scholarly journals Effect of Sensory Deprivation of Nasal Respiratory on Behavior of C57BL/6J Mice

2021 ◽  
Vol 11 (12) ◽  
pp. 1626
Author(s):  
Yongji Zhu ◽  
Yujing Ye ◽  
Chenyang Zhou ◽  
Siqi Sun ◽  
Jingjing Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fear Conditioning ◽  
Memory Retrieval ◽  
Forced Swim Test ◽  
Sensory Deprivation ◽  
Recognition Task ◽  
Contextual Fear Conditioning ◽  
Nasal Breathing ◽  
Y Maze ◽  
General Locomotor Activity

Nasal breathing is a dynamic cortical organizer involved in various behaviors and states, such as locomotion, exploration, memory, emotion, introspection. However, the effect of sensory deprivation of nasal respiratory breath (NRD) on behavior remain poorly understood. Herein, general locomotor activity, emotion, learning and memory, social interaction, and mechanical pain were evaluated using a zinc sulfate nasal irrigation induced nasal respiratory sensory deprivation animal model (ZnSO4-induced mouse model). In the open field test, the elevated O-maze test, and forced swim test, NRD mice exhibited depressive and anxiety-like behaviors. In memory-associated tests, NRD mice showed cognitive impairments in the hippocampal-dependent memory (Y maze, object recognition task, and contextual fear conditioning (CFC)) and amygdala-dependent memory (the tone-cued fear conditioning test (TFC)). Surprisingly, NRD mice did not display deficits in the acquisition of conditional fear in both CFC and TFC tests. Still, they showed significant memory retrieval impairment in TFC and enhanced memory retrieval in CFC. At the same time, in the social novelty test using a three-chamber setting, NRD mice showed impaired social and social novelty behavior. Lastly, in the von Frey filaments test, we found that the pain sensitivity of NRD mice was reduced. In conclusion, this NRD mouse model showed a variety of behavioral phenotypic changes, which could offer an important insight into the behavioral impacts of patients with anosmia or those with an impaired olfactory bulb (OB) (e.g., in COVID-19, Alzheimer’s disease, Parkinson’s disease, etc.).

Memory retrieval after contextual fear conditioning induces c-Fos and JunB expression in CA1 hippocampus

2003 ◽  
Vol 2 (1) ◽  
pp. 3-10 ◽  
Author(s):  
T. Strekalova ◽  
B. Zörner ◽  
C. Zacher ◽  
G. Sadovska ◽  
T. Herdegen ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Retrieval ◽  
Contextual Fear Conditioning ◽  
Contextual Fear

Synaptic Correlates of Anterograde Amnesia and Intact Retrograde Memory in a Mouse Model of Alzheimer’s Disease

2020 ◽  
Vol 17 (3) ◽  
pp. 259-268 ◽  
Author(s):  
Emanuela Rizzello ◽  
Silvia Middei ◽  
Cristina Marchetti
Keyword(s):  
Alzheimer’S Disease ◽  
Patch Clamp ◽  
Mouse Model ◽  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Anterior Cingulate ◽  
Wild Type ◽  
Synaptic Currents ◽  
Contextual Fear ◽  
Tg2576 Mice

Background: Clinical evidence indicates that patients affected by Alzheimer's Disease (AD) fail to form new memories although their memories for old events are intact. This amnesic pattern depends on the selective vulnerability to AD-neurodegeneration of the hippocampus, the brain region that sustains the formation of new memories, while cortical regions that store remote memories are spared. Objective: To identify the cellular mechanisms underlying impaired recent memories and intact remote memories in a mouse model of AD. Method: Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected to the Contextual Fear Conditioning (CFC) task or in naïve conditions. Results: Glutamatergic synaptic currents were recorded by patch-clamp in acute hippocampal and anterior Cingulate Cortical (aCC) slices of AD-like Tg2576 mice and Wild-type (Wt) littermates subjected to the Contextual Fear Conditioning (CFC) task or in naïve conditions. Conclusion: Our data suggest that in the early AD stages synaptic plasticity of CA1 synapses, crucial to form new memories, is lost, while plasticity of aCC synapses is intact and contributes to the persistence of long-term memories.

scholarly journals REAC technology modifies pathological neuroinflammation and motor behaviour in an Alzheimer’s disease mouse model

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Luca Lorenzini ◽  
Alessandro Giuliani ◽  
Sandra Sivilia ◽  
Vito Antonio Baldassarro ◽  
Mercedes Fernandez ◽  
...  
Keyword(s):  
Mouse Model ◽  
Contextual Fear Conditioning ◽  
Innovative Technology ◽  
Motor Behaviour ◽  
New Therapeutic Approaches ◽  
Y Maze ◽  
Complex Motor ◽  
Gfap Immunoreactivity ◽  
N Treatment ◽  
Tg2576 Mice

Abstract The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. In this scenario, biotechnologies play an important role. Here, it is demonstrated that the Radio Electric Asymmetric Conveyer (REAC), an innovative technology platform for neuro- and bio-modulation, used according to the neuro-regenerative protocol (RGN-N), significantly increases astroglial reaction around the amyloid plaques in an AD mouse model, as evaluated by GFAP-immunoreactivity, and reduces microglia-associated neuroinflammation markers, as evaluated by Iba1-immunoreactivity and mRNA expression level of inflammatory cytokines TREM. IL1beta, iNOS and MRC1 were not affected neither by the genotype or by REAC RGN-N treatment. Also observed was an increase in locomotion in treated animals. The study was performed in 24-month-old male Tg2576 mice and age-matching wild-type animals, tested for Y-maze, contextual fear conditioning and locomotion immediately after the end of a specific REAC treatment administered for 15 hours/day for 15 days. These results demonstrated that REAC RGN-N treatment modifies pathological neuroinflammation, and mitigates part of the complex motor behaviour alterations observed in very old Tg2576 mice.

