following repeated preexposure of the to-be-conditioned stimulus. Female Lister-hooded rats were pretreated with phencyclidine or saline twice/day for 5 days, then remained drug-free for 10 days before Latent Inhibition testing. Saline pretreated animals showed Latent Inhibition, as expected. However, phencyclidine pretreated animals showed no Latent Inhibition: the effect of preexposure was attenuated, with no change in basic learning. Thus subchronic phencyclidine pretreatment does disrupt Latent Inhibition, and, importantly, this occurs after withdrawal from the drug, implicating changes in brain function enduring well beyond the time that the drug is present in the brain. In a separate task, discrimination of a novel object was significantly impaired by phencyclidine pretreatment confirming that five days of subchronic pretreatment was sufficient to invoke behavioural impairment previously reported after seven days pretreatment.
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GABA transmission in the ventral pallidum is not involved in the control of Latent Inhibition in the rat
Neuroscience, 2003Co-Authors: Natalia Lawrence, Jeffrey A. Gray, Trevor Sharp, S.p. Peters, Andrew M. J. YoungAbstract:Latent Inhibition describes a process of learning to ignore stimuli of no consequence, and is disrupted in acute, positive-symptomatic schizophrenia. Understanding the neural basis of Latent Inhibition in animals may help to elucidate the neural dysfunction underlying positive schizophrenic symptoms in man. Evidence suggests a crucial role for dopamine transmission in the nucleus accumbens in the control of Latent Inhibition. The present studies investigated the role of the GABA-ergic efferent from the nucleus accumbens to the ventral pallidum in Latent Inhibition. The GABA(A) agonist muscimol (4.56 ng/microl), and antagonist picrotoxin (0.2 microg/microl), were infused into the ventral pallidum, and effects on Latent Inhibition were assessed using a conditioned suppression procedure. Neither drug produced specific effects on Latent Inhibition when given alone and, in the case of muscimol, failed to reverse the disruption of Latent Inhibition induced by systemic amphetamine. In addition to significant non-specific drug effects, a positive control experiment revealed that intra-pallidal picrotoxin significantly enhanced locomotion, suggesting that our manipulations of ventral pallidal GABA function were behaviourally effective. We conclude that modulating ventral pallidal GABA transmission does not affect Latent Inhibition. The implications of this finding for theories of the neural circuitry mediating Latent Inhibition and for understanding the functional role of ventral pallidal GABA transmission are discussed.
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Modulation of Latent Inhibition in the rat by altered dopamine transmission in the nucleus accumbens at the time of conditioning
Neuroscience, 2000Co-Authors: M.h. Joseph, Andrew M. J. Young, Paula M. Moran, S.l. Peters, G.a. Grigoryan, Jeffrey A. GrayAbstract:Latent Inhibition describes a process by which pre-exposure of a stimulus without consequence retards the learning of subsequent conditioned associations with that stimulus. It is well established that Latent Inhibition in rats is impaired by increased dopamine function and potentiated by reduced dopamine function. Previous evidence has suggested that these effects are modulated via the meso-accumbens dopamine projections. We have now undertaken three experiments to examine this issue directly, especially in the light of one study in which Latent Inhibition was reported to be unaffected by direct injection of amphetamine into the accumbens. Latent Inhibition was studied using the effect of pre-exposure of a tone stimulus on the subsequent formation of a conditioned emotional response to the tone. 6-Hydroxydopamine-induced lesions of dopamine terminals in the nucleus accumbens resulted in potentiation of Latent Inhibition. Bilateral local injections of the dopamine antagonist haloperidol into the nucleus accumbens (0.5 microg/side) before conditioning also potentiated Latent Inhibition. Moreover, such injections were able to reverse the disruptive effect of systemic amphetamine (1mg/kg, i.p.) on Latent Inhibition. Bilateral local injection of amphetamine (5 microg/side) into the nucleus accumbens before conditioning was able to disrupt Latent Inhibition, provided that it was preceded by a systemic injection of amphetamine (1mg/kg) 24h earlier.We conclude that the attenuation of Latent Inhibition by increased dopamine function in the nucleus accumbens is brought about by impulse-dependent release of the neurotransmitter occurring at the time of conditioning. The previously reported failure to disrupt Latent Inhibition with intra-accumbens amphetamine is probably due to impulse-independent release of dopamine. The implications of these conclusions for theories linking disrupted Latent Inhibition to the attentional deficits in schizophrenia, and to the dopamine theory of this disorder, are discussed.
