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Fear Memory (fear + memory)

Distribution by Scientific Domains

Life Sciences	94%

Selected Abstracts

Dissociated theta phase synchronization in amygdalo- hippocampal circuits during various stages of fear memory

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2007
Rajeevan T. Narayanan
Abstract The amygdala and the hippocampus are critically involved in the formation and retention of fear memories. However, their precise contribution to, and their interplay during, fear memory formation are not fully understood. In the present study we investigated network activities in the amygdalo-hippocampal system of freely behaving mice at different stages of fear memory consolidation and retention. Our data show enhanced theta phase synchronization in this pathway during the retrieval of fear memory at long-term (24 h post-training), but not short-term (2 min, 30 min and 2 h post-training) stages, following both contextual and auditory cued conditioning. However, retrieval of remotely conditioned fear (30 days post-training) failed to induce an increase in synchronization despite there still being memory retention. Thus, our data indicate that the amygdalo-hippocampal interaction reflects a dynamic interaction of ensemble activities related to various stages of fear memory consolidation and/or retention, and support the notion that recent and remote memories are organized through different network principles. [source]

Fear learning induces persistent facilitation of amygdala synaptic transmission

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2005
Bradley W. Schroeder
Abstract In the maintenance phase of fear memory, synaptic transmission is potentiated and the stimulus requirements and signalling mechanisms are altered for long-term potentiation (LTP) in the cortico-lateral amygdala (LA) pathway. These findings link amygdala synaptic plasticity to the coding of fear memories. Behavioural experiments suggest that the amygdala serves to store long-term fear memories. Here we provide electrophysiological evidence showing that synaptic alterations in rats induced by fear conditioning are evident in vitro 10 days after fear conditioning. We show that synaptic transmission was facilitated and that high-frequency stimulation dependent LTP (HFS,LTP) of the cortico-lateral amygdala pathway remained attenuated 10 days following fear conditioning. Additionally, we found that the low-frequency stimulation dependent LTP (LFS,LTP) measured 24 h after fear conditioning was absent 10 days post-training. The persistent facilitation of synaptic transmission and occlusion of HFS,LTP suggests that, unlike hippocampal coding of contextual fear memory, the cortico-lateral amygdala synapse is involved in the storage of long-term fear memories. However, the absence of LFS,LTP 10 days following fear conditioning suggests that amygdala physiology 1 day following fear learning may reflect a dynamic state during memory stabilization that is inactive during the long-term storage of fear memory. Results from these experiments have significant implications regarding the locus of storage for maladaptive fear memories and the synaptic alterations induced by these memories. [source]

Activation of histaminergic H3 receptors in the rat basolateral amygdala improves expression of fear memory and enhances acetylcholine release

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2002
Iacopo Cangioli
Abstract The basolateral amygdala (BLA) is involved in learning that certain environmental cues predict threatening events. Several studies have shown that manipulation of neurotransmission within the BLA affects the expression of memory after fear conditioning. We previously demonstrated that blockade of histaminergic H3 receptors decreased spontaneous release of acetylcholine (ACh) from the BLA of freely moving rats, and impaired retention of fear memory. In the present study, we examined the effect of activating H3 receptors within the BLA on both ACh release and expression of fear memory. Using the microdialysis technique in freely moving rats, we found that the histaminergic H3 agonists R-,-methylhistamine (RAMH) and immepip, directly administered into the BLA, augmented spontaneous release of ACh in a similar manner. Levels of ACh returned to baseline on perfusion with control medium. Rats receiving intra-BLA, bilateral injections of the H3 agonists at doses similar to those enhancing ACh spontaneous release, immediately after contextual fear conditioning, showed stronger memory for the context,footshock association, as demonstrated by longer freezing assessed at retention testing performed 72 h later. Post-training, bilateral injections of 15 ng oxotremorine also had a similar effect on memory retention, supporting the involvement of the cholinergic system. Thus, our results further support a physiological role for synaptically released histamine, that in addition to affecting cholinergic transmission in the amygdala, modulates consolidation of fear memories [source]

Time-dependent involvement of the dorsal hippocampus in trace fear conditioning in mice

HIPPOCAMPUS, Issue 4 2005
Ilga Misane
Abstract Hippocampal and amygdaloid neuroplasticity are important substrates for Pavlovian fear conditioning. The hippocampus has been implicated in trace fear conditioning. However, a systematic investigation of the significance of the trace interval has not yet been performed. Therefore, this study analyzed the time-dependent involvement of N-methyl- D -aspartate (NMDA) receptors in the dorsal hippocampus in one-trial auditory trace fear conditioning in C57BL/6J mice. The NMDA receptor antagonist APV was injected bilaterally into the dorsal hippocampus 15 min before training. Mice were exposed to tone (conditioned stimulus [CS]) and footshock (unconditioned stimulus [US]) in the conditioning context without delay (0 s) or with CS-US (trace) intervals of 1,45 s. Conditioned auditory fear was determined 24 h after training by the assessment of freezing and computerized evaluation of inactivity in a new context; 2 h later, context-dependent memory was tested in the conditioning context. NMDA receptor blockade by APV markedly impaired conditioned auditory fear at trace intervals of 15 s and 30 s, but not at shorter trace intervals. A 45-s trace interval prevented the formation of conditioned tone-dependent fear. Context-dependent memory was always impaired by APV treatment independent of the trace interval. The results indicate that the dorsal hippocampus and its NMDA receptors play an important role in auditory trace fear conditioning at trace intervals of 15,30-s length. In contrast, NMDA receptors in the dorsal hippocampus are unequivocally involved in contextual fear conditioning independent of the trace interval. The results point at a time-dependent role of the dorsal hippocampus in encoding of noncontingent explicit stimuli. Preprocessing of long CS-US contingencies in the hippocampus appears to be important for the final information processing and execution of fear memories through amygdala circuits. © 2005 Wiley-Liss, Inc. [source]

