scholarly journals The Physiology of Fear: Reconceptualizing the Role of the Central Amygdala in Fear Learning

Physiology ◽  
2015 ◽  
Vol 30 (5) ◽  
pp. 389-401 ◽  
Author(s):  
Orion P. Keifer ◽  
Robert C. Hurt ◽  
Kerry J. Ressler ◽  
Paul J. Marvar
Keyword(s):  
Lateral Hypothalamus ◽  
Recent Literature ◽  
Brain Structures ◽  
Memory Formation ◽  
Fear Learning ◽  
Central Amygdala ◽  
A Site ◽  
The Brain ◽  
Human And Mouse

The historically understood role of the central amygdala (CeA) in fear learning is to serve as a passive output station for processing and plasticity that occurs elsewhere in the brain. However, recent research has suggested that the CeA may play a more dynamic role in fear learning. In particular, there is growing evidence that the CeA is a site of plasticity and memory formation, and that its activity is subject to tight regulation. The following review examines the evidence for these three main roles of the CeA as they relate to fear learning. The classical role of the CeA as a routing station to fear effector brain structures like the periaqueductal gray, the lateral hypothalamus, and paraventricular nucleus of the hypothalamus will be briefly reviewed, but specific emphasis is placed on recent literature suggesting that the CeA 1) has an important role in the plasticity underlying fear learning, 2) is involved in regulation of other amygdala subnuclei, and 3) is itself regulated by intra- and extra-amygdalar input. Finally, we discuss the parallels of human and mouse CeA involvement in fear disorders and fear conditioning, respectively.

scholarly journals Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

2021 ◽  
Vol 22 (11) ◽  
pp. 6071
Author(s):  
Suzanne Gascon ◽  
Jessica Jann ◽  
Chloé Langlois-Blais ◽  
Mélanie Plourde ◽  
Christine Lavoie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factors ◽  
Signaling Pathways ◽  
Brain Structures ◽  
Therapeutic Strategies ◽  
Native Proteins ◽  
Receptor Sites ◽  
The Brain

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.

scholarly journals Consciousness, decision making, and volition: freedom beyond chance and necessity

2021 ◽  
Author(s):  
Hans Liljenström
Keyword(s):  
Decision Making ◽  
Free Will ◽  
Brain Activity ◽  
Brain Structures ◽  
Complex Process ◽  
Neural Information ◽  
Neural Information Processing ◽  
Stochastic Population Model ◽  
The Brain

AbstractWhat is the role of consciousness in volition and decision-making? Are our actions fully determined by brain activity preceding our decisions to act, or can consciousness instead affect the brain activity leading to action? This has been much debated in philosophy, but also in science since the famous experiments by Libet in the 1980s, where the current most common interpretation is that conscious free will is an illusion. It seems that the brain knows, up to several seconds in advance what “you” decide to do. These studies have, however, been criticized, and alternative interpretations of the experiments can be given, some of which are discussed in this paper. In an attempt to elucidate the processes involved in decision-making (DM), as an essential part of volition, we have developed a computational model of relevant brain structures and their neurodynamics. While DM is a complex process, we have particularly focused on the amygdala and orbitofrontal cortex (OFC) for its emotional, and the lateral prefrontal cortex (LPFC) for its cognitive aspects. In this paper, we present a stochastic population model representing the neural information processing of DM. Simulation results seem to confirm the notion that if decisions have to be made fast, emotional processes and aspects dominate, while rational processes are more time consuming and may result in a delayed decision. Finally, some limitations of current science and computational modeling will be discussed, hinting at a future development of science, where consciousness and free will may add to chance and necessity as explanation for what happens in the world.

scholarly journals In amygdala we trust: different contributions of the basolateral and central amygdala in learning whom to trust

2021 ◽  
Author(s):  
Ronald Sladky ◽  
Federica Riva ◽  
Lisa Rosenberger ◽  
Jack van Honk ◽  
Claus Lamm
Keyword(s):  
Basolateral Amygdala ◽  
Human Subjects ◽  
Brain Structures ◽  
Trust Game ◽  
Rodent Models ◽  
Mutual Trust ◽  
Central Amygdala ◽  
Interaction Partners ◽  
Improved Learning

