Contextual learning increases dendrite complexity and EphrinB2 levels in hippocampal mouse neurons

Trabalza, Antonio; Colazingari, Sandra; Sgobio, Carmelo; Bevilacqua, Arturo

doi:10.1016/j.bbr.2011.11.008

Cited by 19 publications

(9 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ephrins are expressed in brain regions that have been shown to be involved in memory formation such as the hippocampus (eg, mouse: Carmona et al, 2009 ; primates: Xiao et al, 2006 ), amygdala (eg, mouse: Trabalza et al, 2012 ; primates: Xiao et al, 2006 ), and cortex (eg, mouse: Theus et al, 2014 ; primates: Xiao et al, 2006 ). It is therefore possible that ephrins that are involved in synaptic transmission, plasticity, and neuronal morphogenesis (see below), cellular processes involved in memory formation, mediate memory formation in these brain regions.…”

Section: Ephrins In Memory Formationmentioning

confidence: 99%

“…These data show a role for ephrinB3 in performing a hippocampus-dependent learning task, independent of its cytoplasmic domain. Mice trained for contextual and auditory fear conditioning showed changes in dendritic morphology in hippocampus and lateral amygdala 24 hours after training compared with naïve or pseudoconditioned mice ( Trabalza et al, 2012 ). Conditioned but not pseudoconditioned or naive mice showed a specific increase in the amount of ephrinB2 in the hippocampus CA1 region but not cortex or amygdala ( Trabalza et al, 2012 ).…”

Section: Ephrins In Memory Formationmentioning

confidence: 99%

“…Mice trained for contextual and auditory fear conditioning showed changes in dendritic morphology in hippocampus and lateral amygdala 24 hours after training compared with naïve or pseudoconditioned mice ( Trabalza et al, 2012 ). Conditioned but not pseudoconditioned or naive mice showed a specific increase in the amount of ephrinB2 in the hippocampus CA1 region but not cortex or amygdala ( Trabalza et al, 2012 ). These results suggest that an increase in ephrinB2 levels in hippocampal CA1 neurons is involved in the behavioral and neuronal changes induced by contextual fear conditioning.…”

Section: Ephrins In Memory Formationmentioning

confidence: 99%

See 2 more Smart Citations

The Role of Ephs and Ephrins in Memory Formation

Dines

Lamprecht

2015

IJNPPY

View full text Add to dashboard Cite

The ability to efficiently store memories in the brain is a fundamental process and its impairment is associated with multiple human mental disorders. Evidence indicates that long-term memory formation involves alterations of synaptic efficacy produced by modifications in neural transmission and morphology. The Eph receptors and their cognate ephrin ligands have been shown to be involved in these key neuronal processes by regulating events such as presynaptic transmitter release, postsynaptic glutamate receptor conductance and trafficking, synaptic glutamate reuptake, and dendritic spine morphogenesis. Recent findings show that Ephs and ephrins are needed for memory formation in different organisms. These proteins participate in the formation of various types of memories that are subserved by different neurons and brain regions. Ephs and ephrins are involved in brain disorders and diseases with memory impairment symptoms, including Alzheimer’s disease and anxiety. Drugs that agonize or antagonize Ephs/ephrins signaling have been developed and could serve as therapeutic agents to treat such diseases. Ephs and ephrins may therefore induce cellular alterations mandatory for memory formation and serve as a target for pharmacological intervention for treatment of memory-related brain diseases.

show abstract

Section: Ephrins In Memory Formationmentioning

confidence: 99%

Section: Ephrins In Memory Formationmentioning

confidence: 99%

Section: Ephrins In Memory Formationmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Ephs and Ephrins in Memory Formation

Dines

Lamprecht

2015

IJNPPY

View full text Add to dashboard Cite

show abstract

“…Disruption of ephrin-B reverse signaling in neurons was also implicated in impaired hippocampal-dependent learning and memory in EphB2 KO mice (Grunwald et al, 2001). In addition, ephrin-B2 expression is upregulated in CA1 neurons but not the cortex or amygdala following fear conditioning without changes in levels of EphA4 receptor (Trabalza et al, 2012). While ephrin-B2 can activate both EphA4 and EphB receptors, ephrin-B1 is known for its high affinity for EphB but not EphA4 receptors.…”

Section: Introductionmentioning

confidence: 96%

Astrocytic Ephrin-B1 Controls Synapse Formation in the Hippocampus During Learning and Memory

Nguyen

Koeppen

Woodruff

et al. 2020

Front. Synaptic Neurosci.

