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Latent Inhibition (latent + inhibition)
Selected AbstractsEffects of insular cortex lesions on conditioned taste aversion and latent inhibition in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2007Christopher Roman Abstract The present study tested the hypothesis that lesions of the insular cortex of the rat retard the acquisition of conditioned taste aversions (CTAs) because of an impairment in the detection of the novelty of taste stimuli. Demonstrating the expected latent inhibition effect, nonlesioned control subjects acquired CTAs more rapidly when the conditioned stimulus (0.15% sodium saccharin) was novel rather than familiar (achieved by pre-exposure to the to-be-conditioned taste cue). However, rats with insular cortex lesions acquired taste aversions at the same slow rate regardless of whether the saccharin was novel or familiar. The pattern of behavioural deficits obtained cannot be interpreted as disruptions of taste detection or stimulus intensity, but is consistent with the view that insular cortex lesions disrupt taste neophobia, a dysfunction that consequently retards CTA acquisition because of a latent inhibition-like effect. [source] Double dissociation of the effects of selective nucleus accumbens core and shell lesions on impulsive-choice behaviour and salience learning in ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2005Helen H. J. Pothuizen Abstract The nucleus accumbens can be subdivided into at least two anatomically distinct subregions: a dorsolateral ,core' and a ventromedial ,shell', and this distinction may extend to a functional dissociation. Here, we contrasted the effects of selective excitotoxic core and medial shell lesions on impulsive-choice behaviour using a delayed reward choice paradigm and a differential reward for low rates of responding (DRL) test, against a form of salience learning known as latent inhibition (LI). Core lesions led to enhanced impulsive choices as evidenced by a more pronounced shift from choosing a continuously reinforced lever to a partially reinforced lever, when a delay between lever press and reward delivery was imposed selectively on the former. The core lesions also impaired performance on a DRL task that required withholding the response for a fixed period of time in order to earn a reward. Medial shell lesions had no effect on these two tasks, but abolished the LI effect, as revealed by the failure of stimulus pre-exposure to retard subsequent conditioning to that stimulus in an active avoidance procedure in the lesioned animals. As expected, selective core lesions spared LI. The double dissociations demonstrated here support a functional segregation between nucleus accumbens core and shell, and add weight to the hypothesis that the core, but not the shell, subregion of the nucleus accumbens is preferentially involved in the control of choice behaviour under delayed reinforcement conditions and in the inhibitory control of goal-directed behaviour. [source] The influence of selective lesions to components of the hippocampal system on the orienting response, habituation and latent inhibitionEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2002Article first published online: 28 JUN 200 First page of article [source] Personality, creativity and latent inhibitionEUROPEAN JOURNAL OF PERSONALITY, Issue 2 2006Giles St J. Burch The current study set out to investigate the relationship between creativity, multi-dimensional schizotypy and personality more generally. This was achieved by analysing scores on a range of personality scales and measures of creativity, where it was found that the creativity measures were more closely related to asocial-schizotypy than positive-schizotypy. The study also sought to test Eysenck's prediction (1993, 1995) that, given the putative relationship between creativity and psychosis-proneness, high psychosis-prone scoring individuals and high creativity scoring individuals would demonstrate the same cognitive style of ,overinclusiveness' on latent inhibition. However, the results failed to demonstrate any evidence of a shared ,widening of the associative horizon' between high creativity and high psychosis-prone scorers. The findings are discussed in relation to multi-dimensional schizotypy. Copyright © 2006 John Wiley & Sons, Ltd. [source] Enhanced dopamine function in DISC1-L100P mutant mice: implications for schizophreniaGENES, BRAIN AND BEHAVIOR, Issue 7 2010T. V. Lipina Significant advances have been made in understanding the role of disrupted-in-schizophrenia-1 (DISC1) in the brain and accumulating findings suggest the possible implication of DISC1 in the regulation of dopamine (DA) function. A mutation in the second exon of DISC1 at L100P leads to the development of schizophrenia-related behavior in mutant mice (DISC1-L100P). We investigated here the role of DA in the expression of schizophrenia-related endophenotypes in the DISC1-L100P genetic mouse model. The mutated DISC1 resulted in facilitation of the psychostimulant effect of amphetamine in DISC1-L100P mutant mice assessed in the open field and prepulse inhibition (PPI) tests. Biochemical studies detected a 2.1-fold increase in the proportion of striatal Dreceptors without significant changes in DA release in vivo in the striatum of DISC1-L100P mutants in response to the low dose of amphetamine. The D2 receptor antagonist haloperidol reversed the hyperactivity, PPI and latent inhibition (LI) deficits and blocked the psychostimulant effect of amphetamine in DISC1-L100P mutants. Taken together, our findings show the role of DISC1 in D2 -related pathophysiological mechanism of schizophrenia, linking DISC1 with well-established DA hypothesis of schizophrenia. [source] Genetic loss of D-amino acid oxidase activity reverses schizophrenia-like phenotypes in miceGENES, BRAIN AND BEHAVIOR, Issue 1 2010V. Labrie Reduced function of the N -methyl- d -aspartate receptor (NMDAR) has been implicated in the pathophysiology of schizophrenia. The NMDAR contains a glycine binding site in its NR1 subunit that may be a useful target for the treatment of schizophrenia. In this study, we assessed the therapeutic potential of long-term increases in the brain levels of the endogenous NMDAR glycine site agonist D-serine, through the genetic inactivation of its catabolic enzyme D-amino acid oxidase (DAO) in mice. The effects of eliminating DAO function were investigated in mice that display schizophrenia-related behavioral deficits due to a mutation (Grin 1D481N) in the NR1 subunit that results in a reduction in NMDAR glycine affinity. Grin 1D481N mice show deficits in sociability, prolonged latent inhibition, enhanced startle reactivity and impaired spatial memory. The hypofunctional Dao 1G181R mutation elevated brain levels of D-serine, but alone it did not affect performance in the behavioral measures. Compared to animals with only the Grin 1D481N mutation, mice with both the Dao1G181R and Grin 1D481N mutations displayed an improvement in social approach and spatial memory retention, as well as a reversal of abnormally persistent latent inhibition and a partial normalization of startle responses. Thus, an increased level of D-serine resulting from decreased catalysis corrected the performance of mice with deficient NMDAR glycine site activation in behavioral tasks relevant to the negative and cognitive symptoms of schizophrenia. Diminished DAO activity and elevations in D-serine may serve as an effective therapeutic intervention for the treatment of psychiatric symptoms. [source] | ||||||||||