Efficacy of traumatic memory reactivation with or without propranolol in PTSD with high dissociative experiences.

Post-traumatic stress disorder (PTSD) with dissociative symptoms is now a full-fledged subtype of this disorder. The dissociative subtype is associated with a greater number of psychiatric comorbidities. To date, the impact of dissociation on the efficacy of PTSD treatment remains unclear.

Traumatic memory reactivation with or without propranolol for PTSD and comorbid MD symptoms: a randomised clinical trial.

Post-traumatic stress disorder (PTSD) is difficult to treat but one promising strategy is to block memory reconsolidation of the traumatic event. This study aimed to evaluate the efficacy of traumatic memory reactivation under the influence of propranolol, a noradrenergic beta-receptor blocker, in reducing PTSD symptoms as well as comorbid major depression (MD) symptoms. We conducted a double blind, placebo-controlled, randomised clinical trial in 66 adults diagnosed with longstanding PTSD.

Influence of early stress on memory reconsolidation: Implications for post-traumatic stress disorder treatment.

Post-traumatic stress disorder (PTSD) is a common consequence of exposure to a life-threatening event. Currently, pharmacological treatments are limited by high rates of relapse, and novel treatment approaches are needed. We have recently demonstrated that propranolol, a β-adrenergic antagonist, inhibited aversive memory reconsolidation in animals.

HDAC inhibition promotes both initial consolidation and reconsolidation of spatial memory in mice.

Accumulating evidence suggests a critical role for epigenetic regulations in long term memory (LTM) formation. Among them, post-translational modifications of proteins, as histone acetylation, are an important regulator of chromatin remodelling and gene transcription. While the implication of histone acetylation in memory consolidation is widely accepted, less is known about its role in memory reconsolidation i.

Effects of Propranolol, a β-noradrenergic Antagonist, on Memory Consolidation and Reconsolidation in Mice.

Memory reconsolidation impairment using the β-noradrenergic receptor blocker propranolol is a promising novel treatment avenue for patients suffering from pathogenic memories, such as post-traumatic stress disorder (PTSD). However, in order to better inform targeted treatment development, the effects of this compound on memory need to be better characterized via translational research. We examined the effects of systemic propranolol administration in mice undergoing a wide range of behavioral tests to determine more specifically which aspects of the memory consolidation and reconsolidation are impaired by propranolol.

Characterization of spatial memory reconsolidation.

Reconsolidation is necessary for the restabilization of reactivated memory traces. However, experimental parameters have been suggested as boundary conditions for this process. Here we investigated the role of a spatial memory trace's age, strength, and update on the reconsolidation process in mice.

Cortical abnormalities and non-spatial learning deficits in a mouse model of CranioFrontoNasal syndrome.

Eph receptors and their ephrin ligands play critical roles in the development of the nervous system, however, less is known about their functions in the adult brain. Here, we investigated the function of ephrinB1, an ephrinB family member that is mutated in CranioFrontoNasal Syndrome. We show that ephrinB1 deficient mice (EfnB1(Y/-)) demonstrate spared spatial learning and memory but exhibit exclusive impairment in non-spatial learning and memory tasks.

Involvement of protein degradation by the ubiquitin proteasome system in opiate addictive behaviors.

Plastic changes in the nucleus accumbens (NAcc), a structure occupying a key position in the neural circuitry related to motivation, are among the critical cellular processes responsible for drug addiction. During the last decade, it has been shown that memory formation and related neuronal plasticity may rely not only on protein synthesis but also on protein degradation by the ubiquitin proteasome system (UPS). In this study, we assess the role of protein degradation in the NAcc in opiate-related behaviors.

Ventral striatal plasticity and spatial memory.

Spatial memory formation is a dynamic process requiring a series of cellular and molecular steps, such as gene expression and protein translation, leading to morphological changes that have been envisaged as the structural bases for the engram. Despite the role suggested for medial temporal lobe plasticity in spatial memory, recent behavioral observations implicate specific components of the striatal complex in spatial information processing. However, the potential occurrence of neural plasticity within this structure after spatial learning has never been investigated.

