Co-learning facilitates memory in mice: A new avenue in social neuroscience

Lipina, Tatiana V.; Roder, John

doi:10.1016/j.neuropharm.2012.06.054

Cited by 26 publications

(14 citation statements)

References 63 publications

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“…For instance, Lipina and Roder have recently demonstrated that paired co-learning (simultaneous involvement to the same activity) with a familiar BL6 mouse rescued the deficit in episodic memory in BTBR mice. Co-learning reduced the anxiety level, increased the exploratory behavior and mediated the learning-facilitation in a novel environment (Lipina and Roder, 2013). Therefore, our expectation of the positive effect would be reduced anxiety-like behavior and improved learning in DBA/2 mice when BL6 and DBA/2 strains were mixed.…”

Section: Discussionmentioning

confidence: 99%

“…Re-socialization (group-housing with normally developed peers) rescued the prosocial deficit induced by post-weaning social isolation in rats (Tulogdi et al, 2014). The effectiveness of group-learning and social enrichment in facilitation of learning and memory was also validated in an animal model of Alzheimer's disease (Kiryk et al, 2011) and in BTBR mice (Lipina and Roder, 2013). …”

Section: Introductionmentioning

confidence: 99%

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Mixed housing with DBA/2 mice induces stress in C57BL/6 mice: implications for interventions based on social enrichment

Kulesskaya

Karpova

et al. 2014

Front. Behav. Neurosci.

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Several behavioral interventions, based on social enrichment and observational learning are applied in treatment of neuropsychiatric disorders. However, the mechanism of such modulatory effect and the safety of applied methods on individuals involved in social support need further investigation. We took advantage of known differences between inbred mouse strains to reveal the effect of social enrichment on behavior and neurobiology of animals with different behavioral phenotypes. C57BL/6 and DBA/2 female mice displaying multiple differences in cognitive, social, and emotional behavior were group-housed either in same-strain or in mixed-strain conditions. Comprehensive behavioral phenotyping and analysis of expression of several plasticity- and stress-related genes were done to measure the reciprocal effects of social interaction between the strains. Contrary to our expectation, mixed housing did not change the behavior of DBA/2 mice. Nevertheless, the level of serum corticosterone and the expression of glucocorticoid receptor Nr3c1 in the brain were increased in mixed housed DBA/2 as compared with those of separately housed DBA/2 mice. In contrast, socially active C57BL/6 animals were more sensitive to the mixed housing, displaying several signs of stress: alterations in learning, social, and anxiety-like behavior and anhedonia. These behavioral impairments were accompanied by the elevated serum corticosterone and the reduced expression of Nr3c1, as well as the elevated Bdnf levels in the cortex and hippocampus. Our results demonstrate the importance of social factors in modulation of both behavior and the underlying neurobiological mechanisms in stress response, and draw attention to the potential negative impact of social interventions for individuals involved in social support.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mixed housing with DBA/2 mice induces stress in C57BL/6 mice: implications for interventions based on social enrichment

Kulesskaya

Karpova

et al. 2014

Front. Behav. Neurosci.

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“…Its morphology is altered in the BTBR mice (Mercier et al 2012). Amygdala-dependent fear learning is impaired, both in the classic conditioning paradigm (MacPherson et al 2008) and during social co-learning of fear responses (Lipina and Roder, 2013). The activation of several nuclei of amygdala was also dampened, as compared with B6 mice, in response to emotional information transfer from a conspecific (Meyza et al 2015).…”

Section: Future Directionsmentioning

confidence: 99%

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Meyza

Blanchard

2017

Neuroscience & Biobehavioral Reviews

126

109

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Autism spectrum disorder (ASD) is the most commonly diagnosed neurodevelopmental disorder, with current estimates of more than 1% of affected children across nations. The patients form a highly heterogeneous group with only the behavioral phenotype in common. The genetic heterogeneity is reflected in a plethora of animal models representing multiple mutations found in families of affected children. Despite many years of scientific effort, for the majority of cases the genetic cause remains elusive. It is therefore crucial to include well-validated models of idiopathic autism in studies searching for potential therapeutic agents. One of these models is the BTBR T+Itpr3tf/J mouse. The current review summarizes data gathered in recent research on potential molecular mechanisms responsible for the autism-like behavioral phenotype of this strain.

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“…There is now a large literature demonstrating disturbances in spine morphology and signaling cascades at excitatory synapses in animal models of cognitive disability (Belichenko et al, 2007;Kramar et al, 2012), including disorders on the autism spectrum (Chen et al, 2010;Hung et al, 2008;Seese et al, 2012;Tropea et al, 2009). Learning and executive functions are impaired in BTBR mice (Amodeo et al, 2012;Lipina and Roder, 2013;MacPherson et al, 2008;Ribeiro et al, 2013;Rutz and Rothblat, 2012;Silverman et al, 2013;Yang et al, 2012), but thorough analyses of associated synaptic abnormalities and evidence for pharmacological normalization of these measures are lacking.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Memory Deficits are Associated with Elevated Synaptic ERK1/2 Activation and Reversed by mGluR5 Antagonism in an Animal Model of Autism

Seese

Maske

Lynch

et al. 2014

Neuropsychopharmacol

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A significant proportion of patients with autism exhibit some degree of intellectual disability. The BTBR T þ Itpr3 tf /J mouse strain exhibits behaviors that align with the major diagnostic criteria of autism. To further evaluate the BTBR strain's cognitive impairments, we quantified hippocampus-dependent object location memory (OLM) and found that one-third of the BTBR mice exhibited robust memory, whereas the remainder did not. Fluorescence deconvolution tomography was used to test whether synaptic levels of activated extracellular signal-regulated kinase 1/2 (ERK1/2), a protein that contributes importantly to plasticity, correlate with OLM scores in individual mice. In hippocampal field CA1, the BTBRs had fewer post-synaptic densities associated with high levels of phosphorylated (p-) ERK1/2 as compared with C57BL/6 mice. Although counts of p-ERK1/2 immunoreactive synapses did not correlate with OLM performance, the intensity of synaptic p-ERK1/2 immunolabeling was negatively correlated with OLM scores across BTBRs. Metabotropic glutamate receptor (mGluR) 5 signaling activates ERK1/2. Therefore, we tested whether treatment with the mGluR5 antagonist MPEP normalizes synaptic and learning measures in BTBR mice: MPEP facilitated OLM and decreased synaptic p-ERK1/2 immunolabeling intensity without affecting numbers of p-ERK1/2 þ synapses. In contrast, semi-chronic ampakine treatment, which facilitates memory in other models of cognitive impairment, had no effect on OLM in BTBRs. These results suggest that intellectual disabilities associated with different neurodevelopmental disorders on the autism spectrum require distinct therapeutic strategies based on underlying synaptic pathology.

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Co-learning facilitates memory in mice: A new avenue in social neuroscience

Cited by 26 publications

References 63 publications

Mixed housing with DBA/2 mice induces stress in C57BL/6 mice: implications for interventions based on social enrichment

Mixed housing with DBA/2 mice induces stress in C57BL/6 mice: implications for interventions based on social enrichment

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Long-Term Memory Deficits are Associated with Elevated Synaptic ERK1/2 Activation and Reversed by mGluR5 Antagonism in an Animal Model of Autism

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