View full text Add to dashboard Cite

Astrocytes play a fundamental role in synapse formation, pruning, and plasticity, which are associated with learning and memory. However, the role of astrocytes in learning and memory is still largely unknown. Our previous study showed that astrocytespecific ephrin-B1 knockout (KO) enhanced but ephrin-B1 overexpression (OE) in hippocampal astrocytes impaired contextual memory recall following fear conditioning. The goal of this study was to understand the mechanism by which astrocytic ephrin-B1 influences learning; specifically, learning-induced remodeling of synapses and dendritic spines in CA1 hippocampus using fear-conditioning paradigm. While we found a higher dendritic spine density and clustering on c-Fos-positive (+) neurons activated during contextual memory recall in both wild-type (WT) and KO mice, overall spine density and mEPSC amplitude were increased in CA1 neurons of KO compared to WT. In contrast, ephrin-B1 OE in hippocampal astrocytes impaired dendritic spine formation and clustering, specifically on c-Fos(+) neurons, coinciding with an overall decrease in vGlut1/PSD95 co-localization. Although astrocytic ephrin-B1 influenced learninginduced spine formation, the changes in astrocytic ephrin-B1 levels did not affect spine enlargement as no genotype differences in spine volume were observed between trained WT, KO, and OE groups. Our results suggest that a reduced formation of new spines rather than spine maturation in activated CA1 hippocampal neurons is most likely responsible for impaired contextual learning in OE mice due to abundantly high ephrin-B1 levels in astrocytes. The ability of astrocytic ephrin-B1 to negatively influence new spine formation during learning can potentially regulate new synapse formation at specific dendritic domains and underlie memory encoding.

show abstract

“…The brain is remarkably adaptive. Neuroimaging studies in animals and humans have shown multiple facets of plasticity, 1 , 2 manifested as structural changes induced by environment, 3 learning, 4 behavior 1 , 5 and emotions. 6 Similar to structural plasticity, emotions alter neural responsivity.…”

Section: Introductionmentioning

confidence: 99%

Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder

et al. 2016

View full text Add to dashboard Cite

Patients with anxiety disorders exhibit excessive neural reactivity in the amygdala, which can be normalized by effective treatment like cognitive behavior therapy (CBT). Mechanisms underlying the brain's adaptation to anxiolytic treatments are likely related both to structural plasticity and functional response alterations, but multimodal neuroimaging studies addressing structure–function interactions are currently missing. Here, we examined treatment-related changes in brain structure (gray matter (GM) volume) and function (blood–oxygen level dependent, BOLD response to self-referential criticism) in 26 participants with social anxiety disorder randomly assigned either to CBT or an attention bias modification control treatment. Also, 26 matched healthy controls were included. Significant time × treatment interactions were found in the amygdala with decreases both in GM volume (family-wise error (FWE) corrected PFWE=0.02) and BOLD responsivity (PFWE=0.01) after successful CBT. Before treatment, amygdala GM volume correlated positively with anticipatory speech anxiety (PFWE=0.04), and CBT-induced reduction of amygdala GM volume (pre–post) correlated positively with reduced anticipatory anxiety after treatment (PFWE⩽0.05). In addition, we observed greater amygdala neural responsivity to self-referential criticism in socially anxious participants, as compared with controls (PFWE=0.029), before but not after CBT. Further analysis indicated that diminished amygdala GM volume mediated the relationship between decreased neural responsivity and reduced social anxiety after treatment (P=0.007). Thus, our results suggest that improvement-related structural plasticity impacts neural responsiveness within the amygdala, which could be essential for achieving anxiety reduction with CBT.

show abstract

Contextual learning increases dendrite complexity and EphrinB2 levels in hippocampal mouse neurons

Cited by 19 publications

References 59 publications

The Role of Ephs and Ephrins in Memory Formation

The Role of Ephs and Ephrins in Memory Formation

Astrocytic Ephrin-B1 Controls Synapse Formation in the Hippocampus During Learning and Memory

Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder

Contact Info

Product

Resources

About