scholarly journals Hippocampal Regulation of Postsynaptic Density Homer1 by Associative Learning

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Nicholas E. Clifton ◽  
Darren Cameron ◽  
Simon Trent ◽  
Lucy H. Sykes ◽  
Kerrie L. Thomas ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Novelty Detection ◽  
Postsynaptic Density ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Fear Learning ◽  
Contextual Fear ◽  
Postsynaptic Density Proteins ◽  
Genes Encoding

Genes involved in synaptic plasticity, particularly genes encoding postsynaptic density proteins, have been recurrently linked to psychiatric disorders including schizophrenia and autism. Postsynaptic density Homer1 proteins contribute to synaptic plasticity through the competing actions of short and long isoforms. The activity-induced expression of shortHomer1isoforms,Homer1aandAnia-3, is thought to be related to processes of learning and memory. However, the precise regulation ofHomer1aandAnia-3with different components of learning has not been investigated. Here, we used in situ hybridization to quantify short and longHomer1expression in the hippocampus following consolidation, retrieval, and extinction of associative fear memory, using contextual fear conditioning in rats.Homer1aandAnia-3, but not longHomer1, were regulated by contextual fear learning or novelty detection, although their precise patterns of expression in hippocampal subregions were dependent on the isoform. We also show for the first time that the two short Homer1 isoforms are regulated after the retrieval and extinction of contextual fear memory, albeit with distinct temporal and spatial profiles. These findings support a role of activity-induced Homer1 isoforms in learning and memory processes in discrete hippocampal subregions and suggest that Homer1a and Ania-3 may play separable roles in synaptic plasticity.

scholarly journals Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning

Hippocampus ◽  
2013 ◽  
Vol 24 (2) ◽  
pp. 204-213 ◽  
Author(s):  
W. Bailey Glen ◽  
Bryant Horowitz ◽  
Gregory C. Carlson ◽  
Tyrone D. Cannon ◽  
Konrad Talbot ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Contextual Fear Conditioning ◽  
Contextual Fear

scholarly journals Npas4a expression in the teleost forebrain is associated with stress coping style differences in fear learning

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Baker ◽  
Ryan Y. Wong
Keyword(s):  
Neural Plasticity ◽  
Coping Style ◽  
Molecular Mechanisms ◽  
Conditioned Fear ◽  
Coping Styles ◽  
Brain Regions ◽  
Contextual Fear Conditioning ◽  
Fear Learning ◽  
Stress Coping ◽  
Contextual Fear

AbstractLearning to anticipate potentially dangerous contexts is an adaptive behavioral response to coping with stressors. An animal’s stress coping style (e.g. proactive–reactive axis) is known to influence how it encodes salient events. However, the neural and molecular mechanisms underlying these stress coping style differences in learning are unknown. Further, while a number of neuroplasticity-related genes have been associated with alternative stress coping styles, it is unclear if these genes may bias the development of conditioned behavioral responses to stressful stimuli, and if so, which brain regions are involved. Here, we trained adult zebrafish to associate a naturally aversive olfactory cue with a given context. Next, we investigated if expression of two neural plasticity and neurotransmission-related genes (npas4a and gabbr1a) were associated with the contextual fear conditioning differences between proactive and reactive stress coping styles. Reactive zebrafish developed a stronger conditioned fear response and showed significantly higher npas4a expression in the medial and lateral zones of the dorsal telencephalon (Dm, Dl), and the supracommissural nucleus of the ventral telencephalon (Vs). Our findings suggest that the expression of activity-dependent genes like npas4a may be differentially expressed across several interconnected forebrain regions in response to fearful stimuli and promote biases in fear learning among different stress coping styles.

scholarly journals Neurotrophin signalling in amygdala-dependent cued fear learning

2020 ◽  
Vol 382 (1) ◽  
pp. 161-172 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Volkmar Lessmann
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Neurotrophic Factor ◽  
Memory Formation ◽  
Fear Learning ◽  
Mammalian Brain ◽  
Pavlovian Fear Conditioning ◽  
Cortical Afferents ◽  
Trkb Receptors ◽  
Tropomyosin Related Kinase B

Abstract The amygdala is a central hub for fear learning assessed by Pavlovian fear conditioning. Indeed, the prevailing hypothesis that learning and memory are mediated by changes in synaptic strength was shown most convincingly at thalamic and cortical afferents to the lateral amygdala. The neurotrophin brain-derived neurotrophic factor (BDNF) is known to regulate synaptic plasticity and memory formation in many areas of the mammalian brain including the amygdala, where BDNF signalling via tropomyosin-related kinase B (TrkB) receptors is prominently involved in fear learning. This review updates the current understanding of BDNF/TrkB signalling in the amygdala related to fear learning and extinction. In addition, actions of proBDNF/p75NTR and NGF/TrkA as well as NT-3/TrkC signalling in the amygdala are introduced.

scholarly journals Fear Memory

2016 ◽  
Vol 96 (2) ◽  
pp. 695-750 ◽  
Author(s):  
Ivan Izquierdo ◽  
Cristiane R. G. Furini ◽  
Jociane C. Myskiw
Keyword(s):  
Fear Conditioning ◽  
Basolateral Amygdala ◽  
Inhibitory Avoidance ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Fear Learning ◽  
Term Potentiation ◽  
Mechanisms Of Memory

Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre- and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

scholarly journals Neurogenesis-induced forgetting is associated with reduced neuronal activity in CA1 during context fear memory retrieval

2021 ◽  
Author(s):  
Alexandria Evans ◽  
Gavin A. Scott ◽  
Jonathan R. Epp
Keyword(s):  
Memory Retrieval ◽  
Wheel Running ◽  
Fear Memory ◽  
Hippocampal Neurogenesis ◽  
Contextual Fear Conditioning ◽  
Early Gene ◽  
Population Activity ◽  
Contextual Fear ◽  
Induced Forgetting

AbstractHippocampal neurogenesis has a role in many essential learning and memory processes, including forgetting. This forgetting process is important because it prevents proactive interference between old and new memories. While several studies have now established the role of neurogenesis in forgetting, the specific mechanisms mediating neurogenesis-induced forgetting have not been elucidated. The goal of this study was to examine how increased neurogenesis affects the recall of context fear memory in addition to its effects on population activity within hippocampal subregions. We trained mice in contextual fear conditioning and then increased neurogenesis via 4 weeks of voluntary wheel running. Increased neurogenesis led to a reduction in freezing behaviour during context testing, replicating previous studies showing that increased neurogenesis causes forgetting of context fear memories. Additionally, we mapped the expression of the immediate early gene c-Fos within hippocampal subregions and found that increasing neurogenesis led to reduced CA1 c-Fos expression during context testing. The results suggest that reduced CA1 population activity may underlie the association between increased neurogenesis and forgetting.

Sign in / Sign up

Export Citation Format

Share Document