D1 receptor modulation of memory retrieval performance is associated with changes in pCREB and pDARPP-32 in rat prefrontal cortex

Hotte, Maïté; Thuault, Sébastien; Lachaise, Fabienne; Dineley, Kelly T.; Hemmings, Hugh C.; Nairn, Angus C.; Jay, Thérèse M.

doi:10.1016/j.bbr.2006.03.026

Cited by 67 publications

(43 citation statements)

References 43 publications

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“…Furthermore, it shows that H 1 receptor activation in the CA1 is necessary for IA-LTM retrieval. This finding adds strong support to the view that retrieval is a dynamic process that requires neuromodulatory signaling, just like acquisition, consolidation, reconsolidation, and memory maintenance (6,33,34), and identifies a crucial role for the neurotransmitter histamine in this process. Indeed, rats temporarily depleted of histamine through infusion of a-FMHis, an irreversible inhibitor of histidine decarboxylase, into the LV 24 h either before or after IA training displayed amnesia of IA training 48 h posttraining.…”

Section: Discussionsupporting

confidence: 56%

Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus

Fabbri

Furini

Passani

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Retrieval represents a dynamic process that may require neuromodulatory signaling. Here, we report that the integrity of the brain histaminergic system is necessary for retrieval of inhibitory avoidance (IA) memory, because rats depleted of histamine through lateral ventricle injections of α-fluoromethylhistidine (a-FMHis), a suicide inhibitor of histidine decarboxylase, displayed impaired IA memory when tested 2 d after training. a-FMHis was administered 24 h after training, when IA memory trace was already formed. Infusion of histamine in hippocampal CA1 of brain histamine-depleted rats (hence, amnesic) 10 min before the retention test restored IA memory but was ineffective when given in the basolateral amygdala (BLA) or the ventral medial prefrontal cortex (vmPFC). Intra-CA1 injections of selective H 1 and H 2 receptor agonists showed that histamine exerted its effect by activating the H 1 receptor. Noteworthy, the H 1 receptor antagonist pyrilamine disrupted IA memory retrieval in rats, thus strongly supporting an active involvement of endogenous histamine; 90 min after the retention test, c-Fos-positive neurons were significantly fewer in the CA1s of a-FMHis-treated rats that displayed amnesia compared with in the control group. We also found reduced levels of phosphorylated cAMP-responsive element binding protein (pCREB) in the CA1s of a-FMHis-treated animals compared with in controls. Increases in pCREB levels are associated with retrieval of associated memories. Targeting the histaminergic system may modify the retrieval of emotional memory; hence, histaminergic ligands might reduce dysfunctional aversive memories and improve the efficacy of exposure psychotherapies.emory determines the uniqueness of our personal history and is decisive for each individual to survive and prosper. It is a multistate process that includes acquisition, consolidation, and retrieval (1). Whereas considerable advancement has been made toward understanding the specific brain structures (e.g., amygdala, prefrontal cortex, and hippocampus) and molecular mechanisms (receptors and signaling pathways) that underlie acquisition and consolidation (2, 3), the understanding of retrieval has lagged behind, although it is ultimately the only possible measure of memory (4-6). Indeed, retrieval is not simply a static readout of stored information; rather, it represents a dynamic process that can be studied separately from either acquisition or consolidation, with which it shares similar mechanisms (1, 7, 8). Furthermore, retrieval can elicit specific processes that modify the recalled memory (9). In this regard, protein synthesis, a necessary step in the transfer of a labile short-term memory into a stable long-term memory (LTM) (2), is required to enable retrieval, because infusion of protein synthesis inhibitors in the amygdala 10 min before retrieval impaired fear memory expression (10). An interesting question is whether neuromodulatory signaling is required for not only memory acquisition and consolidation (11) but also, retrieval. The...

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Section: Discussionsupporting

confidence: 56%

Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus

Fabbri

Furini

Passani

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Extensive evidence supports the idea that CREB plays an essential role in memory formation. Inhibition of CREB phosphorylation within the hippocampus (Bourtchuladze et al, 1994) or the PFC (Hotte et al, 2006) impairs the induction of long-term potentiation within these brain regions, leading to a significant deficit in spatial tasks (Laroche et al, 2000;Conejo et al, 2010). Therefore, the decrease in hippocampal CREB activity observed here likely accounts for the spatial learning deficit in drug-reinforced mice.…”

Section: Discussionmentioning

confidence: 72%

Disrupting Effect of Drug-Induced Reward on Spatial But Not Cue-Guided Learning: Implication of the Striatal Protein Kinase A/cAMP Response Element-Binding Protein Pathway

