scholarly journals Endogenous Estrogen Influences Predator Odor-Induced Impairment of Cognitive and Social Behaviors in Aromatase Gene Deficiency Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Yaner Gao ◽  
Lei Ma ◽  
Feng Gao ◽  
Zuoli Sun ◽  
Zhengrong Zhang ◽  
...  
Keyword(s):  
Object Recognition ◽  
Social Behavior ◽  
Social Behaviors ◽  
Estrogen Deficiency ◽  
Predator Odor ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Aromatase Gene ◽  
Endogenous Estrogen

Epidemiological studies have suggested that traumatic stress increases vulnerability to various mental disorders, such as dementia and psychiatric disorders. While women are more vulnerable than men to depression and anxiety, it is unclear whether endogenous estrogens are responsible for the underlying sex-specific mechanisms. In this study, the aromatase gene heterozygous (Ar+/-) mice were used as an endogenous estrogen deficiency model and age- and sex-matched wild type mice (WT) as controls to study the predator odor 2,3,5-trimethyl-3-thiazoline- (TMT-) induced short- and long-term cognitive and social behavior impairments. In addition, the changes in brain regional neurotransmitters and their associations with TMT-induced changes in behaviors were further investigated in these animals. Our results showed TMT induced immediate fear response in both Ar+/- and WT mice regardless of sexes. TMT induced an acute impairment of novel object recognition memory and long-term social behavior impairment in WT mice, particularly in females, while Ar+/- mice showed impaired novel object recognition in both sexes and TMT-elevated social behaviors, particularly in males. TMT failed to induce changes in the prepulse inhibition (PPI) test in both groups. TMT resulted in a slight increase of DOPAC/DA ratio in the cortex and a significant elevation of this ratio in the striatum of WT mice. In addition, the ratio of HIAA/5-HT was significantly elevated in the cortex of TMT-treated WT mice, which was not found in TMT-treated Ar+/- mice. Taken together, our results indicate that TMT exposure can cause cognitive and social behavior impairments as well as change catecholamine metabolism in WT mice, and endogenous estrogen deficiency might desensitize the behavioral and neurochemical responses to TMT in Ar+/- mice.

scholarly journals Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

2021 ◽  
Vol 15 ◽  
Author(s):  
Yin Feng ◽  
Keguo Li ◽  
Elizabeth Roth ◽  
Dongman Chao ◽  
Christina M. Mecca ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Object Recognition ◽  
Brain Injury ◽  
Neuronal Activity ◽  
Home Cage ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Closed Head

A major hurdle preventing effective interventions for patients with mild traumatic brain injury (mTBI) is the lack of known mechanisms for the long-term cognitive impairment that follows mTBI. The closed head impact model of repeated engineered rotational acceleration (rCHIMERA), a non-surgical animal model of repeated mTBI (rmTBI), mimics key features of rmTBI in humans. Using the rCHIMERA in rats, this study was designed to characterize rmTBI-induced behavioral disruption, underlying electrophysiological changes in the medial prefrontal cortex (mPFC), and associated mitochondrial dysfunction. Rats received 6 closed-head impacts over 2 days at 2 Joules of energy. Behavioral testing included automated analysis of behavior in open field and home-cage environments, rotarod test for motor skills, novel object recognition, and fear conditioning. Following rmTBI, rats spent less time grooming and less time in the center of the open field arena. Rats in their home cage had reduced inactivity time 1 week after mTBI and increased exploration time 1 month after injury. Impaired associative fear learning and memory in fear conditioning test, and reduced short-term memory in novel object recognition test were found 4 weeks after rmTBI. Single-unit in vivo recordings showed increased neuronal activity in the mPFC after rmTBI, partially attributable to neuronal disinhibition from reduced inhibitory synaptic transmission, possibly secondary to impaired mitochondrial function. These findings help validate this rat rmTBI model as replicating clinical features, and point to impaired mitochondrial functions after injury as causing imbalanced synaptic transmission and consequent impaired long-term cognitive dysfunction.

scholarly journals Conversion of short-term to long-term memory in the novel object recognition paradigm

2013 ◽  
Vol 105 ◽  
pp. 174-185 ◽  
Author(s):  
Shannon J. Moore ◽  
Kaivalya Deshpande ◽  
Gwen S. Stinnett ◽  
Audrey F. Seasholtz ◽  
Geoffrey G. Murphy
Keyword(s):  
Object Recognition ◽  
Long Term Memory ◽  
Novel Object Recognition ◽  
The Novel ◽  
Short Term ◽  
Term Memory ◽  
Novel Object

scholarly journals Early-life status epilepticus induces long-term deficits in anxiety and spatial learning in mice

