Object exploration and reactions to spatial and nonspatial changes in hooded rats following damage to parietal cortex or hippocampal formation.

Save, Étienne; Poucet, Bruno; Foreman, Nigel; Buhot, Marie-Christine

doi:10.1037/0735-7044.106.3.447

Cited by 365 publications

(295 citation statements)

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“…The behavioral testing procedure was that described by Save et al (1992) for rat and by Roullet et al (1996) for mice (Figure 1). On the test day, each mouse was placed individually into the empty open field for a 6 min session (S1), in order to become familiar with the apparatus.…”

Section: Intracerebral Injection and Behavioral Testing Proceduresmentioning

confidence: 99%

“…During sessions S2-S6, object exploration was scored as the time the animal spent in contact with an object. A contact was defined as the mouse's snout actually touching an object (for details, see Save et al, 1992;Roullet et al, 1996;Sargolini et al, 1999).…”

Section: Data Collection and Statistical Analysismentioning

confidence: 99%

“…Control mice usually spend more time exploring the displaced objects (DO) as well as the novel one compared to the other objects. This response is interpreted as an index of rodent's ability to encode (or use) spatial and non-spatial relationships between discrete stimuli (Poucet, 1989;Save et al, 1992;Roullet et al, 1996). This task does not involve an explicit reinforcement and does not involve learning of rules, but it is based entirely on the spontaneous exploratory behavior of animals toward objects.…”

Section: Introductionmentioning

confidence: 99%

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D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Rinaldi

Mandillo

Oliverio

et al. 2006

Neuropsychopharmacol

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The prefrontal cortex (PFC) is a cortical area involved in selecting and retaining information to produce complex behaviors. Within the PFC, the dopaminergic system plays an important role in information processing. Thus, the objective of this study was to test whether bilateral administration of the D1 and D2 receptor antagonists in the prelimbic region of the PFC influenced the performance of mice in a non-associative spatial learning task. CD1 mice were bilaterally microinjected in the PFC with either the D1 receptor antagonist, SCH23390 (SCH 6.25; 12.5; 50 ng), or the D2 receptor antagonist, sulpiride (SULP 12.5; 50; 100 ng) and placed into an open field containing five different objects. After three sessions of habituation two objects were repositioned (spatial change) and in the subsequent session one of the objects was substituted (non-spatial change). No significant alteration was observed in the habituation pattern of the animals after D1 or D2 receptor blockade. When two of the objects were displaced, control mice explored the displaced objects far more than the non-displaced ones, while mice treated with SCH or SULP spent a comparable amount of time re-exploring the two object categories. Conversely, DA antagonists had no effects on the discrimination of the new object. Thus, the administration of both SCH and SULP selectively impaired the ability of mice to discriminate a spatial change, without affecting any other behavioral parameter. These findings could provide a model to study the role of the PFC dopaminergic system in spatial learning and to study the neural mechanisms underlying cognitive and attention deficits often observed in psychiatric disorders.

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Section: Intracerebral Injection and Behavioral Testing Proceduresmentioning

confidence: 99%

Section: Data Collection and Statistical Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Rinaldi

Mandillo

Oliverio

et al. 2006

Neuropsychopharmacol

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“…When administered immediately after fear conditioning, TSA selectively enhances long-term contextual fear memory (Vecsey et al 2007). Using the same method of post-training intrahippocampal delivery for the GABA receptor type A agonist muscimol, reversible inactivation of the hippocampus prevents memory formation in the object-location memory task (Oliveira et al 2010).The hippocampus-dependent object-location memory task exploits the observation that mice explore objects more when the position of the object is changed relative to previous experiences (Save et al 1992). Training and testing in this task were performed as previously described (Oliveira et al 2010).…”

mentioning

confidence: 99%

“…The hippocampus-dependent object-location memory task exploits the observation that mice explore objects more when the position of the object is changed relative to previous experiences (Save et al 1992). Training and testing in this task were performed as previously described (Oliveira et al 2010).…”

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confidence: 99%

Post-training intrahippocampal inhibition of class I histone deacetylases enhances long-term object-location memory

Hawk¹,

Florian²,

Abel³

2011

Learn. Mem.

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Long-term memory formation involves covalent modification of the histone proteins that package DNA. Reducing histone acetylation by mutating histone acetyltransferases impairs long-term memory, and enhancing histone acetylation by inhibiting histone deacetylases (HDACs) improves long-term memory. Previous studies using HDAC inhibitors to enhance longterm memory have focused on the fear-conditioning task using broad-spectrum HDAC inhibitors. We have found that post-training intrahippocampal administration of the broad-spectrum HDAC inhibitor trichostatin A (TSA) or the class I HDAC-selective inhibitor MS275 enhances long-term object-location memory, supporting a role for class I HDACs in the enhancement of hippocampus-dependent memory induced by HDAC inhibition.The formation of a long-term memory requires de novo gene transcription in the hours following learning . Covalent modifications, such as acetylation, occur on the histone proteins that package genes to guide transcription (Jenuwein and Allis 2001). It has become clear that histone acetylation contributes to memory formation (Wood et al. 2006b;Barrett and Wood 2008;Sweatt 2009;Morris et al. 2010). Histone acetylation increases after learning (Levenson et al. 2004;Chwang et al. 2006;Bredy et al. 2007;Peleg et al. 2010), and the histone acetyltransferase CREB-binding protein (CBP) is critical for memory storage (Oike et al. 1999;Alarcon et al. 2004;Korzus et al. 2004;Wood et al. 2005Wood et al. , 2006a. Specific point mutations in CBP that block the recruitment of CBP to CREB (Wood et al. 2006a) or that eliminate the histone acetyltransferase activity of CBP (Korzus et al. 2004) selectively impair long-term memory. Also, the contextual fear memory deficit observed in mice lacking one copy of CBP is ameliorated by pharmacologically inhibiting the histone deacetylases (HDACs) that oppose CBP (Alarcon et al. 2004), presumably through enhancing the efficacy of histone acetylation by the CBP that remains.Treatment of rodents with inhibitors of HDACs enhances long-term memory (Alarcon et al. 2004;Korzus et al. 2004;Levenson et al. 2004;Yeh et al. 2004;Lattal et al. 2007;Vecsey et al. 2007;Bredy and Barad 2008;Guan et al. 2009;Stefanko et al. 2009;Peleg et al. 2010;Roozendaal et al. 2010). Most previous studies examined the hippocampus-dependent contextual fear-conditioning task (Alarcon et al. 2004;Levenson et al. 2004;Vecsey et al. 2007;Guan et al. 2009;Peleg et al. 2010) or extinction of fear memory Bredy and Barad 2008). Recently, memory enhancement by HDAC inhibitor treatment was observed for object-recognition memory (Stefanko et al. 2009) and object-location memory (Haettig et al. 2011). In contrast to object-location memory (Haettig et al. 2011) and contextual fear conditioning (Vecsey et al. 2007), the effect of HDAC inhibition on object-recognition memory does not require the CREB-CBP interaction (Stefanko et al. 2009). This mechanistic distinction is supported by an anatomical dissociation in the effect of HDAC inhibitors on different forms of object-bas...

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Novelty-induced increased expression of immediate-early genes c-fos and arg 3.1 in the mouse brain

et al. 1999

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Object exploration and reactions to spatial and nonspatial changes in hooded rats following damage to parietal cortex or hippocampal formation.

Cited by 365 publications

References 53 publications

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Post-training intrahippocampal inhibition of class I histone deacetylases enhances long-term object-location memory

Novelty-induced increased expression of immediate-early genes c-fos and arg 3.1 in the mouse brain

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