Symptoms of traumatic stress in mothers of children victims of a motor vehicle accident.

Background: Motor vehicle accidents (MVAs) are the main cause of Posttraumatic stress disorder (PTSD) in industrialized countries. This includes the frequently occurring but understudied situation of parents learning that their children were injured. However, unlike in other types of trauma survivors, little is known about the predictors of PTSD symptoms in mothers whose child has suffered an MVA.

Pharmacological intervention of hippocampal CA3 NMDA receptors impairs acquisition and long-term memory retrieval of spatial pattern completion task.

Pattern completion is the ability to retrieve complete information on the basis of incomplete retrieval cues. Although it has been demonstrated that this cognitive capacity depends on the NMDA receptors (NMDA-Rs) of the hippocampal CA3 region, the role played by these glutamatergic receptors in the pattern completion process has not yet been specified. In the present study, we investigated the function of the CA3 NMDA-Rs during the different memory stages (acquisition, memory consolidation, and retrieval) in a spatial pattern completion task (when some visual cues were removed from the environment) in comparison to a standard spatial water maze task (when all visual cues were available in the environment).

Recruitment of adult-generated neurons into functional hippocampal networks contributes to updating and strengthening of spatial memory.

The dentate gyrus (DG), a hippocampal subregion, continuously produces new neurons in the adult mammalian brain that become functionally integrated into existing neural circuits. To what extent this form of plasticity contributes to memory functions remains to be elucidated. Using mapping of activity-dependent gene expression, we visualized in mice injected with the birthdating marker 5-bromo-2'-deoxyuridine the recruitment of new neurons in a set of controlled water maze procedures that engage specific spatial memory processes and require hippocampal-cortical networks.

Protein degradation, as with protein synthesis, is required during not only long-term spatial memory consolidation but also reconsolidation.

The formation of long-term memory requires protein synthesis, particularly during initial memory consolidation. This process also seems to be dependant upon protein degradation, particularly degradation by the ubiquitin-proteasome system. The aim of this study was to investigate the temporal requirement of protein synthesis and degradation during the initial consolidation of allocentric spatial learning.

Reactivation with a simple exposure to the experimental environment is sufficient to induce reconsolidation requiring protein synthesis in the hippocampal CA3 region in mice.

Our understanding of the memory reconsolidation process is at an earlier stage than that of consolidation. For example, it is unclear if, as for memory consolidation, reconsolidation of a memory trace necessitates protein synthesis. In fact, conflicting results appear in the literature and this discrepancy may be due to differences in the experimental reactivation procedure.

Effects of intra-accumbens NMDA and AMPA receptor antagonists on short-term spatial learning in the Morris water maze task.

Glutamatergic transmission within the nucleus accumbens (Nac) is considered to subserve the transfer of different types of information from the cortical and limbic regions. In particular, it has been suggested that glutamatergic afferences from the hippocampus and the prefrontal cortex provide the main source of contextual information to the Nac. Accordingly, several authors have demonstrated that the blockade of glutamate receptors within the Nac impairs various spatial tasks.

CREB antisense oligodeoxynucleotide administration into the dorsal hippocampal CA3 region impairs long- but not short-term spatial memory in mice.

The transcription factor cAMP response-element binding protein (CREB) has a pivotal role in hippocampal synaptic plasticity and hippocampus-dependent long-term memory. We recently demonstrated that the dorsal hippocampal CA3 region is involved in memory consolidation of spatial information tested on a Morris water maze in mice. To test whether activation of CREB in the CA3 region is required for memory consolidation of spatial information, bilaterally cannulated mice were infused 18 h before the beginning of the behavioral training with antisense or control sense CREB oligodeoxynucleotides (ODNs) or buffer.

