scholarly journals Neuronal integration in the adult olfactory bulb is a non-selective addition process

2018 ◽  
Author(s):  
Jean-Claude Platel ◽  
Alexandra Angelova ◽  
Stephane Bugeon ◽  
Thibault Ganay ◽  
Ilona Chudotvorova ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Adult Neurogenesis ◽  
Neuronal Death ◽  
Critical Period ◽  
Cell Loss ◽  
Low Doses ◽  
Newborn Neurons ◽  
Selective Addition

AbstractAdult neurogenesis is considered a competition in which neurons scramble during a critical period for integration and survival. Moreover, newborn neurons are thought to replace preexisting ones that die. Despite a wealth of evidence supporting this model, systematic in vivo observations of the process are still scarce. We used 2-photon imaging to study neuronal integration and survival directly in the olfactory bulb (OB) of living mice. Long-term tracking of over 1400 neurons demonstrated that cell-loss in the OB is virtually absent. Neuronal death resembling a critical period was induced by standard doses of BrdU or EdU, but disappeared when low doses of EdU were used, demonstrating toxicity. Finally, we demonstrate that the OB grows throughout life. This shows that neuronal selection during OB-neurogenesis does not occur during integration and argues against the existence of a critical period. Moreover, the OB is not a “turnover” system but shows lifelong neuronal addition.

scholarly journals Neuronal integration in the adult mouse olfactory bulb is a non-selective addition process

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Jean-Claude Platel ◽  
Alexandra Angelova ◽  
Stephane Bugeon ◽  
Jenelle Wallace ◽  
Thibault Ganay ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
In Vivo Imaging ◽  
Adult Mouse ◽  
Indirect Evidence ◽  
Two Photon ◽  
Low Levels ◽  
Newborn Neurons ◽  
Selective Addition

Adult neurogenesis in the olfactory bulb (OB) is considered as a competition in which neurons scramble during a critical selection period for integration and survival. Moreover, newborn neurons are thought to replace pre-existing ones that die. Despite indirect evidence supporting this model, systematic in vivo observations are still scarce. We used two-photon in vivo imaging to study neuronal integration and survival. We show that loss of new neurons in the OB after arrival at terminal positions occurs only at low levels. Moreover, long-term observations showed that no substantial cell death occurred at later stages. Neuronal death was induced by standard doses of thymidine analogs, but disappeared when low doses were used. Finally, we demonstrate that the OB grows throughout life. This shows that neuronal selection during OB-neurogenesis does not occur after neurons reached stable positions. Moreover, this suggests that OB neurogenesis does not represent neuronal turnover but lifelong neuronal addition.

Transient Cerebral Ischemia Induces Active Astrocytosis Without Distinct Neuronal Death in the Gerbil Main Olfactory Bulb: A Long-Term Analysis

2010 ◽  
Vol 35 (10) ◽  
pp. 1588-1598 ◽  
Author(s):  
Jung Hoon Choi ◽  
Ki-Yeon Yoo ◽  
Choong Hyun Lee ◽  
Ok kyu Park ◽  
Bing Chun Yan ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Olfactory Bulb ◽  
Neuronal Death ◽  
Transient Cerebral Ischemia ◽  
Main Olfactory Bulb ◽  
Term Analysis

scholarly journals Murine neonates develop vigorous in vivo cytotoxic and Th1/Th2 responses upon exposure to low doses of NIMA-like alloantigens

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1530-1538 ◽  
Author(s):  
Shannon J. Opiela ◽  
Robert B. Levy ◽  
Becky Adkins
Keyword(s):  
Early Life ◽  
In Vitro Assays ◽  
Low Doses ◽  
Early Life Exposure ◽  
Donor Cells ◽  
Th2 Responses ◽  
In Vivo Cytotoxicity

