scholarly journals piRNAs in the Olfactory Bulb Related to Fear Conditioning can Migrate from the Brain to the Germline

2021 ◽  
Vol 3 (5) ◽  
pp. 132-136
Author(s):  
Sicong Chen
Keyword(s):  
Olfactory Bulb ◽  
Fear Conditioning ◽  
Small Rnas ◽  
Memory Formation ◽  
Virus Vector ◽  
Single Nucleotide ◽  
The Brain ◽  
Fear Conditioning Test

Small RNAs have been shown to be crucial in the mechanisms of transgenerational memory. Precisely, piRNAs have previously been thought to only exist in the germline and are related to transgenerational memory. To determine if the offspring inherits memory due to piRNA transmission, we conducted odor fear-conditioning tests and identified a piRNA that increased in abundance. That piRNA is thought to be involved in memory formation of the fear-conditioning test. We then used a virus vector to manipulate a single nucleotide of that piRNA sequence to see if it can migrate from the olfactory bulb to the germline. The data should theoretically indicate whether the mutant piRNA has migrated from the olfactory bulb to the germline of the mice.

scholarly journals Odor hedonics coding in the vertebrate olfactory bulb

2021 ◽  
Vol 383 (1) ◽  
pp. 485-493 ◽  
Author(s):  
Florence Kermen ◽  
Nathalie Mandairon ◽  
Laura Chalençon
Keyword(s):  
Social Interaction ◽  
Olfactory Bulb ◽  
Physicochemical Properties ◽  
Olfactory Perception ◽  
Hedonic Value ◽  
Odor Hedonics ◽  
The Brain

AbstractWhether an odorant is perceived as pleasant or unpleasant (hedonic value) governs a range of crucial behaviors: foraging, escaping danger, and social interaction. Despite its importance in olfactory perception, little is known regarding how odor hedonics is represented and encoded in the brain. Here, we review recent findings describing how odorant hedonic value is represented in the first olfaction processing center, the olfactory bulb. We discuss how olfactory bulb circuits might contribute to the coding of innate and learned odorant hedonics in addition to the odorant’s physicochemical properties.

scholarly journals The role of single nucleotide polymorphism of val66met (rs6265) of the brain-derived neurotropic factor in formation of endpoints after st-segment elevation myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
O.V Petyunina ◽  
M.P Kopytsya ◽  
A.E Berezin ◽  
A.A Berezin
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Bdnf Gene ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
St Segment Elevation ◽  
Acute Stemi ◽  
End Point ◽  
St Segment ◽  
The Brain

Abstract Background The single nucleotide polymorphism (SNP) Val66Met (rs6265) of the brain-derived neurotrophic factor (BDNF) gene is a possible candidate that is associated with the development of psychopathology and combines it with cardiovascular events. Purpose To research the possible associations of single-nucleotide polymorphism of Val66Met BDNF gene with the occurrence of endpoints after 6 months of follow-up after ST segment elevation myocardial infarction (STEMI). Methods 256 acute STEMI patients after successful primary percutaneous coronary intervention (PCI) were enrolled in the study. TIMI III blood flow restoring through culprit artery was determined. The study of SNP of Val66Met (rs6265) of the BDNF gene was performed by real-time polymerase chain reaction. The emotional state of the patients and its relationship with stress were assessed with the questionnaire “Depression, Anxiety and Stress-21”. All acute STEMI patients received adjuvant treatment due to current ESC recommendations. All procedures performed in the study involving human participants were in accordance with the ethical standards and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards and approved by the local ethics committee. Written inform consent was obtained from each patient. The primary endpoint was combined event (follow-up major adverse cardiac events – MACEs and hospitalization) that occurred within 6-month of the discharge from the hospital. MACEs were defined as the composite of CV death, recurrent angina, newly diagnosed heart failure. Results The frequency of genotypes Val66Met gene for BDNF in STEMI patients (n=256) was the following: 66ValVal=74.2% (n=190), 66ValMet + 66MetMet – 25.8% (n=66). The 66ValMet + 66MetMet polymorphism in the BDNF gene, stress and anxiety on 10–14 days before the event, as well as reduced left ventricular ejection fraction (LVEF), were independently associated with combined 6 months clinical end point after STEMI. Severity of depression according to depression scale was more profound in individuals with 66ValMet+66MetMet polymorphysms in BDNF gene (P=0.045) than in patients with 66ValVal genotype. Univariate and multivariate linear regressions has shown that 66ValMet+66MetMet genotype in BDNF gene, anxiety and stress before event, LVEF had independent power on dependent variable entitled combined end point after 6 month observation for STEMI patients with successful revascularization (P=0.0395). Kaplan-Meier curves demonstrated that STEMI patients with 66ValVal genotype in BDNF gene had a lower accumulation of combined end point compared with acute STEMI patients with 66ValMet+66ValMet polymorphism (Cox-criterion, P=0.019; log-rang criterion, P=0.03). Conclusion The Val66Met polymorphism in BDNF gene was found as an independent predictor for combined 6-month clinical end points after acute STEMI treated primary PCI. Funding Acknowledgement Type of funding source: None

