Method for Stimulation of Hippocampal Neurogenesis by Transient Microneedle Insertion

Author(s):  
Shijie Song ◽  
Xiaoyung Kong ◽  
Juan Sanchez-Ramos
2011 ◽  
Vol 26 (S2) ◽  
pp. 655-655
Author(s):  
M. Moreno ◽  
E. Glennon ◽  
L. Thiru ◽  
C. Sexton ◽  
J.D. Coplan ◽  
...  

BackgroundIn this study we examine potential mechanisms by which the stimulation of hippocampal neurogenesis may generate an antidepressant effect.MethodsStudy-1: Adult male rats (N = 24) were trained to segregate relevant from irrelevant spatial cues (spatial segregation); tested on this task four and 8-weeks late; then exposed (on week 8) to a modified version of the task that conflicted with the memory of the initially learned experience (mnemonic segregation); and then euthanized to detect hippocampal neurogenesis. Study-2: Adult rats (N = 24) were trained in the spatial segregation task; three-days later, half were re-tested on the same task and half the tested on the modified task (mnemonic segregation); and euthanized immediately to detect neurons that were synaptically active during task performance.ResultsStudy-1: Good performers on the modified task (mnemonic segregation) had significantly greater rates of hippocampal neurogenesis, but the increase was only in immature neurons and not in new neurons that had completed maturation. Performance on spatial segregation task was unrelated to proficiency in mnemonic segregation or rates of neurogenesis. Study-2: Performance on the mnemonic segregation unrelated to neurogenesis rates, but inversely correlated to synaptic activation of mature hippocampal neurons, which in turn inversely correlated with immature neuron rates.ConclusionTaken together, the data suggests that neurogenesis facilitates detection of subtle changes to experiences established over several weeks (not days); this occurs prior to forming synapses; and maybe associated with suppression of mature hippocampal neurons that presumably mediate older, interfering, experiences.


2016 ◽  
Vol 17 (3) ◽  
pp. 534-543 ◽  
Author(s):  
Jin-il Kim ◽  
Seong Gak Jeon ◽  
Kyoung Ah Kim ◽  
Yong Jun Kim ◽  
Eun Ji Song ◽  
...  

2014 ◽  
Vol 7 (2) ◽  
pp. 304-307 ◽  
Author(s):  
Tiffany Scarcelli ◽  
Jessica F. Jordão ◽  
Meaghan A. O'Reilly ◽  
Nicholas Ellens ◽  
Kullervo Hynynen ◽  
...  

2021 ◽  
pp. 113114
Author(s):  
Farah Chamaa ◽  
Batoul Darwish ◽  
Ziad Nahas ◽  
Elie D. Al-Chaer ◽  
Nayef E. Saadé ◽  
...  

2008 ◽  
Vol 108 (1) ◽  
pp. 132-138 ◽  
Author(s):  
Hiroki Toda ◽  
Clement Hamani ◽  
Adrian P. Fawcett ◽  
William D. Hutchison ◽  
Andres M. Lozano

Object To examine the influence of deep brain stimulation on hippocampal neurogenesis in an adult rodent model. Methods Rats were anesthetized and treated for 1 hour with electrical stimulation of the anterior nucleus of the thalamus (AN) or sham surgery. The animals were injected with 5′-bromo-2′-deoxyuridine (BrdU) 1–7 days after surgery and killed 24 hours or 28 days later. The authors counted the BrdU-positive cells in the dentate gyrus (DG) of the hippocampus. To investigate the fate of these cells, they also stained sections for doublecortin, NeuN, and GFAP and analyzed the results with confocal microscopy. In a second set of experiments they assessed the number of DG BrdU-positive cells in animals treated with corticosterone (a known suppressor of hippocampal neurogenesis) and sham surgery, corticosterone and AN stimulation, or vehicle and sham surgery. Results Animals receiving AN high-frequency stimulation (2.5 V, 90 μsec, 130 Hz) had a 2- to 3-fold increase in the number of DG BrdU-positive cells compared with nonstimulated controls. This increase was not seen with stimulation at 10 Hz. Most BrdU-positive cells assumed a neuronal cell fate. As expected, treatment with corticosterone significantly reduced the number of DG BrdU-positive cells. This steroid-induced reduction of neurogenesis was reversed by AN stimulation. Conclusions High-frequency stimulation of the AN increases the hippocampal neurogenesis and restores experimentally suppressed neurogenesis. Interventions that increase hippocampal neurogenesis have been associated with enhanced behavioral performance. In this context, it may be possible to use electrical stimulation to treat conditions associated with impairment of hippocampal function.