AbstractEarly life exposure to noninherited maternal antigens (NIMAs) may occur via transplacental transfer and/or breast milk. There are indications that early life exposure to NIMAs may lead to lifelong tolerance. However, there is mounting evidence that exposure to NIMAs may also lead to immunologic priming. Understanding how these different responses arise could be critical in transplantation with donor cells expressing NIMAs. We recently reported that murine neonates that received a transplant of low doses of NIMA-like alloantigens develop vigorous memory cytotoxic responses, as assessed by in vitro assays. Here, we demonstrate that robust allospecific cytotoxicity is also manifest in vivo. Importantly, at low doses, NIMA-expressing cells induced the development of in vivo cytotoxicity during the neonatal period. NIMA-exposed neonates also developed vigorous primary and memory allospecific Th1/Th2 responses that exceeded the responses of adults. Overall, we conclude that exposure to low doses of NIMA-like alloantigens induces robust in vivo cytotoxic and Th1/Th2 responses in neonates. These findings suggest that early exposure to low levels of NIMA may lead to long-term immunologic priming of all arms of T-cell adaptive immunity, rather than tolerance.

scholarly journals Advances in Cell Transplantation Therapy for Diseased Myocardium

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Outi M. Villet ◽  
Antti Siltanen ◽  
Tommi Pätilä ◽  
M. Ali A. Mahar ◽  
Antti Vento ◽  
...  
Keyword(s):  
Cell Transplantation ◽  
Cultured Cells ◽  
Systolic Function ◽  
Cell Loss ◽  
Engineering Technology ◽  
Term Survival ◽  
3 Dimensional ◽  
Bone Marrow Derived Cells

The overall objective of cell transplantation is to repopulate postinfarction scar with contractile cells, thus improving systolic function, and to prevent or to regress the remodeling process. Direct implantation of isolated myoblasts, cardiomyocytes, and bone-marrow-derived cells has shown prospect for improved cardiac performance in several animal models and patients suffering from heart failure. However, direct implantation of cultured cells can lead to major cell loss by leakage and cell death, inappropriate integration and proliferation, and cardiac arrhythmia. To resolve these problems an approach using 3-dimensional tissue-engineered cell constructs has been investigated. Cell engineering technology has enabled scaffold-free sheet development including generation of communication between cell graft and host tissue, creation of organized microvascular network, and relatively long-term survival afterin vivotransplantation.

scholarly journals Low Doses of Fentanyl Block Central Sensitization in the Rat Spinal Cord In Vivo

2004 ◽  
Vol 100 (6) ◽  
pp. 1545-1551 ◽  
Author(s):  
Justus Benrath ◽  
Christina Brechtel ◽  
Eike Martin ◽  
Jürgen Sandkühler
Keyword(s):  
Spinal Cord ◽  
High Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Low Doses ◽  
Term Potentiation ◽  
C Fiber ◽  
Frequency Stimulation

Background mu-Opioid receptor agonists are strong analgesics. However, their usefulness for preemptive analgesia is controversial. The authors tested antinociceptive and preemptive properties of fentanyl as a mu-opioid receptor agonist in a model of spinal nociception in vivo. Methods C fiber-evoked potentials were recorded in the superficial laminae I-II of the rat lumbar spinal cord with glass microelectrodes in response to electrical stimulation of the sciatic nerve. High-frequency stimulation was applied on the sciatic nerve to induce long-term potentiation of C fiber-evoked field potentials, a form of central sensitization. To test the effect of fentanyl on acute nociception, fentanyl was infused intravenously at increasing doses (6-192 microg.kg(-1).h(-1)). One hour after start of infusion, high-frequency stimulation was applied to evaluate effects of fentanyl on the induction of long-term potentiation. Results In the absence of fentanyl, high-frequency stimulation potentiated C fiber-evoked field potentials to 149 +/-12% of controls (mean +/-SEM; n = 6) for at least 1 h. Increasing doses of fentanyl led to a significant reduction of C fiber-evoked potentials in a dose-dependent manner. The induction of long-term potentiation was blocked by low doses of fentanyl (infusion 12-48 microg.kg(1).h(-1)). At high doses, fentanyl did not block the induction of long-term potentiation (infusion 96-192 microg.kg(-1).h(-1)). Conclusions : Low doses of fentanyl block the synaptic form of central sensitization in the rat spinal cord in vivo, but higher doses do not have this effect.