Post-training intrahippocampal injection of synthetic poly-alpha-2,8-sialic acid-neural cell adhesion molecule mimetic peptide improves spatial long-term performance in mice.

Several data have shown that the neural cell adhesion molecule (NCAM) is necessary for long-term memory formation and might play a role in the structural reorganization of synapses. The NCAM, encoded by a single gene, is represented by several isoforms that differ with regard to their content of alpha-2,8-linked sialic acid residues (PSA) on their extracellular domain. The carbohydrate PSA is known to promote plasticity, and PSA-NCAM isoforms remain expressed in the CA3 region of the adult hippocampus.

Co-activation of glutamate and dopamine receptors within the nucleus accumbens is required for spatial memory consolidation in mice.

Rationale: The nucleus accumbens receives glutamatergic and dopaminergic inputs converging onto common dendrites. Recent behavioral data demonstrated that intra-accumbens administrations of either glutamate or dopamine (DA) antagonist impair spatial memory consolidation. Thus, also based on the biochemical and molecular findings demonstrating interactions among the different receptors subtypes for glutamate and dopamine, it is conceivable that memory consolidation within this structure might be modulated by glutamate-dopamine receptor interactions.

Hippocampal CA3-region is crucial for acquisition and memory consolidation in Morris water maze task in mice.

This experiment investigated the involvement of the dorsal hippocampal CA3-region in the different phases of learning and memory in spatial and non-spatial tasks. To do so, we temporarily inactivated the CA3-subfield by a focal injection of diethyldithiocarbamate (DDC) which chelates most of the heavy metals present in this region. The effects of temporary inactivation of the CA3-region were examined in an associative task, the Morris water maze (MWM).

Consolidation of memory for odour-reward association requires transient polysialylation of the neural cell adhesion molecule in the rat hippocampal dentate gyrus.

Cell adhesion molecule function is involved in hippocampal synaptic plasticity and is associated with memory consolidation. At the infragranular zone of the dentate gyrus, neurons expressing the polysialylated form of the neural cell adhesion molecule (NCAM PSA) transiently increase their frequency at the 12-hr posttraining time in behaviours elicited by stressful stimuli, such as those associated with conditioned avoidance, water maze, and fear conditioning paradigms. To determine whether learning-induced modulation of NCAM polysialylation is limited to stressful paradigms, we employed a reward-based odour discrimination task.

Differential involvement of NMDA and AMPA receptors within the nucleus accumbens in consolidation of information necessary for place navigation and guidance strategy of mice.

Recent evidence now points to a role of glutamate transmission within the nucleus accumbens (Nacc) in spatial learning and memory. Unfortunately, the role of the distinct classes of glutamate receptors within this structure in mediating the different steps of the memorization process is not clear. The aim of this study therefore was to further investigate this issue, trying to assess the involvement of the two classes of glutamate receptors within the Nacc in consolidation of spatial information using an associative spatial task, the water maze.

Involvement of the hippocampal CA3-region in acquisition and in memory consolidation of spatial but not in object information in mice.

This study investigates the implication of the hippocampal CA3-region in the different phases of learning and memory in spatial and non-spatial tasks. For that purpose, we performed focal injections of diethyldithiocarbamate (DDC) into the CA3-region of the dorsal hippocampus. The DDC chelates most of the heavy metals in the brain which blocks selectively and reversibly the synapses containing heavy metals, i.

Effects of intra-accumbens focal administrations of glutamate antagonists on object recognition memory in mice.

Generally recognition memory is distinguished into spatial and object memories that have been suggested to relay at a cortical level on different neural substrates. Recent studies point to a possible involvement of the nucleus accumbens (Nac) in spatial memory, demonstrating that blockade of glutamate antagonists within this structure impairs acquisition and consolidation of spatial information, while not many data are available on the potential role of this structure in object recognition. Thus in this study we wanted to investigate the effects of intra-accumbens focal administrations of NMDA antagonist, AP-5 (0.