scholarly journals Synaptic plasticity-dependent competition rule influences memory formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yire Jeong ◽  
Hye-Yeon Cho ◽  
Mujun Kim ◽  
Jung-Pyo Oh ◽  
Min Soo Kang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Specific Pattern ◽  
Memory Encoding ◽  
Competition Rule ◽  
Term Potentiation ◽  
Input Activity

AbstractMemory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

scholarly journals Murine Olfactory Bulb Interneurons Survive Infection with a Neurotropic Coronavirus

2017 ◽  
Vol 91 (22) ◽  
Author(s):  
D. Lori Wheeler ◽  
Jeremiah Athmer ◽  
David K. Meyerholz ◽  
Stanley Perlman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Olfactory Bulb ◽  
Hepatitis Virus ◽  
Large Fraction ◽  
Acute Infection ◽  
Virus Antigen ◽  
Host Cells ◽  
Virulent Virus ◽  
The Brain

ABSTRACT Viral infection of the central nervous system (CNS) is complicated by the mostly irreplaceable nature of neurons, as the loss of neurons has the potential to result in permanent damage to brain function. However, whether neurons or other cells in the CNS sometimes survive infection and the effects of infection on neuronal function is largely unknown. To address this question, we used the rJHM strain (rJ) of mouse hepatitis virus (MHV), a neurotropic coronavirus that causes acute encephalitis in susceptible strains of mice. To determine whether neurons or other CNS cells survive acute infection with this virulent virus, we developed a recombinant JHMV that expresses Cre recombinase (rJ-Cre) and infected mice that universally expressed a silent (floxed) version of tdTomato. Infection of these mice with rJ-Cre resulted in expression of tdTomato in host cells. The results showed that some cells were able to survive the infection, as demonstrated by continued tdTomato expression after virus antigen could no longer be detected. Most notably, interneurons in the olfactory bulb, which are known to be inhibitory, represented a large fraction of the surviving cells. In conclusion, our results indicated that some neurons are resistant to virus-mediated cell death and provide a framework for studying the effects of prior coronavirus infection on neuron function. IMPORTANCE We developed a novel recombinant virus that allows the study of cells that survive an infection by a central nervous system-specific strain of murine coronavirus. Using this virus, we identified neurons and, to a lesser extent, nonneuronal cells in the brain that were infected during the acute phase of the infection and survived for approximately 2 weeks until the mice succumbed to the infection. We focused on neurons and glial cells within the olfactory bulb because the virus enters the brain at this site. Our results show that interneurons of the olfactory bulb were the primary cell type able to survive infection. Further, these results indicate that this system will be useful for functional and gene expression studies of cells in the brain that survive acute infection.

scholarly journals Human brain harbors single nucleotide somatic variations in functionally relevant genes possibly mediated by oxidative stress

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2520 ◽  
Author(s):  
Anchal Sharma ◽  
Asgar Hussain Ansari ◽  
Renu Kumari ◽  
Rajesh Pandey ◽  
Rakhshinda Rehman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corpus Callosum ◽  
Human Brain ◽  
Frontal Cortex ◽  
Oxidative Stress Marker ◽  
Somatic Variation ◽  
Single Nucleotide ◽  
Normal Human Brain ◽  
Normal Human ◽  
The Brain