Human societies are built on cooperation and mutual trust, but not everybody is trustworthy. Research on rodents suggests an essential role of the basolateral amygdala (BLA) in learning from social experiences (Hernandez-Lallement J et al., 2016), which was also confirmed in human subjects with selective bilateral BLA damage as they failed to adapt their trust behavior towards trustworthy vs. untrustworthy interaction partners (Rosenberger LA et al., 2019). However, neuroimaging in neurotypical populations did not consistently report involvement of the amygdala in trust behavior. This might be explained by the difficulty of differentiating between amygdala's structurally and functionally different subnuclei, i.e., the BLA and central amygdala (CeA), which have even antagonistic features particularly in trust behavior (van Honk J et al., 2013). Here, we used fMRI of the amygdala subnuclei of neurotypical adults (n=31f/31m) engaging in the repeated trust game. Our data show that both the BLA and the CeA play a role and indeed differentially: While the BLA was most active when obtaining feedback on whether invested trust had been reciprocated or not, the CeA was most active when subjects were preparing their next trust decision. In the latter phase, improved learning was associated with higher activation differences in response to untrustworthy vs. trustworthy trustees, in both BLA and CeA. Our data not only translate to rodent models and support our earlier findings in BLA-damaged subjects, but also show the specific contributions of other brain structures in the amygdala-centered network in learning whom to trust, and better not to trust.

scholarly journals Role of Thalamus in Recovery of Traumatic Brain Injury

2016 ◽  
Vol 07 (S 01) ◽  
pp. S076-S079 ◽  
Author(s):  
Ashok Munivenkatappa ◽  
Amit Agrawal
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Structures ◽  
Thalamic Nuclei ◽  
Posttraumatic Symptoms ◽  
Injured Brain ◽  
Recovery Mechanisms ◽  
The Brain ◽  
Degree Of Recovery

ABSTRACTDegree of recovery after traumatic brain injury is highly variable that lasts for many weeks to months. The evidence of brain structures involved in recovery mechanisms is limited. This review highlights evidence of the brain structure particularly thalamus in neuroplasticity mechanism. Thalamus with its complex global networking has potential role in refining the cortical and other brain structures. Thalamic nuclei activation both naturally or by neurorehabilitation in injured brain can enhance and facilitate the improvement of posttraumatic symptoms. This review provides evidence from literature that thalamus plays a key role in recovery mechanism after injury. The study also emphasize that thalamus should be specifically targeted in neurorehabilitation following brain injury.

scholarly journals The Role of the Entorhinal Cortex in Extinction: Influences of Aging

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Lia R. M. Bevilaqua ◽  
Janine I. Rossato ◽  
Juliana S. Bonini ◽  
Jociane C. Myskiw ◽  
Julia R. Clarke ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Entorhinal Cortex ◽  
Amyloid Plaques ◽  
Memory Formation ◽  
Amygdaloid Nucleus ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Glutamate Nmda Receptors ◽  
The Brain

The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer's disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its effect may be in part mediated by the entorhinal cortex.

Behavioral Neuroscience of Circuits Involved in Fear Processing

2016 ◽  
Author(s):  
Elizabeth P. Bauer ◽  
Denis Paré
Keyword(s):  
Fear Conditioning ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Current Knowledge ◽  
Brain Structures ◽  
Fear Learning ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
The Brain ◽  
Insight Into

Normal fear regulation includes the ability to learn by experience that some circumstances predict danger. This process, which can be modeled in the laboratory using Pavlovian fear conditioning, appears to be disrupted in individuals with post-traumatic stress disorder (PTSD). Understanding of the mechanisms underlying fear learning has progressed tremendously in the last 25 years, and constitutes a promising paradigm to study the neural bases of PTSD. This chapter first reviews current knowledge of the brain structures involved in fear learning, expression and extinction, including the contributions of the amygdala and prefrontal cortex. It then addresses how these circuits are affected by PTSD and how fear processing is altered in PTSD. Understanding PTSD within a fear-conditioning and extinction framework provides insight into why certain individuals are susceptible to developing PTSD and suggests potential therapies.

scholarly journals An Emerging Role of m6A in Memory: A Case for Translational Priming

2020 ◽  
Vol 21 (20) ◽  
pp. 7447
Author(s):  
Amanda M. Leonetti ◽  
Ming Yin Chu ◽  
Fiona O. Ramnaraign ◽  
Samuel Holm ◽  
Brandon J. Walters
Keyword(s):  
Learning And Memory ◽  
Memory Consolidation ◽  
Protein Translation ◽  
Memory Formation ◽  
Current Data ◽  
Neuron Development ◽  
Neuronal Functions ◽  
The Brain ◽  
Fine Tune

Investigation into the role of methylation of the adenosine base (m6A) of RNA has only recently begun, but it quickly became apparent that m6A is able to control and fine-tune many aspects of mRNA, from splicing to translation. The ability of m6A to regulate translation distally, away from traditional sites near the nucleus, quickly caught the eye of neuroscientists because of implications for selective protein translation at synapses. Work in the brain has demonstrated how m6A is functionally required for many neuronal functions, but two in particular are covered at length here: The role of m6A in 1) neuron development; and 2) memory formation. The purpose of this review is not to cover all data about m6A in the brain. Instead, this review will focus on connecting mechanisms of m6A function in neuron development, with m6A’s known function in memory formation. We will introduce the concept of “translational priming” and discuss how current data fit into this model, then speculate how m6A-mediated translational priming during memory consolidation can regulate learning and memory locally at the synapse.

