Corticosterone administration after a single-trial contextual fear conditioning does not influence the strength and specificity of recent and remote memory in rats

Bueno, Ana Paula Arantes; Paiva, Joselisa Péres Queiroz de; Corrêa, Moisés dos Santos; Tiba, Paula Ayako; Fornari, Raquel Vecchio

doi:10.1016/j.physbeh.2017.01.011

Cited by 12 publications

(17 citation statements)

References 35 publications

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“…NPSR deficiency and high CORT levels during fear memory consolidation support the generalization of fear memory, here induced by incubation time. Previous studies have shown that CORT injections after fear conditioning training or incubation time alone lead to a generalization of fear memories in wildtype animals (e.g., Cordero and Sandi, 1998;Siegmund and Wotjak, 2007;Kaouane et al, 2012;Sauerhofer et al, 2012) (but see: Bueno et al, 2017). We could not observe such a generalization in our NPSR+/+ littermates and NPSR+/− mice.…”

Section: Discussioncontrasting

confidence: 54%

“…We could not observe such a generalization in our NPSR+/+ littermates and NPSR+/− mice. However, it has been shown that exposing animals to more than one retention test improves the specificity of fear memories in the long term, i.e., prevents the development of generalized fear memory (De Oliveira Alvares et al, 2013;Bueno et al, 2017). These findings explain the absence of fear generalization in our NPSR+/+ littermates and NPSR+/− mice after CORT treatment and incubation time.…”

Section: Discussionmentioning

confidence: 62%

“…Then, specificity and strength of the fear memory were examined in recent and remote retention tests in the same groups of animals to evaluate the potential development of fear memory generalization. Importantly, intense foot shocks, CORT injections, and 1-month incubation time are all factors known to induce a generalization of fear memory (Kaouane et al, 2012;Sauerhofer et al, 2012), whereas the recent memory test is able to reduce or prevent fear memory generalization (De Oliveira Alvares et al, 2013;Bueno et al, 2017). In addition to the fear memory, the startle response, anxiety-like behavior in the light-dark box, and the response to a stimulus that was presented explicitly unpaired during fear conditioning were tested.…”

Section: Introductionmentioning

confidence: 99%

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Corticosterone Treatment and Incubation Time After Contextual Fear Conditioning Synergistically Induce Fear Memory Generalization in Neuropeptide S Receptor-Deficient Mice

Kolodziejczyk

Fendt

2020

Front. Neurosci.

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Fear memory generalization is a learning mechanism that promotes flexible fear responses to novel situations. While fear generalization has adaptive value, overgeneralization of fear memory is a characteristic feature of the pathology of anxiety disorders. The neuropeptide S (NPS) receptor (NPSR) has been shown to be associated with anxiety disorders and has recently been identified as a promising target for treating anxiety disorders. Moreover, stress hormones play a role in regulating both physiological and pathological fear memories and might therefore also be involved in anxiety disorders. However, little is known about the interplay between stress hormone and the NPS system in the development of overgeneralized fear. Here, we hypothesize that NPSR-deficient mice with high corticosterone (CORT) levels during the fear memories consolidation are more prone to develop generalized fear. To address this hypothesis, NPSR-deficient mice were submitted to a contextual fear conditioning procedure. Immediately after conditioning, mice received CORT injections (2.5 or 5 mg/kg). One day and 1 month later, the mice were tested for the specificity and strength of their fear memory, their anxiety level, and their startle response. Moreover, CORT blood levels were monitored throughout the experiment. Using this protocol, a specific contextual fear memory was observed in all experimental groups, despite the 5-mg/kg CORTtreated NPSR-deficient mice. This group of mice showed a generalization of contextual fear memory and a decreased startle response, and the females of this group had significantly less body weight gain. These findings indicate that interplay between CORT and the NPS system during the consolidation of fear memories is critical for the generalization of contextual fear.

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Section: Discussioncontrasting

confidence: 54%

Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

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Corticosterone Treatment and Incubation Time After Contextual Fear Conditioning Synergistically Induce Fear Memory Generalization in Neuropeptide S Receptor-Deficient Mice

Kolodziejczyk

Fendt

2020

Front. Neurosci.

