ErbB4 Receptors in the Medial Habenula Regulate Contextual Fear Memory

Geng, Fei; Liu, Jiayun; Chen, Xiaowen; Zou, Wen-Jun; Wu, Jianlin; Rodríguez, Guadalupe; Peng, Chao; Tian, Jianwei; Lu, Gui-Feng

doi:10.1159/000495064

Cited by 3 publications

(2 citation statements)

References 31 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The implication of the MHb in trace fear conditioning has not yet been investigated. This region in rodents (Yamaguchi et al 2013;Zhang et al 2016;Geng et al 2019), or its equivalent in zebrafish (the dorsal habenula; Agetsuma et al 2010), modulate fear responses, although Hsu et al (2016) found no contextual fear conditioning deficits following its lesion. The LHb is also included in these two factors, but with regional specificity.…”

Section: Discussionmentioning

confidence: 97%

Involvement of the lateral habenula in fear memory

et al. 2020

View full text Add to dashboard Cite

Increasing evidence points to the engagement of the lateral habenula (LHb) in the selection of appropriate behavioral responses in aversive situations. However, very few data have been gathered with respect to its role in fear memory formation, especially in learning paradigms in which brain areas involved in cognitive processes like the hippocampus (HPC) and the medial prefrontal cortex (mPFC) are required. A paradigm of this sort is trace fear conditioning, in which an aversive event is preceded by a discrete stimulus, generally a tone, but without the close temporal contiguity allowing for their association based on amygdala-dependent information processing. In a first experiment, we analyzed cellular activations (c-Fos expression) induced by trace fear conditioning in subregions of the habenular complex, HPC, mPFC and amygdala using a factorial analysis to unravel functional networks through correlational analysis of data. This analysis suggested that distinct LHb subregions engaged in different aspects of conditioning, e.g. associative processes and onset of fear responses. In a second experiment, we performed chemogenetic LHb inactivation during the conditioning phase of the trace fear conditioning paradigm and subsequently assessed contextual and tone fear memories. Whereas LHb inactivation did not modify rat's behavior during conditioning, it induced contextual memory deficits and enhanced fear to the tone. These results demonstrate the involvement of the LHb in fear memory. They further suggest that the LHb is engaged in learning about threatening environments through the selection of relevant information predictive of a danger.

show abstract

Section: Discussionmentioning

confidence: 97%

Involvement of the lateral habenula in fear memory

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In addition, postsynaptic nAChRs located on IPn neurons can generate retrograde signaling molecules, including endocannabinoids and nitric oxide, that provide a source of feedback inhibition onto mHb inputs ( Rodrigo et al, 1994 ; Ables et al, 2017 ; Quina et al, 2017 ; Melani et al, 2019 ). Little is currently known about the function of the mHb-IPn circuit, although available data suggest that mHb-derived cholinergic, glutamatergic, and substance P transmission in the IPn modulated by GABA B , cannabinoid 1 (CB1), or glycine receptors regulates the encoding of memories related to aversive stimuli or events ( Thompson, 1960 ; Donovick et al, 1970 ; Agetsuma et al, 2010 ; Yamaguchi et al, 2013 ; Soria-Gomez et al, 2015; Zhang et al, 2016 ; Koppensteiner et al, 2017 ; Geng et al, 2019 ; Melani et al, 2019 ). The mHb-IPn circuit may also coordinate adaptive physiologic and behavioral responses to stressful or anxiety-provoking stimuli ( Lisoprawski et al, 1981 ; Murray et al, 1994 ; Shumake et al, 2003 ; Hsu et al, 2012, 2016 ; Xu et al, 2018 ; Duncan et al, 2019 ; Sherafat et al, 2020 ).…”

Section: Nondopamine Mechanisms Of Nicotine Aversionmentioning

confidence: 99%

Neurobiological Mechanisms of Nicotine Reward and Aversion

et al. 2022

View full text Add to dashboard Cite

show abstract

Inhibitory Neural Network’s Impairments at Hippocampal CA1 LTP in an Aged Transgenic Mouse Model of Alzheimer’s Disease

Seo

Park

Choi

et al. 2021

IJMS

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a rapid accumulation of amyloid β (Aβ) protein in the hippocampus, which impairs synaptic structures and neuronal signal transmission, induces neuronal loss, and diminishes memory and cognitive functions. The present study investigated the impact of neuregulin 1 (NRG1)-ErbB4 signaling on the impairment of neural networks underlying hippocampal long-term potentiation (LTP) in 5xFAD mice, a model of AD with greater symptom severity than that of TG2576 mice. Specifically, we observed parvalbumin (PV)-containing hippocampal interneurons, the effect of NRG1 on hippocampal LTP, and the functioning of learning and memory. We found a significant decrease in the number of PV interneurons in 11-month-old 5xFAD mice. Moreover, synaptic transmission in the 5xFAD mice decreased at 6 months of age. The 11-month-old transgenic AD mice showed fewer inhibitory PV neurons and impaired NRG1-ErbB4 signaling than did wild-type mice, indicating that the former exhibit the impairment of neuronal networks underlying LTP in the hippocampal Schaffer-collateral pathway. In conclusion, this study confirmed the impaired LTP in 5xFAD mice and its association with aberrant NRG1-ErbB signaling in the neuronal network.

show abstract

ErbB4 Receptors in the Medial Habenula Regulate Contextual Fear Memory

Cited by 3 publications

References 31 publications

Involvement of the lateral habenula in fear memory

Involvement of the lateral habenula in fear memory

Neurobiological Mechanisms of Nicotine Reward and Aversion

Inhibitory Neural Network’s Impairments at Hippocampal CA1 LTP in an Aged Transgenic Mouse Model of Alzheimer’s Disease

Contact Info

Product

Resources

About