Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acetylcholine Regulates Olfactory Perceptual Learning through Effects on Adult Neurogenesis.

ABSTRACT: Learning to perceptually discriminate between chemical signals in the environment (olfactory perceptual learning [OPL]) is critical for survival. Multiple mechanisms have been implicated in OPL, including modulation of neurogenesis and manipulation of cholinergic activity. However, whether these represent distinct processes regulating OPL or if cholinergic effects on OPL depend upon neurogenesis has remained an unresolved question. Using a combination of pharmacological and optogenetic approaches, cholinergic activity was shown to be both necessary and sufficient to drive OPL, and this process was dependent on the presence of newly born cells in the olfactory bulb (OB). This study is the first to directly demonstrate that cholinergic effects on OPL require adult OB neurogenesis.

SUBMITTER: Schilit Nitenson A

PROVIDER: S-EPMC6926271 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Acetylcholine Regulates Olfactory Perceptual Learning through Effects on Adult Neurogenesis.

Schilit Nitenson Arielle A Manzano Nieves Gabriela G Poeta Devon Lynn DL Bahar Ryan R Rachofsky Carolyn C Mandairon Nathalie N Bath Kevin G KG

iScience 20191114

Learning to perceptually discriminate between chemical signals in the environment (olfactory perceptual learning [OPL]) is critical for survival. Multiple mechanisms have been implicated in OPL, including modulation of neurogenesis and manipulation of cholinergic activity. However, whether these represent distinct processes regulating OPL or if cholinergic effects on OPL depend upon neurogenesis has remained an unresolved question. Using a combination of pharmacological and optogenetic approache ...[more]

PMID: 31855767

Similar Datasets

Olfactory perceptual learning requires adult neurogenesis.

Project description:Perceptual learning is required for olfactory function to adapt appropriately to changing odor environments. We here show that newborn neurons in the olfactory bulb are not only involved in, but necessary for, olfactory perceptual learning. First, the discrimination of perceptually similar odorants improves in mice after repeated exposure to the odorants. Second, this improved discrimination is accompanied by an elevated survival rate of newborn inhibitory neurons, preferentially involved in processing of the learned odor, within the olfactory bulb. Finally, blocking neurogenesis before and during the odorant exposure period prevents this learned improvement in discrimination. Olfactory perceptual learning is thus mediated by the reinforcement of functional inhibition in the olfactory bulb by adult neurogenesis.

| S-EPMC2764902 | biostudies-literature

Inhibitory muscarinic acetylcholine receptors enhance aversive olfactory learning in adult Drosophila.

Project description:Olfactory associative learning in Drosophila is mediated by synaptic plasticity between the Kenyon cells of the mushroom body and their output neurons. Both Kenyon cells and their inputs from projection neurons are cholinergic, yet little is known about the physiological function of muscarinic acetylcholine receptors in learning in adult flies. Here, we show that aversive olfactory learning in adult flies requires type A muscarinic acetylcholine receptors (mAChR-A), particularly in the gamma subtype of Kenyon cells. mAChR-A inhibits odor responses and is localized in Kenyon cell dendrites. Moreover, mAChR-A knockdown impairs the learning-associated depression of odor responses in a mushroom body output neuron. Our results suggest that mAChR-A function in Kenyon cell dendrites is required for synaptic plasticity between Kenyon cells and their output neurons.

| S-EPMC6641838 | biostudies-literature

Polycomb repressive complex 2 regulates basal cell fate during adult olfactory neurogenesis.

Project description:Adult neurogenesis occurs in the mammalian olfactory epithelium to maintain populations of neurons that are vulnerable to injury yet essential for olfaction. Multipotent olfactory basal stem cells are activated by damage, although mechanisms regulating lineage decisions are not understood. Using mouse lesion models, we focused on defining the role of Polycomb repressive complexes (PRCs) in olfactory neurogenesis. PRC2 has a well-established role in developing tissues, orchestrating transcriptional programs via chromatin modification. PRC2 proteins are expressed in olfactory globose basal cells (GBCs) and nascent neurons. Conditional PRC2 loss perturbs lesion-induced neuron production, accompanied by altered histone modifications and misexpression of lineage-specific transcription factors in GBCs. De-repression of Sox9 in PRC2-mutant GBCs is accompanied by increased Bowman's gland production, defining an unrecognized role for PRC2 in regulating gland versus neuron cell fate. Our findings support a model for PRC2-dependent mechanisms promoting sensory neuronal differentiation in an adult neurogenic niche.

| S-EPMC10679661 | biostudies-literature

Neurovascular EGFL7 regulates adult neurogenesis in the subventricular zone and thereby affects olfactory perception.

