The consolidation of inhibitory avoidance memory in mice depends on the intensity of the aversive stimulus: The involvement of the amygdala, dorsal hippocampus and medial prefrontal cortex

Canto-de-Souza, Lucas; Mattioli, Rosana

doi:10.1016/j.nlm.2016.01.012

Cited by 21 publications

(11 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We also assessed plasma levels of multiple stress-associated signal molecules in group-housed and isolated Kpna1 KO mice. In our study, we found Kpna1 deletion decreases anxiety-like behavior, impairs short-term memory and sensorimotor gating, and increases depression-like behavior, suggesting that hypofunction of KPNA1 results in behavioral changes associated with psychiatric disorders [32,[39][40][41][42][43][44][45]49]. Furthermore, the administration of adolescent social isolation stress, an environmental risk factor known to interact with genetic risk factors in the development of psychiatric disorders [25,27], resulted in significant impairment of aversive learning and/or memory in the IA and increased depression-like behavior in the FS in Kpna1 KO mice.…”

Section: Discussionmentioning

confidence: 99%

“…Inhibitory avoidance test. The inhibitory avoidance test assesses aversive learning and memory by measuring the latency to enter into a 'dark' chamber paired with an aversive [32,43]. Three-way repeated measures ANOVA analysis revealed a significant main effect of trial (day) on the latency to enter the 'dark' chamber (F (1,34) = 265.1, p<0.001), indicating that mice were able to learn the contingency between the chamber and the shock with which it had been paired on day 1.…”

Section: Memory-related Tasksmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Importin α1/KPNA1 deletion and adolescent social isolation stress on psychiatric disorder-associated behaviors in mice

et al. 2021

View full text Add to dashboard Cite

Importin α1/KPNA1 is a member of the Importin α family widely present in the mammalian brain and has been characterized as a regulator of neuronal differentiation, synaptic functionality, and anxiety-like behavior. In humans, a de novo mutation of the KPNA1 (human Importin α5) gene has been linked with schizophrenia; however, the precise roles of KPNA1 in disorder-related behaviors are still unknown. Moreover, as recent studies have highlighted the importance of gene-environment interactions in the development of psychiatric disorders, we investigated the effects of Kpna1 deletion and social isolation stress, a paradigm that models social stress factors found in human patients, on psychiatric disorder-related behaviors in mice. Through assessment in a behavioral battery, we found that Kpna1 knockout resulted in the following behavioral phenotype: (1) decreased anxiety-like behavior in an elevated plus maze test, (2) short term memory deficits in novel object recognition test (3) impaired sensorimotor gating in a prepulse inhibition test. Importantly, exposure to social isolation stress resulted in additional behavioral abnormalities where isolated Kpna1 knockout mice exhibited: (1) impaired aversive learning and/or memory in the inhibitory avoidance test, as well as (2) increased depression-like behavior in the forced swim test. Furthermore, we investigated whether mice showed alterations in plasma levels of stress-associated signal molecules (corticosterone, cytokines, hormones, receptors), and found that Kpna1 knockout significantly altered levels of corticosterone and LIX (CXCL5). Moreover, significant decreases in the level of prolactin were found in all groups except for group-housed wild type mice. Our findings demonstrate that Kpna1 deletion can trigger widespread behavioral abnormalities associated with psychiatric disorders, some of which were further exacerbated by exposure to adolescent social isolation. The use of Kpna1 knockout mice as a model for psychiatric disorders may show promise for further investigation of gene-environment interactions involved in the pathogenesis of psychiatric disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Memory-related Tasksmentioning

confidence: 99%

Effects of Importin α1/KPNA1 deletion and adolescent social isolation stress on psychiatric disorder-associated behaviors in mice

et al. 2021

View full text Add to dashboard Cite

show abstract

“…For instance, different involvement of the amygdala (AMG), pre-frontal cortex (PFC) and hippocampus (HPC) was found under different intensities (Canto-de-Souza & Mattioli, 2016;Garín-Aguilar et al, 2014;Matos et al, 2019). In addition, corticosterone levels correlate with the intensity of conditioning Dos Santos Corrêa et al, 2019;Ponce-Lina et al, 2020), which in turns determines the ability of glucocorticoid antagonists to regulate fear memory .…”