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Latent Inhibition of conditioned dopamine release in rat nucleus accumbens
Neuroscience, 1993Co-Authors: Andrew M. J. Young, M.h. Joseph, Jeffrey A. GrayAbstract:Classical conditioning both to rewarding and to aversive stimuli is sensitive to drugs which act on the dopaminergic system: amphetamine enhances conditioning and neuroteptics attenuate it.3,25 Many lines of evidence point to the nucleus accumbens as being part of an anatomical substrate for reward.8,34 We have examined the release of dopamine in the nucleus accumbens during classical aversive conditioning using microdialysis in the unrestrained rat. Two mild footshocks caused a release of dopamine, which was potentiated when each footshock was immediately preceded by a novel tone or light stimulus. Presentation of either of these stimuli after conditioning elicited an increase in dopamine, only to that stimulus which had been conditioned; presentation of either stimulus after footshock alone without conditioning produced no dopamine response. Latent Inhibition is a process whereby pre-exposure to a stimulus without consequence impairs learning about that stimulus at subsequent conditioning.20,21 This process too is believed to be under the control of dopaminergic systems,30 particularly in nucleus accumbens.28 Pre-exposure to the tone stimulus both markedly attenuated the potentiation of dopamine release at conditioning and abolished the conditioned release of dopamine at subsequent tone presentation. This is the first report of direct measurement of potentiated dopamine release during conditioning, and may provide a neurochemical basis for the effects of dopaminergic drugs on conditioning and Latent Inhibition. The results also support the hypothesis that disrupted Latent Inhibition in schizophrenia reflects increased mesolimbic dopamine function.
Elias Tsakanikos - One of the best experts on this subject based on the ideXlab platform.
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Relationship between behavioral measures of anxiety and Latent Inhibition in mature rats.
Learning & behavior, 2018Co-Authors: Elias Tsakanikos, Phil ReedAbstract:This study adopted a novel approach to relating nonhuman and human studies of anxiety and Latent Inhibition, by exploring the degree to which rats' "temperaments" in relation to anxiety predicted the development of Latent Inhibition. It investigated whether anxiety levels in one situation (i.e., an elevated-plus maze) involving 38 intact, mature rats, could predict performance on a Latent Inhibition task (i.e., an animal model of attention), and, thus, reproduce findings from human studies. Rats were subjected to two tasks: a novel within-subject, appetitive stimulus pre-exposure procedure, and an elevated-plus maze task. In the stimulus pre-exposure task, non-reinforced exposure to a light led to facilitation of conditioning (perceptual learning) during the first 3 days, and to retardation of conditioning (Latent Inhibition) during the last 5 days. In the elevated-plus maze task, moderate levels of anxiety were observed. Regression analyses revealed that anxiety levels (plus maze) were a significant predictor of Latent Inhibition (stimulus pre-exposure). Measures of locomotor activity did not predict performance on the Latent Inhibition task. Rats with moderate levels of anxiety had better performance in the late Inhibition task than animals with low levels of anxiety. These data and the methodology have implications for understanding nonhuman models of schizophrenia, and for the design of studies investigating these issues with nonhumans.
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Latent Inhibition, visual pop-out and schizotypy: is disruption of Latent Inhibition due to enhanced stimulus salience?