Somatic variation in DNA can cause cells to deviate from the preordained genomic path in both disease and healthy conditions. Here, using exome sequencing of paired tissue samples, we show that the normal human brain harbors somatic single base variations measuring up to 0.48% of the total variations. Interestingly, about 64% of these somatic variations in the brain are expected to lead to non-synonymous changes, and as much as 87% of these represent G:C>T:A transversion events. Further, the transversion events in the brain were mostly found in the frontal cortex, whereas the corpus callosum from the same individuals harbors the reference genotype. We found a significantly higher amount of 8-OHdG (oxidative stress marker) in the frontal cortex compared to the corpus callosum of the same subjects (p<0.01), correlating with the higher G:C>T:A transversions in the cortex. We found significant enrichment for axon guidance and related pathways for genes harbouring somatic variations. This could represent either a directed selection of genetic variations in these pathways or increased susceptibility of some loci towards oxidative stress. This study highlights that oxidative stress possibly influence single nucleotide somatic variations in normal human brain.

Expression of IGF-I and -II mRNA in the brain and craniofacial region of the rat fetus

Development ◽  
1991 ◽  
Vol 111 (1) ◽  
pp. 105-115 ◽  
Author(s):  
C. Ayer-le Lievre ◽  
P.A. Stahlbom ◽  
V.R. Sara
Keyword(s):  
Nervous System ◽  
Olfactory Bulb ◽  
Endocrine Function ◽  
Target Cells ◽  
Pars Intermedia ◽  
Sensory Ganglia ◽  
Rat Fetus ◽  
Amino Terminal ◽  
Igf I ◽  
The Brain

Insulin-like growth factors (IGF-I and -II) are present in the brain during development, with high levels of both being also found in the periphery particularly in the embryo. IGFs in the brain are believed to stimulate the proliferation of neuronal and glial precursors and their phenotypic differentiation. Using in situ hybridization, we have investigated the distribution of cells producing IGF-I and -II in the rat fetus during the second half of prenatal development with special emphasis on the peripheral and central nervous system. High levels of IGF-I mRNA were found in the olfactory bulb and in discrete neurons of the cranial sensory ganglia, notably in the trigeminal ganglion, as early as 13 days of gestation, in the pineal primordium of 18 day old fetuses, and in discrete groups of cells in the cochlear epithelium located laterally outside the forming spiral organ, in day 13 to 21 fetuses. High levels of IGF-II mRNA in the brain, besides the choroid plexus and the leptomeninges, were detected in hypothalamus, in the floor of the 3rd ventricle at all stages studied, in the pineal primordium at 18 days and in the pars intermedia of the pituitary or in the Rathke's pouch epithelium from which it is derived, with progressive fading towards the end of the gestation. In the peripheral nervous system the IGF-II mRNA was only found in association with the vascular endothelia of the ganglia. IGF-II mRNA in the nervous system was found in highly vascularized areas, meninges, blood vessels and choroid plexuses. It is thus associated with structures involved in the production of extracellular fluids and/or substrate transport and supply in the nervous tissues. A more specific role in the differentiation or fetal endocrine function should be considered for IGF-II in cells producing melatonin and melanocyte stimulating hormone (MSH) in the pineal and pituitary glands, respectively. The presence of IGF-I mRNA in the nervous system could be associated with fiber outgrowth and synaptogenesis in the cases of olfactory bulb and developing iris. The role of IGF-I in restricted populations of cells of the cochlear epithelium and in the pineal gland is unclear and requires further investigations including a search for IGF-I receptors in possible target cells. In the sensory ganglia, the presence of high levels of IGF-I mRNA eventually corresponds to the production, by post-translational processing, of the amino-terminal tripeptide of IGF-I, which might represent a neurotransmitter for these sensory neurons.

scholarly journals Metabolic learning and memory formation by the brain influence systemic metabolic homeostasis

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Yumin Zhang ◽  
Gang Liu ◽  
Jingqi Yan ◽  
Yalin Zhang ◽  
Bo Li ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Formation ◽  
Metabolic Homeostasis ◽  
The Brain

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.

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