scholarly journals Interneuron activity-structural plasticity association is driven by context-dependent sensory experience

2021 ◽  
Author(s):  
Soham Saha ◽  
John Hongyu Meng ◽  
Hermann Riecke ◽  
Georgios Agoranos ◽  
Kurt A. Sailor ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Population Level ◽  
Plasticity Mechanism ◽  
Spine Stability ◽  
Odor Memory ◽  
New Information ◽  
Spine Plasticity ◽  
Network Mechanism ◽  
Spine Dynamics

AbstractNeuronal dendritic spine dynamics provide a plasticity mechanism for altering brain circuit connectivity to integrate new information for learning and memory. Previous in vivo studies in the olfactory bulb (OB) showed that regional increases in activity caused localized spine stability, at a population level, yet how activity affects spine dynamics at an individual neuron level remains unknown. In this study, we tracked in vivo the correlation between an individual neuron’s activity and its dendritic spine dynamics of OB granule cell (GC) interneurons. Odor experience caused a consistent correlation between individual GC activity and spine stability. Dissecting the components of the OB circuit showed that increased principal cell (MC) activity was sufficient to drive this correlation, whereas cell-autonomously driven GC activity had no effect. A mathematical model was able to replicate the GC activity-spine stability correlation and showed MC output having improved odor discriminability while retaining odor memory. These results reveal that GC spine plasticity provides a sufficient network mechanism to decorrelate odors and maintain a memory trace.

scholarly journals Repeated Exposure to Ketamine–Xylazine during Early Development Impairs Motor Learning–dependent Dendritic Spine Plasticity in Adulthood

2015 ◽  
Vol 122 (4) ◽  
pp. 821-831 ◽  
Author(s):  
Lianyan Huang ◽  
Guang Yang
Keyword(s):  
Motor Learning ◽  
Early Development ◽  
Dendritic Spine ◽  
Primary Motor Cortex ◽  
Underlying Mechanism ◽  
Stages Of Development ◽  
Behavioral Impairment ◽  
Anesthetic Exposure ◽  
Spine Plasticity

Abstract Background: Recent studies in rodents suggest that repeated and prolonged anesthetic exposure at early stages of development leads to cognitive and behavioral impairments later in life. However, the underlying mechanism remains unknown. In this study, we tested whether exposure to general anesthesia during early development will disrupt the maturation of synaptic circuits and compromise learning-related synaptic plasticity later in life. Methods: Mice received ketamine–xylazine (20/3 mg/kg) anesthesia for one or three times, starting at either early (postnatal day 14 [P14]) or late (P21) stages of development (n = 105). Control mice received saline injections (n = 34). At P30, mice were subjected to rotarod motor training and fear conditioning. Motor learning–induced synaptic remodeling was examined in vivo by repeatedly imaging fluorescently labeled postsynaptic dendritic spines in the primary motor cortex before and after training using two-photon microscopy. Results: Three exposures to ketamine–xylazine anesthesia between P14 and P18 impair the animals’ motor learning and learning-dependent dendritic spine plasticity (new spine formation, 8.4 ± 1.3% [mean ± SD] vs. 13.4 ± 1.8%, P = 0.002) without affecting fear memory and cell apoptosis. One exposure at P14 or three exposures between P21 and P25 has no effects on the animals’ motor learning or spine plasticity. Finally, enriched motor experience ameliorates anesthesia-induced motor learning impairment and synaptic deficits. Conclusions: Our study demonstrates that repeated exposures to ketamine–xylazine during early development impair motor learning and learning-dependent dendritic spine plasticity later in life. The reduction in synaptic structural plasticity may underlie anesthesia-induced behavioral impairment.

scholarly journals Layer 4 Pyramidal Neurons Exhibit Robust Dendritic Spine Plasticity In Vivo after Input Deprivation

2015 ◽  
Vol 35 (18) ◽  
pp. 7287-7294 ◽  
Author(s):  
A. Miquelajauregui ◽  
S. Kribakaran ◽  
R. Mostany ◽  
A. Badaloni ◽  
G. G. Consalez ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Layer 4 ◽  
Spine Plasticity

Ibotenic acid induced lesions impair the modulation of dendritic spine plasticity in the prefrontal cortex and amygdala, a phenomenon that underlies working memory and social behavior

2021 ◽  
Vol 896 ◽  
pp. 173883
Author(s):  
Néstor I. Martínez-Torres ◽  
Nallely Vázquez-Hernández ◽  
Fabiola L. Martín-Amaya-Barajas ◽  
Mario Flores-Soto ◽  
Ignacio González-Burgos
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Social Behavior ◽  
Dendritic Spine ◽  
Ibotenic Acid ◽  
Spine Plasticity

Toxicokinetic and Genotoxicity Study of NNK in Male Sprague-Dawley Rats Following Nose-Only Inhalation Exposure, Intraperitoneal Injection, and Oral Gavage