scholarly journals Apolipoprotein E Antibodies Affect the Retention of Passive Avoidance Memory in the Chick

1998 ◽  
Vol 6 (3) ◽  
pp. 29-40 ◽  
Author(s):  
Chris Lancashire ◽  
Radmila Mileusnic ◽  
Steven P.R. Rose
Keyword(s):  
Risk Factors ◽  
Apolipoprotein E ◽  
Passive Avoidance ◽  
Residence Time ◽  
Memory Formation ◽  
Avoidance Task ◽  
Brain Distribution ◽  
The Brain ◽  
Avoidance Memory

Isoforms of apolipoprotein E (ApoE) have been implicated as risk factors in Alzheimer’s disease. We have, therefore, examined the possible role of ApoE in memory formation, using a one-trial passive avoidance task in day-old chicks. Birds were trained on the task and then at various times pre or post-training were injected intracerebrally with anti-ApoE. Immunofluorescence staining demonstrated the presence of the antibody bound to the neuropil, close to the injection site and adjacent to the ventricle, with a residence time in the brain of up to 30 min. Chicks that were injected 30 min pre-training or just post-training with 5μg/ hemisphere of the antibody learned the task, but were amnesic when tested at 30 min or at subsequent times up to 24 hr Post-training. When tested at 24 hr, birds injected 5.5 hr post-training showed unimpaired retention. Birds injected with 5μg/hemisphere of anti-ApoA-I (which has a brain distribution similar to that of anti-ApoE) at 30 min pretraining showed no amnesia, indicating the specificity of the effect to the ApoE. Possible mechanisms for this effect are discussed.

Ethanol induced increase of fibroblast growth factor 2 mRNA content in emotiogenic brain structures of rats

2020 ◽  
Vol 66 (5) ◽  
pp. 419-422
Author(s):  
M.I. Airapetov ◽  
S.O. Eresco ◽  
A.A. Lebedev ◽  
E.R. Bychkov ◽  
P.D. Shabanov
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Dopaminergic Neurons ◽  
Mrna Level ◽  
Brain Structures ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Mrna Content ◽  
The Brain

We studied the effects of acute, subacute, and chronic alcohol treatment of rats on the content of fibroblast growth factor 2 (FGF2) mRNA in various brain structures. Results suggest a possible role of FGF2 in the functioning of dopaminergic neurons in the midbrain. In our experiment, ethanol treatment of rats was accompanied by an increase in the FGF2 mRNA level in the emotiogenic structures of the brain. This effect was blocked by pretreatment of animals with chlorpromazine. This suggests FGF2 involvement in the mechanisms of alcohol dependence and can be considered as a possible diagnostic and therapeutic target in alcoholism.

scholarly journals The role of microRNAs in learning and long-term memory

2020 ◽  
Vol 24 (8) ◽  
pp. 885-896
Author(s):  
L. N. Grinkevich
Keyword(s):  
Cognitive Processes ◽  
Regulation Of Gene Expression ◽  
Memory Formation ◽  
Learning Ability ◽  
Long Term Memory ◽  
Term Memory ◽  
Microrna Biogenesis ◽  
The Brain

The mechanisms of long-term memory formation and ways to improve it (in the case of its impairment) remain an extremely difficult problem yet to be solved. Over the recent years, much attention has been paid to microRNAs in this regard. MicroRNAs are unique endogenous non-coding RNAs about 22 nucleotides in length; each can regulate translation of hundreds of messenger RNA targets, thereby controlling entire gene networks. MicroRNAs are widely represented in the central nervous system. A large number of studies are currently being conducted to investigate the role of microRNAs in the brain functioning. A number of microRNAs have been shown to be involved in the process of synaptic plasticity, as well as in the long-term memory formation. Disruption of microRNA biogenesis leads to significant cognitive dysfunctions. Moreover, impaired microRNA biogenesis is one of the causes of the pathogenesis of mental disorders, neurodegenerative illnesses and senile dementia, which are often accompanied by deterioration in the learning ability and by memory impairment. Optimistic predictions are made that microRNAs can be used as targets for therapeutic treatment and for diagnosing the above pathologies. The importance of applications related to microRNAs significantly raises interest in studying their functions in the brain. Thus, this review is focused on the role of microRNAs in cognitive processes. It describes microRNA biogenesis and the role of miRNAs in the regulation of gene expression, as well as the latest achievements in studying the functional role of microRNAs in learning and in long-term memory formation, depending on the activation or inhibition of their expression. The review presents summarized data on the effect of impaired microRNA biogenesis on long-term memory formation, including those associated with sleep deprivation. In addition, analysis is provided of the current literature related to the prospects of improving cognitive processes by influencing microRNA biogenesis via the use of CRISPR/Cas9 technologies and active mental and physical exercises.

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