Project description:Adult neural stem cells reside in a specialized niche in the subventricular zone (SVZ). Throughout life they give rise to adult-born neurons in the olfactory bulb (OB), thus contributing to neural plasticity and pattern discrimination. Here, we show that the neurovascular protein EGFL7 is secreted by endothelial cells and neural stem cells (NSCs) of the SVZ to shape the vascular stem-cell niche. Loss of EGFL7 causes an accumulation of activated NSCs, which display enhanced activity and re-entry into the cell cycle. EGFL7 pushes activated NSCs towards quiescence and neuronal progeny towards differentiation. This is achieved by promoting Dll4-induced Notch signalling at the blood vessel-stem cell interface. Fewer inhibitory neurons form in the OB of EGFL7-knockout mice, which increases the absolute signal conducted from the mitral cell layer of the OB but decreases neuronal network synchronicity. Consequently, EGFL7-knockout mice display severe physiological defects in olfactory behaviour and perception.

| S-EPMC5493759 | biostudies-literature

CBX8-PRC1 regulates adult olfactory neurogenesis and epithelial homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-25 | GSE124442 | GEO

WDR81 regulates adult hippocampal neurogenesis through endosomal SARA-TGFβ signaling.

Project description:Adult hippocampal neurogenesis, a process considered important for hippocampal function, is regulated at multiple molecular levels. Mutations in the gene encoding the WD40 repeat-containing protein WDR81 are associated with neurological disorders, including cerebellar ataxia, mental retardation, quadrupedal locomotion syndrome (CAMRQ2), and microcephaly. In this study, we show that ablation of WDR81 in adult neural progenitor cells (aNPCs) markedly reduced adult hippocampal neurogenesis and impaired hippocampus-dependent learning. WDR81 suppresses endosomal PtdIns3P synthesis, likely by inhibiting the assembly of the PI3K-III complex. In the absence of WDR81, endosomal PtdIns3P levels are greatly elevated, leading to endosomal persistence of the PtdIns3P-binding protein SARA and consequently hyperactivation of SARA-dependent TGFβ signaling. Inhibition of PI3K-III activity or suppression of SARA-dependent TGFβ signaling markedly ameliorated the defective adult neurogenesis in WDR81-deficient mice. Taken together, these findings not only uncover the requirement for the WDR81-SARA-TGFβ axis in adult hippocampal neurogenesis, but also suggest that defective adult hippocampal neurogenesis contributes to the etiology of WDR81-related neurological diseases.

| S-EPMC7850971 | biostudies-literature

Mediator Med23 Regulates Adult Hippocampal Neurogenesis.

Project description:Mammalian Mediator (Med) is a key regulator of gene expression by linking transcription factors to RNA polymerase II (Pol II) transcription machineries. The Mediator subunit 23 (Med23) is a member of the conserved Med protein complex and plays essential roles in diverse biological processes including adipogenesis, carcinogenesis, osteoblast differentiation, and T-cell activation. However, its potential functions in the nervous system remain unknown. We report here that Med23 is required for adult hippocampal neurogenesis in mouse. Deletion of Med23 in adult hippocampal neural stem cells (NSCs) was achieved in Nestin-CreER:Med23flox/flox mice by oral administration of tamoxifen. We found an increased number of proliferating NSCs shown by pulse BrdU-labeling and immunostaining of MCM2 and Ki67, which is possibly due to a reduction in cell cycle length, with unchanged GFAP+/Sox2+ NSCs and Tbr2+ progenitors. On the other hand, neuroblasts and immature neurons indicated by NeuroD and DCX were decreased in number in the dentate gyrus (DG) of Med23-deficient mice. In addition, these mice also displayed defective dendritic morphogenesis, as well as a deficiency in spatial and contextual fear memory. Gene ontology (GO) analysis of hippocampal NSCs revealed an enrichment in genes involved in cell proliferation, Pol II-associated transcription, Notch signaling pathway and apoptosis. These results demonstrate that Med23 plays roles in regulating adult brain neurogenesis and functions.

| S-EPMC7403405 | biostudies-literature

Polycomb Repressive Complex 2 regulates basal cell fate during adult olfactory neurogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-18 | GSE224894 | GEO

CBX8-PRC1 regulates adult olfactory neurogenesis and epithelial homeostasis

Project description:CBX8-PRC1 regulates adult olfactory neurogenesis and epithelial homeostasis

| PRJNA512013 | ENA

Effects of Monocular Perceptual Learning on Binocular Visual Processing in Adolescent and Adult Amblyopia.

Project description:Re-establishing normal binocular visual processing is the key to amblyopia recovery beyond the critical period of visual development. Here, by combining perceptual learning, behavioral testing, and steady-state visually evoked potentials (SSVEPs), we examined how monocular perceptual learning in the amblyopic eye could change binocular visual processing in the adolescent and adult amblyopic visual system. We found that training reduced the interocular difference between amblyopic and fellow eyes and increased the amplitude of a binocular SSVEP component, with a significant negative correlation between the two measures. Our results demonstrate that training in the amblyopic eye primarily improves binocular rather than monocular visual processing in the amblyopic visual system, suggesting that behavioral training could potentially address key neural deficits in adolescent and adult amblyopia.

| S-EPMC7021554 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data