. (2013) 'Overshadowing of geometry learning by discrete landmarks in the water maze : e ects of relative salience and relative validity of competing cues.', Journal of experimental psychology : animal behaviour processes., 39 (2). pp. 126-139.Further information on publisher's website:Publisher's copyright statement:c 2013 APA, all rights reserved. This article may not exactly replicate the nal version published in the APA journal. It is not the copy of record.Additional information: Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-pro t purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details.

Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details.

While palatability depends on the properties of particular foods, it is also determined by prior experience, suggesting that memory affects the hedonic value of a substance. Here, we report two procedures that affect palatability in mice: negative contrast and flavour habituation. A microstructure analysis of licking behaviour was employed, with the lick cluster size (the number of licks made in quick succession before a pause) used as a measure of palatability. It was first confirmed that lick cluster size increased monotonically as a function of sucrose concentration, whereas consumption followed an inverted U-shaped function. In a successive negative contrast procedure it was found that when shifted from a high sucrose concentration (32%) to a low sucrose concentration (4%), mice made smaller lick clusters than a group that only received the low concentration. Mice exposed to flavours (cherry or grape Kool Aid) mixed with sucrose (16%) made larger lick clusters for familiar flavours compared to novel flavours. This habituation effect was evident after short (5 min) and long (24 h) test intervals. Both successive negative contrast and flavour habituation failed to affect levels of consumption. Collectively, the results show that prior experience can have effects on lick cluster size that are equivalent to increasing or decreasing the sweetness of a solution. Thus, palatability is not a fixed property of a substance but is dependent on expectation or familiarity that occurs as a result of memory.

Theories of learning differ in whether they assume that learning reflects the strength of an association between memories or symbolic encoding of the statistical properties of events. We provide novel evidence for symbolic encoding of informational variables by demonstrating that sensitivity to time and number in learning is dissociable. Whereas responding in normal mice was dependent on reinforcement rate, responding in mice that lacked the GluA1 AMPA receptor subunit was insensitive to reinforcement rate and, instead, dependent on the number of times a cue had been paired with reinforcement. This suggests that GluA1 is necessary for weighting numeric information by temporal information in order to calculate reinforcement rate. Sample sizes per genotype varied between seven and 23 across six experiments and consisted of both male and female mice. The results provide evidence for explicit encoding of variables by animals rather than implicit encoding via variations in associative strength.

The GluA1 subunit of the AMPA receptor has been implicated in schizophrenia. While GluA1 is important for cognition, it is not clear what the role of GluA1 is in hedonic responses that are relevant to the negative symptoms of disorders such as schizophrenia. Here, we tested mice that lack GluA1 (Gria1 −/− mice) on consumption of sucrose solutions using a licking microstructure analysis. GluA1 deletion drastically reduced palatability (as measured by the mean lick cluster size) across a range of sucrose concentrations. Although initial lick rates were reduced, measures of consumption across long periods of access to sucrose solutions were not affected by GluA1 deletion and Gria1 −/− mice showed normal satiety responses to high sucrose concentrations. GluA1 deletion also failed to impair flavour conditioning, in which increased intake of a flavour occurred as a consequence of prior pairing with a high sucrose concentration. These results demonstrate that GluA1 plays a role in responding on the basis of palatability rather than other properties, such as the automatic and learnt postingestive, nutritional consequences of sucrose. Therefore, Gria1 −/− mice provide a potential model of anhedonia, adding converging evidence to the role of glutamatergic dysfunction in various symptoms of schizophrenia and related disorders.Glutamatergic dysfunction has been proposed as a potential cause of schizophrenia 1 . Recently the Gria1 gene that encodes for the GluA1 subunit of the AMPA receptor for glutamate has been found to show genome wide association to schizophrenia 2, 3 . Furthermore, post-mortem tests have revealed a reduction in hippocampal GluA1 mRNA 4, 5 , and GluA1 6 and AMPA binding sites 7 in schizophrenia patients. Genetically modified mice that lack a functional Gria1 gene now provide a useful means of studying the causal role of glutamatergic dysfunction in neuropsychiatric disorders.Knockout of Gria1 in mice (Gria1 −/− mice) results in impaired hippocampal plasticity 8-11 and causes cognitive deficits that are associated with dysfunction of the hippocampus 12-14 and amygdala 15,16 . Furthermore, Gria1 −/− mice show behavioural abnormalities that are relevant to schizophrenia suggesting that Gria1 deletion models components of the disorder [17][18][19] . In particular Gria1 −/− mice fail to reduce attention to recently experienced stimuli as a consequence of impaired short-term habituation 14,[20][21][22] , suggesting that GluA1 deletion may model aspects of aberrant salience in disorders such as schizophrenia 23,24 .There is evidence that Gria1 −/− mice show behavioural changes that mimic negative symptoms, such as anhedonia, in schizophrenia. Ruling out potential confounds, however, has proved difficult. For example, there are reports of reduced social behaviour 18,19,25 , but while these deficits may reflect an aspect of social anhedonia, it is possible that these tests are confounded by deficits in spatial habituation 14,20,26 . Similarly, it is possible that other demonstrations of emotional blunting in Gria...