Combining pharmacotherapy with cognitive behavioral therapy: Traditional and new approaches

JOURNAL OF TRAUMATIC STRESS, Issue 5 2006
Michael Davis
Given the ever-increasing sources of trauma both nationally and globally, it is imperative to develop new and better treatments for anxiety disorders such as posttraumatic stress disorder (PTSD). This review is a collection of presentations that seek to do just that, either by using pharmacotherapy to try to prevent or erase the formation of traumatic fear memories, or to enhance exposure-based cognitive,behavioral therapy using pharmacological agents that have been effective in enhanced extinction of fear in rodents. [source]

Glucocorticoid receptors in the basolateral nucleus of amygdala are required for postreactivation reconsolidation of auditory fear memory

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2007
Xin-Chun Jin
Abstract It is well known that initial consolidation requires de novo gene transcription and protein synthesis in order for memory to become stable. The consolidated memory again becomes labile and temporarily sensitive to disruption when retrieved, requiring a reconsolidation process to become permanent. Although it is well established that glucocorticoid receptors (GR) in the basolateral nucleus of amygdala (BLA) are required for consolidation of fear memory, little is known about their role in reconsolidation of fear memory. In the present study, we first examined the effect of a GR antagonist on postconditioning consolidation of auditory fear memory (AFM). Intra-BLA infusion of the GR antagonist RU486 0 h postconditioning impaired long-term AFM, leaving short-term AFM intact. RU486 had no effect if infusion was performed 6 h postconditioning. We then investigated the effect of the RU486 treatment on postretrieval reconsolidation of AFM. Severe amnesia took place when RU486 was infused into the BLA 0 h postretrieval (reactivation) of AFM, regardless of whether the retrieval was performed 1 day or 10 days postconditioning. RU486 produced no amnesia if the memory retrieval was omitted or if the drug was administered 6 h postretrieval. Treatment with RU486 0 h postretrieval produced no deficit in postretrieval short-term memory but impaired postretrieval long-term memory, and the amnesia exhibited no spontaneous recovery 6 days after retrieval. The present results provide strong evidence that glucocorticoid receptors in the BLA are required for reconsolidation as well as consolidation of AFM. [source]

Dissociated theta phase synchronization in amygdalo- hippocampal circuits during various stages of fear memory

Fear learning induces persistent facilitation of amygdala synaptic transmission

Activation of histaminergic H3 receptors in the rat basolateral amygdala improves expression of fear memory and enhances acetylcholine release

Differential regulation of CaMKII inhibitor , protein expression after exposure to a novel context and during contextual fear memory formation

GENES, BRAIN AND BEHAVIOR, Issue 6 2010
K. Radwa
Understanding of the molecular basis of long-term fear memory (fear LTM) formation provides targets in the treatment of emotional disorders. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is one of the key synaptic molecules involved in fear LTM formation. There are two endogenous inhibitor proteins of CaMKII, CaMKII N, and N,, which can regulate CaMKII activity in vitro. However, the physiological role of these endogenous inhibitors is not known. Here, we have investigated whether CaMKII N, protein expression is regulated after contextual fear conditioning or exposure to a novel context. Using a novel CaMKII N, -specific antibody, CaMKII N, expression was analysed in the naïve mouse brain as well as in the amygdala and hippocampus after conditioning and context exposure. We show that in naïve mouse forebrain CaMKII N, protein is expressed at its highest levels in olfactory bulb, prefrontal and piriform cortices, amygdala and thalamus. The protein is expressed both in dendrites and cell bodies. CaMKII N, expression is rapidly and transiently up-regulated in the hippocampus after context exposure. In the amygdala, its expression is regulated only by contextual fear conditioning and not by exposure to a novel context. In conclusion, we show that CaMKII N, expression is differentially regulated by novelty and contextual fear conditioning, providing further insight into molecular basis of fear LTM. [source]

Altered conditioned fear behavior in glutamate decarboxylase 65 null mutant mice

GENES, BRAIN AND BEHAVIOR, Issue 2 2003
O. Stork
We investigated the involvement of the 65 kDa isoform of glutamic acid decarboxylase (GAD65) and GAD65-mediated ,-aminobutyric acid (GABA) synthesis in the formation and expression of Pavlovian fear memory. To this end, behavioral, endocrine and autonomic parameters were examined during conditioned fear retrieval of mice with targeted ablation of the GAD65 gene (GAD65,/, mice). These mutant mice were found to display specific fear behavior (freezing, escape), as well as autonomic (increased defecation) and endocrine activation (increased plasma corticosterone) during fear memory retrieval. However, freezing was reduced and flight and escape behavior were increased in GAD65,/, mice compared to their wild type and heterozygous littermates, while corticosterone levels and defecation rates did not differ between genotypes. Active defensive behavior of GAD65,/, mice was observed during both auditory cued and contextual retrieval of fear memory, as well as immediately after conditioning. These data indicate a selectively altered behavioral fear response in GAD65,/, mice, most likely due to deficits in threat estimation or the elicitation of appropriate conditioned fear behavior, and suggest that GAD65 is a genetic determinant of conditioned fear behavior. GAD65,/, mice provide a valuable tool to further dissect the GABAergic mechanisms involved in fear and anxiety and to model GABA-related neurological and psychiatric disorders. [source]