Personality and Individual Differences, 2004Co-Authors: Elias TsakanikosAbstract:The disruption of Latent Inhibition (i.e. conditioning rate to a preexposed (PE) stimulus elevated to the level of a non-preexposed (NPE) stimulus) within the schizophrenia continuum has often been attributed to increased attentional distractibility by irrelevant stimuli. It has not been established, however, whether such a putative distractibility is due to a tendency to treat any stimulus as salient on the basis of physical characteristics (enhanced stimulus salience). In order to test this possibility, extreme schizotypy scorers were selected from a larger sample of undergraduate students to take part in a two-experimental investigation. In Experiment 1, Latent Inhibition, as assessed in a visual search paradigm, was disrupted in high-schizotypy scorers, but was intact for low-schizotypy scorers replicating past findings. In Experiment 2, no evidence for an enhanced stimulus salience, as assessed in a visual pop-out task, was found for high-schizotypy scorers. Accuracy rate for both high- and low-schizotypy scorers followed the hierarchically differentiated pattern of the stimulus salience level, failing to support the hypothesis that high-schizotypy scorers tend to treat any stimulus as salient on the basis of physical characteristics. The obtained results suggest that the disruption of Latent Inhibition in high-schizotypy scorers is not associated with a tendency to experience any event (i.e. both PE and NPE stimuli) as perceptually salient.
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Latent Inhibition and context change in psychometrically defined schizotypy
Personality and Individual Differences, 2004Co-Authors: Elias Tsakanikos, Phil ReedAbstract:Abstract The disruption of Latent Inhibition within the schizophrenia spectrum has often been interpreted either as a result of increased attentional distractibility (attentional account) or as a result of deficient interference of past associations (associative account). The aim of the present investigation was to test competing predictions, as derived from the above theoretical accounts. In a visual search paradigm of Latent Inhibition, accuracy was examined as a function of prior experience with the target, and psychometrically defined schizotypy. In Experiment 1 (N=60), no context change was introduced. In accord with past evidence, Latent Inhibition was found to be intact in low-, but disrupted in high-schizotypy scorers, a result predicted both by attentional and associative accounts. In Experiment 2 (N=60), a context change was introduced. As predicted by past evidence, Latent Inhibition was disrupted in low-schizotypy scorers. However, Latent Inhibition was found to be intact in high-schizotypy scorers, a finding accommodated by attentional, but not associative accounts. Theoretical implications and alternative interpretations are also considered.
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Latent Inhibition AND PSYCHOMETRICALLY DEFINED SCHIZOTYPY:AN EXPERIMENTAL INVESTIGATION
2003Co-Authors: Elias TsakanikosAbstract:The review of the literature suggests that the interpretation of the disruption of Latent Inhibition within the schizophrenia continuum remains elusive due to a number of methodological and theoretical problems. This thesis adopted a personality-based approach to experimental psychopathology testing alternative interpretations of Latent Inhibition deficits as a function of psychotic-like features in non-clinical participants. Results from 12 Experiments are discussed in terms of a two-component (attentional + associative) model of Latent Inhibition deficits.
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The influence of a distractor during compound preexposure on Latent Inhibition
Animal Learning & Behavior, 2002Co-Authors: Phil Reed, Elias TsakanikosAbstract:Nonreinforced exposure to a nontarget stimulus that was followed by nonreinforced exposure to a target/nontarget simultaneous compound stimulus resulted in enhanced Latent Inhibition of the target. Conditioning was slower after this treatment than after nonreinforced exposure to the target stimulus alone (Experiment 1). However, a salient auditory stimulus presented immediately after the compound in the second phase reduced levels of Latent Inhibition, relative to the enhanced Latent Inhibition produced when no such extracompound stimulus was presented (Experiments 2 and 3). This effect was not noted if the salient auditory cue was presented 10 sec after the termination of the compound stimulus (Experiment 4). In Experiment 5, there was no disruption of simple Latent Inhibition produced by a salient stimulus. These results are consistent with enhanced Latent Inhibition’s being produced by the formation of within-compound associations, which are disrupted by the salient extracompound stimuli.
Phil Reed - One of the best experts on this subject based on the ideXlab platform.
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Relationship between behavioral measures of anxiety and Latent Inhibition in mature rats.