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“…To evaluate associative emotional memory, animals were submitted to CFC and TFC training in conditioning box (Med-Associates, Inc., St. Albans, VT, United States), following a protocol adapted from previous studies ( Blanchard and Blanchard, 1969 ; LeDoux, 1993 ; Wood and Anagnostaras, 2011 ; Bueno et al, 2017 ). The training of CFC and TFC and also the CFC test (days 34 and 35, respectively) were carried out in the context A, consisting of a conditioning box with striped walls, grid floor and bright light.…”

Section: Methodsmentioning

confidence: 99%

Anandamide Effects in a Streptozotocin-Induced Alzheimer’s Disease-Like Sporadic Dementia in Rats

et al. 2018

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Alzheimer’s disease (AD) is characterized by multiple cognitive deficits including memory and sensorimotor gating impairments as a result of neuronal and synaptic loss. The endocannabinoid system plays an important role in these deficits but little is known about its influence on the molecular mechanism regarding phosphorylated tau (p-tau) protein accumulation – one of the hallmarks of AD –, and on the density of synaptic proteins. Thus, the aim of this study was to investigate the preventive effects of anandamide (N-arachidonoylethanolamine, AEA) on multiple cognitive deficits and on the levels of synaptic proteins (syntaxin 1, synaptophysin and synaptosomal-associated protein, SNAP-25), cannabinoid receptor type 1 (CB1) and molecules related to p-tau degradation machinery (heat shock protein 70, HSP70), and Bcl2-associated athanogene (BAG2) in an AD-like sporadic dementia model in rats using intracerebroventricular (icv) injection of streptozotocin (STZ). Our hypothesis is that AEA could interact with HSP70, modulating the level of p-tau and synaptic proteins, preventing STZ-induced cognitive impairments. Thirty days after receiving bilateral icv injections of AEA or STZ or both, the cognitive performance of adult male Wistar rats was evaluated in the object recognition test, by the escape latency in the elevated plus maze (EPM), by the tone and context fear conditioning as well as in prepulse inhibition tests. Subsequently, the animals were euthanized and their brains were removed for histological analysis or for protein quantification by Western Blotting. The behavioral results showed that STZ impaired recognition, plus maze and tone fear memories but did not affect contextual fear memory and prepulse inhibition. Moreover, AEA prevented recognition and non-associative emotional memory impairments induced by STZ, but did not influence tone fear conditioning. STZ increased the brain ventricular area and this enlargement was prevented by AEA. Additionally, STZ reduced the levels of p-tau (Ser199/202) and increased p-tau (Ser396), although AEA did not affect these alterations. HSP70 was found diminished only by STZ, while BAG2 levels were decreased by STZ and AEA. Synaptophysin, syntaxin and CB1 receptor levels were reduced by STZ, but only syntaxin was recovered by AEA. Altogether, albeit AEA failed to modify some AD-like neurochemical alterations, it partially prevented STZ-induced cognitive impairments, changes in synaptic markers and ventricle enlargement. This study showed, for the first time, that the administration of an endocannabinoid can prevent AD-like effects induced by STZ, boosting further investigations about the modulation of endocannabinoid levels as a therapeutic approach for AD.

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“…For example, glucocorticoid receptors in the ventral hippocampus or BLA are important for contextual fear, and infusion of corticosterone into the hippocampus after fear conditioning prevents mice from discriminating between correct and incorrect predictors of threat (Donley et al, 2005; Kaouane et al, 2012). Although not all studies demonstrate an effect of corticosterone (Bueno et al, 2017), there is significant variation with regard to many key variables, including conditioning parameters, corticosterone regimen, species and strain differences, etc.…”

Section: Molecular and Cellular Mechanisms Of Fear Generalizationmentioning

confidence: 99%

The Neurobiology of Fear Generalization

Asok

Kandel

Rayman

2019

Front. Behav. Neurosci.

131

102

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The generalization of fear memories is an adaptive neurobiological process that promotes survival in complex and dynamic environments. When confronted with a potential threat, an animal must select an appropriate defensive response based on previous experiences that are not identical, weighing cues and contextual information that may predict safety or danger. Like other aspects of fear memory, generalization is mediated by the coordinated actions of prefrontal, hippocampal, amygdalar, and thalamic brain areas. In this review article, we describe the current understanding of the behavioral, neural, genetic, and biochemical mechanisms involved in the generalization of fear. Fear generalization is a hallmark of many anxiety and stress-related disorders, and its emergence, severity, and manifestation are sex-dependent. Therefore, to improve the dialog between human and animal studies as well as to accelerate the development of effective therapeutics, we emphasize the need to examine both sex differences and remote timescales in rodent models.

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Corticosterone administration after a single-trial contextual fear conditioning does not influence the strength and specificity of recent and remote memory in rats

Cited by 12 publications

References 35 publications

Corticosterone Treatment and Incubation Time After Contextual Fear Conditioning Synergistically Induce Fear Memory Generalization in Neuropeptide S Receptor-Deficient Mice

Corticosterone Treatment and Incubation Time After Contextual Fear Conditioning Synergistically Induce Fear Memory Generalization in Neuropeptide S Receptor-Deficient Mice

Anandamide Effects in a Streptozotocin-Induced Alzheimer’s Disease-Like Sporadic Dementia in Rats

The Neurobiology of Fear Generalization

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