Section: Introductionmentioning

confidence: 99%

Hippocampal TRPV1 channels in the modulation of contextual fear conditioning

HdB

et al. 2021

Preprint

View full text Add to dashboard Cite

Psychiatric disorders have been linked to impairments in fear memory circuitry. Thus, pharmacological approaches that impair aversive memories have been investigated as new treatments. The TRPV1 channel modulates biological processes related to memory consolidation and retrieval. However, TRPV1 seems involved in memories generated by high intense conditioning. Anandamide (AEA), the main endocannabinoid, is an agonist of both, TRPV1 channels and CB1 receptors which are colocalized in several brain structures. Remarkably, AEA has twenty-times more affinity for CB1 than for TRPV1, which may be involved in the intensity-dependent recruitment of this channel. In order to evaluate the role of intensity of the conditioning in the recruitment of TRPV1, the animals were submitted to the contextual fear conditioning (CFC) and conditioned with low, moderate or high intensity. Before the retrieval a TRPV1 blocker was administered into the dorsal hippocampus (dHPC). The levels of AEA were quantified by Mass Spectrometry. The RNA levels of Arc, Zif and Trkb, involved in memory and plasticity, were quantified by PCR. Our results showed that TRPV1 blockers impair the retrieval of memory in animals conditioned with moderate and high intensity but not low ones. As revealed by Mass Spectrometry, this different recruitment among intensities seems to be associated with the levels of AEA released. Moreover, the impairment in freezing induced by blocking TRPV1 was prevented by a subeffective dose of the cannabinoid receptor CB1 antagonist which suggest that TRPV1 blockers act increasing AEA availability in the synaptic cleft to act through CB1 receptors. Despite blocking TRPV1 channels impairs freezing in moderate and high intensities, it increases the RNA levels of Arc, Zif and Trkb only in animals conditioned with the moderate intensity. In accordance, the treatment impairs retrieval in both intensities but only in the moderate intensity is able to prevent the reinstatement. Summarizing, our results suggested that intensity of the conditioning modulates AEA levels which in turns determines if TRPV1 will be recruited at the retrieval and which molecular pathways will be engaged due to TRPV1 blocking.

show abstract

“…(Deogracias et al, 2004;Leal et al, 2014). Esses fenômenos neuroplásticos no CPFM e Hpc estão diretamente envolvidos em processos de formação de memória (Brightwell et al, 2004;Canto-de-Souza and Mattioli, 2016;Giustino and Maren, 2015;Impey et al, 1998;Martínez et al, 2014;Zoladz et al, 2012). Estudos demonstram que a deposição da βA modifica a cinética de liberação e captação do glutamato (Brito-Moreira et al, 2011;Pirttimaki et al, 2013;Talantova et al, 2013).…”

Section: Discussionunclassified

“…O BDNF é uma neurotrofina responsável pela ativação do receptor TrkB, que sofre uma fosforilação e leva a uma sequência de eventos celulares, promovendo efeitos neuroprotetores por aumentar o número de conexões entre os neurônios e a formação espinhas dendríticas (Deogracias et al, 2004;Leal et al, 2014). A mediação de tais fenômenos neuroplásticos pela via S-NMDA/CREB/BDNF-TrkB no CPFM e Hpc está envolvida em processos de formação de memória (Brightwell et al, 2004;Canto-de-Souza and Mattioli, 2016;Giustino and Maren, 2015;Impey et al, 1998;Martínez et al, 2014;Zoladz et al, 2012). Além disso, esta mesma via também facilita a potenciação de longo prazo (LTP-long term potentiation), um fenômeno celular subjacente à formação de memória (Bliss and Collingridge, 1993;Korte et al, 1998;Minichiello, 2009;Minichiello et al, 2002;Taylor et al, 2016).…”

Section: Introductionunclassified

Efeitos neuroprotetores do antagonismo dos receptores TRPV1 em um modelo animal da Doença de Alzheimer

Silva¹

View full text Add to dashboard Cite

Aos meus pais, por todo amor, carinho e paciência. Ao meu irmão pela parceria de vida. Aos meus avós por todos os ensinamentos. AGRADECIMENTOS AGRADECIMENTOSA Deus que é essencial em minha vida, é a base que eu tenho para me guiar, iluminar e me fortalecer em todo o meu caminho sem perder a fé. Aos meus familiares, por todo apoio, incentivo e força em todos os momentos dessa jornada.Ao Prof. Leonardo Resstel, meu agradecimento por ter aberto as portas do seu laboratório para que eu pudesse aprender e evoluir cientificamente. Obrigada pela confiança e todos os ensinamentos. Aprendi muito durante esses anos.

show abstract

The consolidation of inhibitory avoidance memory in mice depends on the intensity of the aversive stimulus: The involvement of the amygdala, dorsal hippocampus and medial prefrontal cortex

Cited by 21 publications

References 92 publications

Effects of Importin α1/KPNA1 deletion and adolescent social isolation stress on psychiatric disorder-associated behaviors in mice

Effects of Importin α1/KPNA1 deletion and adolescent social isolation stress on psychiatric disorder-associated behaviors in mice

Hippocampal TRPV1 channels in the modulation of contextual fear conditioning

Efeitos neuroprotetores do antagonismo dos receptores TRPV1 em um modelo animal da Doença de Alzheimer

Contact Info

Product

Resources

About