Learning & behavior, 2018Co-Authors: Elias Tsakanikos, Phil ReedAbstract:This study adopted a novel approach to relating nonhuman and human studies of anxiety and Latent Inhibition, by exploring the degree to which rats' "temperaments" in relation to anxiety predicted the development of Latent Inhibition. It investigated whether anxiety levels in one situation (i.e., an elevated-plus maze) involving 38 intact, mature rats, could predict performance on a Latent Inhibition task (i.e., an animal model of attention), and, thus, reproduce findings from human studies. Rats were subjected to two tasks: a novel within-subject, appetitive stimulus pre-exposure procedure, and an elevated-plus maze task. In the stimulus pre-exposure task, non-reinforced exposure to a light led to facilitation of conditioning (perceptual learning) during the first 3 days, and to retardation of conditioning (Latent Inhibition) during the last 5 days. In the elevated-plus maze task, moderate levels of anxiety were observed. Regression analyses revealed that anxiety levels (plus maze) were a significant predictor of Latent Inhibition (stimulus pre-exposure). Measures of locomotor activity did not predict performance on the Latent Inhibition task. Rats with moderate levels of anxiety had better performance in the late Inhibition task than animals with low levels of anxiety. These data and the methodology have implications for understanding nonhuman models of schizophrenia, and for the design of studies investigating these issues with nonhumans.
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Latent Inhibition and context change in psychometrically defined schizotypy
Personality and Individual Differences, 2004Co-Authors: Elias Tsakanikos, Phil ReedAbstract:Abstract The disruption of Latent Inhibition within the schizophrenia spectrum has often been interpreted either as a result of increased attentional distractibility (attentional account) or as a result of deficient interference of past associations (associative account). The aim of the present investigation was to test competing predictions, as derived from the above theoretical accounts. In a visual search paradigm of Latent Inhibition, accuracy was examined as a function of prior experience with the target, and psychometrically defined schizotypy. In Experiment 1 (N=60), no context change was introduced. In accord with past evidence, Latent Inhibition was found to be intact in low-, but disrupted in high-schizotypy scorers, a result predicted both by attentional and associative accounts. In Experiment 2 (N=60), a context change was introduced. As predicted by past evidence, Latent Inhibition was disrupted in low-schizotypy scorers. However, Latent Inhibition was found to be intact in high-schizotypy scorers, a finding accommodated by attentional, but not associative accounts. Theoretical implications and alternative interpretations are also considered.
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The influence of a distractor during compound preexposure on Latent Inhibition
Animal Learning & Behavior, 2002Co-Authors: Phil Reed, Elias TsakanikosAbstract:Nonreinforced exposure to a nontarget stimulus that was followed by nonreinforced exposure to a target/nontarget simultaneous compound stimulus resulted in enhanced Latent Inhibition of the target. Conditioning was slower after this treatment than after nonreinforced exposure to the target stimulus alone (Experiment 1). However, a salient auditory stimulus presented immediately after the compound in the second phase reduced levels of Latent Inhibition, relative to the enhanced Latent Inhibition produced when no such extracompound stimulus was presented (Experiments 2 and 3). This effect was not noted if the salient auditory cue was presented 10 sec after the termination of the compound stimulus (Experiment 4). In Experiment 5, there was no disruption of simple Latent Inhibition produced by a salient stimulus. These results are consistent with enhanced Latent Inhibition’s being produced by the formation of within-compound associations, which are disrupted by the salient extracompound stimuli.
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Extinction of enhanced Latent Inhibition
Animal Learning & Behavior, 1997Co-Authors: Phil Reed, Pany Petrochilos, Natasha Upal, Martin BaumAbstract:Hungry rats were used in a classical conditioning procedure in which visual stimuli were paired with food. Conditions in which nonreinforced exposure to a nontarget stimulus was followed by exposure to a simultaneous compound nontarget/target stimulus (a blocking procedure) resulted in enhanced Latent Inhibition to the target relative to exposure to the nontarget, followed by exposure to the target stimulus alone. A third phase of nonreinforced exposure training, in which the target was exposed alone following the compound, reduced levels of Latent Inhibition relative to results obtained with the blocking procedure. Experiments also suggested that this was not the result of restoration of associability by the omission of an expected presentation of the nontarget stimulus in the final preexposure phase. These results suggest that enhanced Latent Inhibition is due to summation of a direct-target-no-event association and a second-order association of these elements via target-nontarget and nontarget-no-event association. Exposure to the target after compound exposure extinguished the target-nontarget association and reduced the sources of no-event learning for the target.