scholarly journals OTX2 signals from the choroid plexus to regulate adult neurogenesis

2018 ◽  
Author(s):  
Anabelle Planques ◽  
Vanessa Oliveira Moreira ◽  
Chantal Dubreuil ◽  
Alain Prochiantz ◽  
Ariel A Di Nardo
Keyword(s):  
Extracellular Matrix ◽  
Cerebrospinal Fluid ◽  
Olfactory Bulb ◽  
Choroid Plexus ◽  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Supporting Cells ◽  
Multi Level ◽  
Newborn Neurons ◽  
Migratory Stream

AbstractProliferation and migration during adult neurogenesis are regulated by a microenvironment of signaling molecules originating from local vasculature, from cerebrospinal fluid produced by the choroid plexus, and from local supporting cells including astrocytes. Here, we focus on the function of OTX2 homeoprotein transcription factor in the mouse adult ventricular-subventricular zone (V-SVZ) which generates olfactory bulb neurons. We find that OTX2 secreted by choroid plexus is transferred to supporting cells of the V-SVZ and rostral migratory stream. Deletion of Otx2 in choroid plexus affects neuroblast migration and reduces the number of olfactory bulb newborn neurons. Adult neurogenesis was also decreased by expressing secreted single-chain antibodies to sequester OTX2 in the cerebrospinal fluid, demonstrating the importance of non-cell autonomous OTX2. We show that OTX2 activity modifies extracellular matrix components and signaling molecules produced by supporting astrocytes. Thus, we reveal a multi-level and non-cell autonomous role of a homeoprotein and reinforce the choroid plexus and astrocytes as key niche compartments affecting adult neurogenesis.Significance StatementCerebrospinal fluid, local vasculature and non-neurogenic astrocytes are niche compartments that provide a microenvironment for regulating adult mouse neurogenesis. We show that OTX2 homeoprotein secreted by choroid plexus into the cerebrospinal fluid is transferred into non-neurogenic astrocytes of the ventricular-subventricular zone and rostral migratory stream where it regulates extracellular matrix and signaling factors. This non-cell-autonomous activity impacts the number of newborn neurons that integrate the olfactory bulb. Thus, we reveal a multi-level role for OTX2 and reinforce the choroid plexus as a key niche compartment affecting adult neurogenesis.

scholarly journals Immature olfactory sensory neurons provide behaviorally useful sensory input to the olfactory bulb

2021 ◽  
Author(s):  
Jane S Huang ◽  
Tenzin Kunkhyen ◽  
Beichen Liu ◽  
Ryan J Muggleton ◽  
Jonathan T Avon ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Sensory Neurons ◽  
Sensory Input ◽  
Odorant Receptors ◽  
Projection Neurons ◽  
Olfactory Sensory Neurons ◽  
Odor Processing ◽  
Newborn Neurons ◽  
Behavioral Assays

Postnatal neurogenesis provides an opportunity to understand how newborn neurons functionally integrate into circuits to restore lost function. Newborn olfactory sensory neurons (OSNs) wire into highly organized olfactory bulb (OB) circuits throughout life, enabling lifelong plasticity and regeneration. Immature OSNs can form functional synapses capable of evoking firing in OB projection neurons. However, what contribution, if any, immature OSNs make to odor processing is unknown. Indeed, because immature OSNs can express multiple odorant receptors, any input that they do provide could degrade the odorant selectivity of input to OB glomeruli. Here, we used a combination of in vivo 2-photon calcium imaging, optogenetics, electrophysiology and behavioral assays to show that immature OSNs provide odor input to the OB, where they form monosynaptic connections with excitatory neurons. Importantly, immature OSNs responded as selectively to odorants as mature OSNs. Furthermore, mice successfully performed odor detection tasks using sensory input from immature OSNs alone. Immature OSNs responded more strongly to low odorant concentrations but their responses were less concentration dependent than those of mature OSNs, suggesting that immature and mature OSNs provide distinct odor input streams to each glomerulus. Together, our findings suggest that sensory input mediated by immature OSNs plays a previously unappreciated role in olfactory-guided behavior.

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