scholarly journals Divergent Roles ofp75NTRand Trk Receptors in BDNF's Effects on Dendritic Spine Density and Morphology

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Christopher A. Chapleau ◽  
Lucas Pozzo-Miller
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Dendritic Morphology ◽  
Spine Density ◽  
Trk Receptors ◽  
Trk Receptor ◽  
Dendritic Spine Density ◽  
Trkb Receptors ◽  
Hippocampal Ca1 ◽  
Bdnf Signaling

Activation of TrkB receptors by brain-derived neurotrophic factor (BDNF) followed by MAPK/ERK signaling increases dendritic spine density and the proportion of mature spines in hippocampal CA1 pyramidal neurons. Considering the opposing actions ofp75NTRand Trk receptors in several BDNF actions on CNS neurons, we tested whether these receptors also have divergent actions on dendritic spine density and morphology. A function-blocking anti-p75NTRantibody (REX) did not affect spine density by itself but it prevented BDNF’s effect on spine density. Intriguingly, REX by itself increased the proportion of immature spines and prevented BDNF's effect on spine morphology. In contrast, the Trk receptor inhibitor k-252a increased spine density by itself, and prevented BDNF from further increasing spine density. However, most of the spines in k-252a-treated slices were of the immature type. These effects of k-252a on spine density and morphology required neuronal activity because they were prevented by TTX. These divergent BDNF actions on spine density and morphology are reminiscent of opposing functional signaling byp75NTRand Trk receptors and reveal an unexpected level of complexity in the consequences of BDNF signaling on dendritic morphology.

scholarly journals Five hours total sleep deprivation does not affect CA1 dendritic length or spine density

2021 ◽  
Author(s):  
Alvin T.S. Brodin ◽  
Sarolta Gabulya ◽  
Katrin Wellfelt ◽  
Tobias E. Karlsson
Keyword(s):  
Sleep Deprivation ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Memory Function ◽  
Long Term Memory ◽  
Spine Density ◽  
Dendritic Length ◽  
Dendritic Spine Density ◽  
Hippocampal Ca1

AbstractSleep is essential for long term memory function. However the neuroanatomical consequences of sleep loss are disputed. Sleep deprivation has been reported to cause both decreases and increases of dendritic spine density. Here we use Thy1-GFP expressing transgenic mice to investigate the effects of acute sleep deprivation on the dendritic architecture of hippocampal CA1 pyramidal neurons. We found that five hours of sleep deprivation had no effect on either dendritic length or dendritic spine density. Our work suggests that no major neuroanatomical changes result from one episode of sleep deprivation.

Dendritic Spine Density of Pyramidal Neurons in Field CA1 of the Hippocampus Decreases due to Chronic Tryptophan Restriction

1998 ◽  
Vol 1 (3) ◽  
pp. 237-242 ◽  
Author(s):  
M.I. Pérez-Vega ◽  
G. Barajas-López ◽  
A.R. del Angel-Meza ◽  
I. González-Burgos ◽  
A. Feria-Velasco
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Field Ca1

scholarly journals Hippocampal CA1 Pyramidal Neurons ofMecp2Mutant Mice Show a Dendritic Spine Phenotype Only in the Presymptomatic Stage

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Christopher A. Chapleau ◽  
Elena Maria Boggio ◽  
Gaston Calfa ◽  
Alan K. Percy ◽  
Maurizio Giustetto ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Mutant Mice ◽  
Spine Density ◽  
Ca1 Pyramidal Neurons ◽  
Dendritic Spine Density ◽  
Presymptomatic Stage ◽  
Deficient Mice

Alterations in dendritic spines have been documented in numerous neurodevelopmental disorders, including Rett Syndrome (RTT). RTT, an X chromosome-linked disorder associated with mutations inMECP2, is the leading cause of intellectual disabilities in women. Neurons inMecp2-deficient mice show lower dendritic spine density in several brain regions. To better understand the role of MeCP2 on excitatory spine synapses, we analyzed dendritic spines of CA1 pyramidal neurons in the hippocampus ofMecp2tm1.1Jaemale mutant mice by either confocal microscopy or electron microscopy (EM). At postnatal-day 7 (P7), well before the onset of RTT-like symptoms, CA1 pyramidal neurons from mutant mice showed lower dendritic spine density than those from wildtype littermates. On the other hand, at P15 or later showing characteristic RTT-like symptoms, dendritic spine density did not differ between mutant and wildtype neurons. Consistently, stereological analyses at the EM level revealed similar densities of asymmetric spine synapses in CA1stratum radiatumof symptomatic mutant and wildtype littermates. These results raise caution regarding the use of dendritic spine density in hippocampal neurons as a phenotypic endpoint for the evaluation of therapeutic interventions in symptomaticMecp2-deficient mice. However, they underscore the potential role of MeCP2 in the maintenance of excitatory spine synapses.

scholarly journals Developmental Stage-dependent Persistent Impact of Propofol Anesthesia on Dendritic Spines in the Rat Medial Prefrontal Cortex

2011 ◽  
Vol 115 (2) ◽  
pp. 282-293 ◽  
Author(s):  
Adrian Briner ◽  
Irina Nikonenko ◽  
Mathias De Roo ◽  
Alexandre Dayer ◽  
Dominique Muller ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Prefrontal Cortex ◽  
Developmental Stage ◽  
Medial Prefrontal Cortex ◽  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Postnatal Life ◽  
Spine Density ◽  
Quantitative Electron Microscopy ◽  
Dendritic Spine Density

Background Recent observations demonstrate that anesthetics rapidly impair synaptogenesis during neuronal circuitry development. Whether these effects are lasting and depend on the developmental stage at which these drugs are administered remains, however, to be explored. Methods Wistar rats received propofol anesthesia at defined developmental stages during early postnatal life. The acute and long-term effects of these treatments on neuronal cytoarchitecture were evaluated by Neurolucida and confocal microscopy analysis after iontophoretic injections of Lucifer Yellow into layer 5 pyramidal neurons in the medial prefrontal cortex. Quantitative electron microscopy was applied to investigate synapse density. Results Layer 5 pyramidal neurons of the medial prefrontal cortex displayed intense dendritic growth and spinogenesis during the first postnatal month. Exposure of rat pups to propofol at postnatal days 5 and 10 significantly decreased dendritic spine density, whereas this drug induced a significant increase in spine density when administered at postnatal days 15, 20, or 30. Quantitative electron microscopy revealed that the propofol-induced increase in spine density was accompanied by a significant increase in the number of synapses. Importantly, the propofol-induced modifications in dendritic spine densities persisted up to postnatal day 90. Conclusion These new results demonstrate that propofol anesthesia can rapidly induce significant changes in dendritic spine density and that these effects are developmental stage-dependent, persist into adulthood, and are accompanied by alterations in synapse number. These data suggest that anesthesia in the early postnatal period might permanently impair circuit assembly in the developing brain.

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