2017 ◽  
Vol 04 (01) ◽  
pp. 036-045
Author(s):  
Gregory Smith ◽  
Nowrin Ahmed ◽  
Erin Arbuckle ◽  
Joaquin Lugo
Keyword(s):  
Status Epilepticus ◽  
Object Recognition ◽  
Early Life ◽  
Water Maze ◽  
Elevated Plus Maze ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Plus Maze ◽  
Marble Burying

Abstract Background One of the most devastating aspects of developmental epilepsy is the long-term impact on behavior. Children with epilepsy show a high co-morbidity with anxiety disorders and autism. Methods To examine whether early-life status epilepticus results in altered anxiety, repetitive behavior, social behavior, and learning and memory, we induced status epilepticus in male C57BL/6 mice on postnatal day (PD) 10. The mice received intraperitoneal injections of either kainic acid (2 mg/kg) or 0.9% normal saline. We also included a nontreated control group. Kainic acid induced status epilepticus for approximately 1.5 h. At PD60, the adult mice were then tested in a battery of behavioral tasks, including open field activity, elevated-plus maze, light-dark test, marble burying, social chamber, social partition, conditioned fear, novel object recognition, and Morris water maze. Results The early-life seizure group showed consistent increases in anxiety in the open field test (p < 0.05), elevated plus maze (p < 0.05), and light-dark task (p < 0.01). The seizure group showed significant (p < 0.01) impairment in the Morris water maze. There were no differences observed in marble burying, social partition, social chamber, novel object recognition, or delay fear conditioning tasks. Conclusions These results demonstrate that a single insult of status epilepticus during the neonatal period is sufficient to cause specific, long-term impairments in anxiety and spatial learning.

scholarly journals Perineuronal Net Receptor PTPσ Regulates Retention of Memories

2021 ◽  
Vol 13 ◽  
Author(s):  
Angelina Lesnikova ◽  
Plinio Casarotto ◽  
Rafael Moliner ◽  
Senem Merve Fred ◽  
Caroline Biojone ◽  
...  
Keyword(s):  
Object Recognition ◽  
Fear Conditioning ◽  
Cognitive Flexibility ◽  
Long Term Memory ◽  
Novel Object Recognition ◽  
Short Term ◽  
Perineuronal Net ◽  
Term Memory ◽  
Novel Object

Perineuronal nets (PNNs) have an important physiological role in the retention of learning by restricting cognitive flexibility. Their deposition peaks after developmental periods of intensive learning, usually in late childhood, and they help in long-term preservation of newly acquired skills and information. Modulation of PNN function by various techniques enhances plasticity and regulates the retention of memories, which may be beneficial when memory persistence entails negative symptoms such as post-traumatic stress disorder (PTSD). In this study, we investigated the role of PTPσ [receptor-type tyrosine-protein phosphatase S, a phosphatase that is activated by binding of chondroitin sulfate proteoglycans (CSPGs) from PNNs] in retention of memories using Novel Object Recognition and Fear Conditioning models. We observed that mice haploinsufficient for PTPRS gene (PTPσ+/–), although having improved short-term object recognition memory, display impaired long-term memory in both Novel Object Recognition and Fear Conditioning paradigm, as compared to WT littermates. However, PTPσ+/– mice did not show any differences in behavioral tests that do not heavily rely on cognitive flexibility, such as Elevated Plus Maze, Open Field, Marble Burying, and Forced Swimming Test. Since PTPσ has been shown to interact with and dephosphorylate TRKB, we investigated activation of this receptor and its downstream pathways in limbic areas known to be associated with memory. We found that phosphorylation of TRKB and PLCγ are increased in the hippocampus, prefrontal cortex, and amygdaloid complex of PTPσ+/– mice, but other TRKB-mediated signaling pathways are not affected. Our data suggest that PTPσ downregulation promotes TRKB phosphorylation in different brain areas, improves short-term memory performance but disrupts long-term memory retention in the tested animal models. Inhibition of PTPσ or disruption of PNN-PTPσ-TRKB complex might be a potential target for disorders where negative modulation of the acquired memories can be beneficial.

scholarly journals Mice deficient in the NAAG synthetase II gene Rimkla are impaired in a novel object recognition task

2021 ◽  
Author(s):  
Ivonne Becker ◽  
Lihua Wang‐Eckhardt ◽  
Julia Lodder‐Gadaczek ◽  
Yong Wang ◽  
Agathe Grünewald ◽  
...  
Keyword(s):  
Object Recognition ◽  
Recognition Task ◽  
Novel Object Recognition ◽  
Novel Object ◽  
Object Recognition Task ◽  
Novel Object Recognition Task
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