2019 ◽  
Vol 21 (1) ◽  
pp. 4 ◽  
Author(s):  
Haena Moon ◽  
Seong Gak Jeon ◽  
Jin-il Kim ◽  
Hyeon soo Kim ◽  
Sangho Lee ◽  
...  

Nuclear receptor related-1 (Nurr1) protein performs a crucial role in hippocampal neural stem cell (hNSC) development as well as cognitive functions. We previously demonstrated that the pharmacological stimulation of Nurr1 by amodiaquine (AQ) promotes spatial memory by enhancing adult hippocampal neurogenesis. However, the role of Nurr1 in the cell cycle regulation of the adult hippocampus has not been investigated. This study aimed to examine changes in the cell cycle-related molecules involved in adult hippocampal neurogenesis induced by Nurr1 pharmacological stimulation. Fluorescence-activated cell sorting (FACS) analysis showed that AQ improved the progression of cell cycle from G0/G1 to S phase in a dose-dependent manner, and MEK1 or PI3K inhibitors attenuated this progression. In addition, AQ treatment increased the expression of cell proliferation markers MCM5 and PCNA, and transcription factor E2F1. Furthermore, pharmacological stimulation of Nurr1 by AQ increased the expression levels of positive cell cycle regulators such as cyclin A and cyclin-dependent kinases (CDK) 2. In contrast, levels of CDK inhibitors p27KIP1 and p57KIP2 were reduced upon treatment with AQ. Similar to the in vitro results, RT-qPCR analysis of AQ-administered mice brains revealed an increase in the levels of markers of cell cycle progression, PCNA, MCM5, and Cdc25a. Finally, AQ administration resulted in decreased p27KIP1 and increased CDK2 levels in the dentate gyrus of the mouse hippocampus, as quantified immunohistochemically. Our results demonstrate that the pharmacological stimulation of Nurr1 in adult hNSCs by AQ promotes the cell cycle by modulating cell cycle-related molecules.


2006 ◽  
Vol 59 (9) ◽  
pp. 786-792 ◽  
Author(s):  
Valerie Lemaire ◽  
Stephanie Lamarque ◽  
Michel Le Moal ◽  
Pier-Vincenzo Piazza ◽  
Djoher Nora Abrous

Science ◽  
2018 ◽  
Vol 361 (6406) ◽  
pp. eaan8821 ◽  
Author(s):  
Se Hoon Choi ◽  
Enjana Bylykbashi ◽  
Zena K. Chatila ◽  
Star W. Lee ◽  
Benjamin Pulli ◽  
...  

Adult hippocampal neurogenesis (AHN) is impaired before the onset of Alzheimer’s disease (AD) pathology. We found that exercise provided cognitive benefit to 5×FAD mice, a mouse model of AD, by inducing AHN and elevating levels of brain-derived neurotrophic factor (BDNF). Neither stimulation of AHN alone, nor exercise, in the absence of increased AHN, ameliorated cognition. We successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels. Suppressing AHN later led to worsened cognitive performance and loss of preexisting dentate neurons. Thus, pharmacological mimetics of exercise, enhancing AHN and elevating BDNF levels, may improve cognition in AD. Furthermore, applied at early stages of AD, these mimetics may protect against subsequent neuronal cell death.


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