scholarly journals 4333 The role of the L-type calcium channel, Cav1.3, in motor and associative learning

2020 ◽  
Vol 4 (s1) ◽  
pp. 19-20
Author(s):  
Aislinn Joanmarie Williams ◽  
Marisol Lauffer ◽  
Hsiang Wen ◽  
Bryn Myers
Keyword(s):  
Motor Learning ◽  
Associative Learning ◽  
Fear Conditioning ◽  
Open Field ◽  
Genetic Background ◽  
Forced Swim Test ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Increased Risk ◽  
Deficient Mice

OBJECTIVES/GOALS: Genetic variation in L-type voltage-gated calcium channels, including CaV1.3, is associated with increased risk for psychiatric disorders including bipolar disorder and schizophrenia. Additionally, rare mutations in CaV1.3 have been linked to epilepsy, developmental delay, and autism. Deletion of CaV1.3 in mice is associated with impaired consolidation of contextual fear conditioning. Some studies have also observed affective behavior deficits in CaV1.3-deficient mice, but other studies have not found affective phenotypes, perhaps due to differences in genetic backgrounds, sex ratios, or task protocols. CaV1.3 is important for slow afterhyperpolarization in hippocampal and amygdala neurons, which prevents excessive firing in response to sustained excitatory input, and CaV1.3-deficient amygdala neurons exhibit hyperexcitability and impaired LTP. CaV1.3 is also expressed in the cerebellum, but its functional role there is not well understood. Given its importance in shaping neuronal activity in the hippocampus and amygdala, we hypothesized that loss of CaV1.3 would cause abnormalities in motor learning as well as affective and cognitive behaviors. METHODS/STUDY POPULATION: Wild-type (WT), haploinsufficient (Hap), and knockout (KO) mice were maintained on a congenic C57BL/6NTac genetic background and were subjected to behavioral tasks including open field, rotarod, ErasmusLadder, elevated zero maze, forced swim test, and tail suspension test. Data were analyzed with sexes combined and with sexes separated to assess for sex as a biological variable. Studies were analyzed by one-way ANOVA, two-way ANOVA, or generalized linear mixed model, where appropriate. RESULTS/ANTICIPATED RESULTS: CaV1.3 KO was associated with impaired motor learning in the rotarod task (p < 0.05), as well as impaired associative learning in the ErasmusLadder task (p < 0.01), despite intact locomotor function on both tasks. When examined by sex, the rotarod phenotypes were driven by motor learning impairments in males (both Hap and KO, p < 0.05 and p < 0.01, respectively), whereas the ErasmusLadder associative learning phenotypes were present in both sexes only in the KO condition, consistent with previously reported impairments in CaV1.3-deficient mice in consolidation of contextual fear conditioning. Although KO mice learned the motor aspects of the ErasmusLadder task, they learned more slowly. They also failed to learn start cues, which requires intact associative learning. No differences were observed in overall exploration or locomotor activity in open field or elevated zero maze. Analyses from affective tasks are ongoing. DISCUSSION/SIGNIFICANCE OF IMPACT: These preliminary studies provide new evidence that CaV1.3 is important for the function of neural circuits involved in motor learning, and concur with previous data showing its involvement in associative learning. Our data differ slightly from previous studies of CaV1.3 in motor learning, which could be attributable to differences in task protocols and/or genetic background. These results highlight the importance of CaV1.3 in a variety of behaviors, which may help explain why variation in CaV1.3 expression and function has pleiotropic effects in humans.

Corticosteroid-Binding Globulin Deficiency Specifically Impairs Contextual and Recognition Memory Consolidation in Male Mice

2019 ◽  
Vol 109 (4) ◽  
pp. 322-332
Author(s):  
Gabriela F. de Medeiros ◽  
Pauline Lafenêtre ◽  
Yoottana Janthakhin ◽  
Juan-Carlos Cerpa ◽  
Chun-Lei Zhang ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Performance ◽  
Recognition Task ◽  
Contextual Fear Conditioning ◽  
Long Term Memory ◽  
Male Mice ◽  
Odor Aversion ◽  
Term Memory ◽  
Corticosteroid Binding Globulin

Background/Aims: Glucocorticoids are essential in modulating memory processes of emotionally arousing experiences and we have shown that corticosteroid-binding globulin (CBG) influences glucocorticoid delivery to the brain. Here, we investigated the role of CBG in contextual and recognition long-term memory according to stress intensity. Method: We used adult male mice totally deficient in CBG (Cbg KO) or brain-specific Cbg KO (CbgCamk KO) to examine their performance in contextual fear conditioning (CFC) and au­ditory fear conditioning, both at short (1 h) and long-term (24 h). Long-term memory in Cbg KO was further analyzed in conditioned odor aversion and in novel object recognition task (NORT) with different paradigms, that is, with and without prior habituation to the context, with a mild or strong stressor applied during consolidation. In the NORT experiments, total and free glucocorticoid levels were measured during consolidation. Results: Impaired memory was observed in the Cbg KO but not in the CbgCamk KO in the CFC and the NORT without habituation when tested 24 h later. However, Cbg KO displayed normal behavior in the NORT with previous habituation and in the NORT with a mild stressor. In condition of the NORT with a strong stressor, Cbg KO retained good 24 h memory performance while controls were impaired. Total and free glucocorticoids levels were always higher in controls than in Cbg KO except in NORT with mild stressor where free glucocorticoids were equivalent to controls. Conclusions: These data indicate that circulating but not brain CBG influences contextual and recognition long-term memory in relation with glucocorticoid levels.

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