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ENHANCED Latent Inhibition FOLLOWING COMPOUND PRE-EXPOSURE
The Quarterly journal of experimental psychology. B Comparative and physiological psychology, 1995Co-Authors: Phil ReedAbstract:The influence of non-reinforced exposure to compound stimuli on subsequent appetitive classical conditioning was examined in five experiments with rats as the subjects. Non-reinforced exposure to a visual stimulus retarded subsequent acquisition of conditioned responding relative to a non-pre-exposed condition (Latent Inhibition). If the target stimulus was pre-exposed in compound with a second (non-target) stimulus, then Latent Inhibition was abolished. Exposure to the non-target stimulus prior to compound exposure had varying effects on subsequent conditioning to the target: 40 exposures to the non-target stimulus resulted in Latent Inhibition to the target stimulus that was comparable in magnitude to that observed when the target stimulus was exposed in isolation; 120 exposures to the non-target stimulus enhanced Latent Inhibition to the target stimulus.
Ignacio Morón - One of the best experts on this subject based on the ideXlab platform.
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Latent Inhibition of conditioned taste aversion in rats with amygdaloid or hippocampal lesions
Neuroscience Communications, 2016Co-Authors: Andrés Molero-chamizo, Guadalupe Nathzidy Rivera-urbina, Maria Angeles Ballesteros, Ignacio MorónAbstract:The amygdala and hippocampus play crucial roles in the Latent Inhibition of different conditioned responses, such as fear conditioned. Nevertheless, the involvement of these structures in the Latent Inhibition of conditioned taste aversion (CTA) is uncertain. In the present study, we explore the relevance of the amygdala and hippocampus in Latent Inhibition using a CTA paradigm. The effects of taste pre-exposures vs. non-pre-exposures on taste aversion conditioning were compared in Wistar rats with amygdaloid or hippocampal excitotoxic lesions. All pre-exposed animals consumed significantly more on the test day than did non-pre-exposed animals. Therefore, neither amygdaloid nor hippocampal lesions prevented the Latent Inhibition phenomenon. However, the expected taste neophobia was potentially affected by lesions to either the amygdala or hippocampus. These findings suggest that the amygdala and hippocampus seem to be necessary for taste neophobia but not for the acquisition of Latent Inhibition of CTA. The differential involvement of both structures in Latent Inhibition under different associative learning paradigms is briefly discussed.
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Latent Inhibition of conditioned taste aversion in rats with excitotoxic dorsal hippocampal lesions.
Journal of neuroscience research, 2015Co-Authors: Andrés Molero-chamizo, Ignacio MorónAbstract:The hippocampus plays crucial roles for the acquisition of Latent Inhibition in different associative learning procedures, such as fear conditioning. However, the involvement of the hippocampus in the Latent Inhibition of conditioned taste aversion (CTA) is uncertain. Because different subregions of the hippocampus are associated with distinct functions, it is possible that specific regions of this structure are selectively involved in this learning. To explore the relationship between the dorsal hippocampal region and the Latent Inhibition of CTA, we analyzed the behavioral effects of excitotoxic lesions of the dorsal hippocampus vs. sham lesions in this paradigm. The results provide no evidence that the Latent Inhibition of CTA is compromised in rats with excitotoxic dorsal hippocampal lesions. The differential involvement of specific hippocampal regions in the Latent Inhibition of other associative learning paradigms is briefly discussed.
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Time of day-dependent Latent Inhibition of conditioned taste aversions in rats.
Neurobiology of learning and memory, 2004Co-Authors: Tatiana Manrique, A. Molero, M.angeles Ballesteros, Ignacio Morón, Milagros Gallo, André A. FentonAbstract:We have determined that the temporal context of drinking can modulate Latent Inhibition of learned saline aversions in Wistar rats by changing the time of day of drinking of the preexposure and conditioning phases. Latent Inhibition was absent in the group preexposed and conditioned to saline at different times of the day, but not in the group that was preexposed and conditioned at the same time of day. The results confirm a previous report that the time of day can modulate taste aversion learning independently of other environmental cues. It is proposed that the features and duration of the habituation training to the temporal contexts used may be critical for time-dependent Latent Inhibition to appear.