Baudonnat¹,

Guillou²,

Husson³

et al. 2011

J. Neurosci.

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The multiple memory systems hypothesis posits that different neural circuits function in parallel and may compete for information processing and storage. For example, instrumental conditioning would depend on the striatum, whereas spatial memory may be mediated by a circuit centered on the hippocampus. However, the nature of the task itself is not sufficient to select durably one system over the other. In this study, we investigated the effects of natural and pharmacological rewards on the selection of a particular memory system during learning. We compared the effects of food-or drug-induced activation of the reward system on cue-guided versus spatial learning using a Y-maze discrimination task. Drug-induced reward severely impaired the acquisition of a spatial discrimination task but spared the cued version of the task. Immunohistochemical analysis of the phosphorylated form of the cAMP response element binding (CREB) protein and c-Fos expression induced by behavioral testing revealed that the spatial deficit was associated with a decrease of both markers within the hippocampus and the prefrontal cortex. In contrast, drug reward potentiated the cued learning-induced CREB phosphorylation within the dorsal striatum. Administration of the protein kinase A inhibitor 8-Bromo-adenosine-3',5'-cyclic monophosphorothioate Rp isomer (Rp-cAMPS) into the dorsal striatum before training completely reversed the drug-induced spatial deficit and restored CREB phosphorylation levels within the hippocampus and the prefrontal cortex. Therefore, drug-induced striatal hyperactivity may underlie the declarative memory deficit reported here. This mechanism could represent an important early step toward the development of addictive behaviors by promoting conditioning to the detriment of more flexible forms of memory.

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“…Indeed, the extended access self-administration protocol used in this study has been shown to produce a number of symptoms characteristic of addiction that are not seen following more limited drug access (Ahmed and Koob 1998;Paterson and Markou 2003;Deroche-Gamonet, et al 2004;Vanderschuren and Everitt 2004;Ferrario, et al 2005;Briand, et al 2008). On the other hand, we need to acknowledge that it is not possible conclude conclusively that the deficits described here are due to cocaine compromising hippocampal function Baxter and Murray 2001;Mumby 2001;Zola and Squire 2001), because a number of other brain regions have been implicated in recognition memory, including the nucleus accumbens (Sargolini et al 2003;Ferretti et al 2005), prefrontal cortex (Hotte et al 2006), and perirhinal cortex (Barker et al 2007). …”

Section: Discussionmentioning

confidence: 88%

Impaired object recognition following prolonged withdrawal from extended-access cocaine self-administration

2008

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Cocaine addicts have a number of cognitive deficits that persist following prolonged abstinence. These include impairments in executive functions dependent on the prefrontal cortex, as well as deficits on learning and memory tasks sensitive to hippocampal function. Recent preclinical studies using non-human animals have demonstrated that cocaine treatment can produce persistent deficits in executive functions, but there is relatively little evidence that treatment with cocaine produces persistent deficits in performance on hippocampal-dependent tasks. We recently demonstrated that extended (but not limited) access to self-administered cocaine is especially effective in producing persistent deficits on a test of cognitive vigilance, and therefore, we used this procedure to examine the effects of limited or extended access to cocaine self-administration on recognition memory performance, which is sensitive to hippocampal function. We found that extended access to cocaine produced deficits in recognition memory that persisted for at least 2 weeks after the cessation of drug use. We conclude that the deficits in learning and memory observed in cocaine addicts may be at least in part due to repeated drug use, rather than just due to a pre-existing condition, and that in studying the neural basis of such deficits procedures involving extended access to self-administered cocaine may be especially useful. Keywordsself-administration; memory; cocaine; object recognition Cocaine addicts present with a number of cognitive deficits even following prolonged abstinence. These include impaired performance on tasks involving attention and cognitive flexibility that are thought to be mediated by the medial and orbital prefrontal cortex, as well as spatial, verbal, and recognition memory impairments on tasks thought to be mediated by the hippocampus (Manschreck et al. 1990;Ardila et al. 1991;Berry et al. 1993;Beatty et al. 1995;Hoff et al. 1996;Bolla et al. 2003). Given that cognitive deficits are known to negatively impact treatment outcomes (Aharonovich et al. 2003;Aharonovich et al. 2006), the development of an animal model of persistent cocaine-induced cognitive deficits would be useful in exploring the nature of the deficit. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2009 July 31. Published in final edited form as:Neuroscience. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptA number of preclinical studies have reported that treatment with cocaine produces cognit...

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D1 receptor modulation of memory retrieval performance is associated with changes in pCREB and pDARPP-32 in rat prefrontal cortex

Cited by 67 publications

References 43 publications

Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus

Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus

Disrupting Effect of Drug-Induced Reward on Spatial But Not Cue-Guided Learning: Implication of the Striatal Protein Kinase A/cAMP Response Element-Binding Protein Pathway

Impaired object recognition following prolonged withdrawal from extended-access cocaine self-administration

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D1 receptor modulation of memory retrieval performance is associated with changes in pCREB and pDARPP-32 in rat prefrontal cortex

Cited by 67 publications

References 43 publications

Memory retrieval of inhibitory avoidance requires histamine H 1 receptor activation in the hippocampus

Memory retrieval of inhibitory avoidance requires histamine H 1 receptor activation in the hippocampus

Disrupting Effect of Drug-Induced Reward on Spatial But Not Cue-Guided Learning: Implication of the Striatal Protein Kinase A/cAMP Response Element-Binding Protein Pathway

Impaired object recognition following prolonged withdrawal from extended-access cocaine self-administration

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Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus

Memory retrieval of inhibitory avoidance requires histamine H ₁ receptor activation in the hippocampus