2021 ◽  
Author(s):  
Shu-Chieh Hu ◽  
Matthew S Bryant ◽  
Estatira Sepehr ◽  
Hyun-Ki Kang ◽  
Raul Trbojevich ◽  
...  
Keyword(s):  
Human Lung ◽  
Inhalation Exposure ◽  
Systemic Exposure ◽  
Sprague Dawley ◽  
Oral Gavage ◽  
Sd Rats ◽  
New Information ◽  
Sprague Dawley Rats ◽  
Tissue Specimens

Abstract The tobacco-specific nitrosamine NNK [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] is found in tobacco products and tobacco smoke. NNK is a potent genotoxin and human lung carcinogen; however, there are limited inhalation data for the toxicokinetics (TK) and genotoxicity of NNK in vivo. In the present study, a single dose of 5x10−5, 5x10−3, 0.1, or 50 mg/kg body weight (BW) of NNK, 75% propylene glycol (vehicle control), or air (sham control) was administered to male Sprague-Dawley (SD) rats (9-10 weeks age) via nose-only inhalation (INH) exposure for 1 hour. For comparison, the same doses of NNK were administered to male SD rats via intraperitoneal (IP) injection and oral gavage (PO). Plasma, urine, and tissue specimens were collected at designated timepoints and analyzed for levels of NNK and its major metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and tissue levels of DNA adduct O6-methylguanine by LC/MS/MS. TK data analysis was performed using a non-linear regression program. For the genotoxicity subgroup, tissues were collected at 3 hours post-dosing for comet assay analysis. Overall, the TK data indicated that NNK was rapidly absorbed and metabolized extensively to NNAL after NNK administration via the three routes. The IP route had the greatest systemic exposure to NNK. NNK metabolism to NNAL appeared to be more efficient via INH than IP or PO. NNK induced significant increases in DNA damage in multiple tissues via the three routes. The results of this study provide new information and understanding of the toxicokinetics and genotoxicity of NNK.

The effect of kainic acid on hippocampal dendritic spine dynamics

2016 ◽  
Vol 26 ◽  
pp. S302
Author(s):  
T. Lortkipanidze ◽  
T. Bikashvili ◽  
M. Kiladze
Keyword(s):  
Kainic Acid ◽  
Dendritic Spine ◽  
Spine Dynamics

scholarly journals Pattern and not magnitude of neural activity determines dendritic spine stability in awake mice

2012 ◽  
Vol 15 (7) ◽  
pp. 949-951 ◽  
Author(s):  
Ryan M Wyatt ◽  
Elaine Tring ◽  
Joshua T Trachtenberg
Keyword(s):  
Neural Activity ◽  
Dendritic Spine ◽  
Spine Stability

scholarly journals An in vitro reproduction of stress-induced memory defects: Effects of corticoids on dendritic spine dynamics

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shinichi Saito ◽  
Satoshi Kimura ◽  
Naoki Adachi ◽  
Tadahiro Numakawa ◽  
Akihiko Ogura ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Spine Dynamics

scholarly journals In Bacillus subtilis, the Sirtuin Protein Deacetylase, Encoded by the srtN Gene (Formerly yhdZ), and Functions Encoded by the acuABC Genes Control the Activity of Acetyl Coenzyme A Synthetase

2009 ◽  
Vol 191 (6) ◽  
pp. 1749-1755 ◽  
Author(s):  
Jeffrey G. Gardner ◽  
Jorge C. Escalante-Semerena
Keyword(s):  
Bacillus Subtilis ◽  
Coenzyme A ◽  
Acetyl Coenzyme A ◽  
Acetyl Coenzyme ◽  
New Information ◽  
Low Concentrations ◽  
Dependent Protein ◽  
Protein Deacetylase

ABSTRACT This report provides in vivo evidence for the posttranslational control of the acetyl coenzyme A (Ac-CoA) synthetase (AcsA) enzyme of Bacillus subtilis by the acuA and acuC gene products. In addition, both in vivo and in vitro data presented support the conclusion that the yhdZ gene of B. subtilis encodes a NAD+-dependent protein deacetylase homologous to the yeast Sir2 protein (also known as sirtuin). On the basis of this new information, a change in gene nomenclature, from yhdZ to srtN (for sirtuin), is proposed to reflect the activity associated with the YdhZ protein. In vivo control of B. subtilis AcsA function required the combined activities of AcuC and SrtN. Inactivation of acuC or srtN resulted in slower growth and cell yield under low-acetate conditions than those of the wild-type strain, and the acuC srtN strain grew under low-acetate conditions as poorly as the acsA strain. Our interpretation of the latter result was that both deacetylases (AcuC and SrtN) are needed to maintain AcsA as active (i.e., deacetylated) so the cell can grow with low concentrations of acetate. Growth of an acuA acuC srtN strain on acetate was improved over that of the acuA + acuC srtN strain, indicating that the AcuA acetyltransferase enzyme modifies (i.e., inactivates) AcsA in vivo, a result consistent with previously reported in vitro evidence that AcsA is a substrate of AcuA.

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