Decreased dendritic spine density of neurons of the prefrontal cortex and nucleus accumbens and enhanced amphetamine sensitivity in postpubertal rats after a neonatal amygdala lesion

Synapse ◽  
2009 ◽  
Vol 63 (12) ◽  
pp. 1143-1153 ◽  
Author(s):  
Oscar Solis ◽  
Rubén Antonio Vázquez-Roque ◽  
Israel Camacho-Abrego ◽  
Citlalli Gamboa ◽  
Fidel De La Cruz ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Spine Density ◽  
Amygdala Lesion ◽  
Dendritic Spine Density ◽  
Density Of Neurons

Chronic phencyclidine treatment increases dendritic spine density in prefrontal cortex and nucleus accumbens neurons

Synapse ◽  
2007 ◽  
Vol 61 (12) ◽  
pp. 978-984 ◽  
Author(s):  
Cecilia Flores ◽  
Xianglan Wen ◽  
Cassandre Labelle-Dumais ◽  
Bryan Kolb
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors

2017 ◽  
Vol 114 (35) ◽  
pp. 9469-9474 ◽  
Author(s):  
Ethan M. Anderson ◽  
Anne Marie Wissman ◽  
Joyce Chemplanikal ◽  
Nicole Buzin ◽  
Daniel Guzman ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Morphological Changes ◽  
Dominant Negative ◽  
Addictive Behaviors ◽  
Spine Density ◽  
Nucleus Accumbens Shell ◽  
Self Administration ◽  
Dendritic Spine Density ◽  
Chronic Cocaine

Chronic cocaine use is associated with prominent morphological changes in nucleus accumbens shell (NACsh) neurons, including increases in dendritic spine density along with enhanced motivation for cocaine, but a functional relationship between these morphological and behavioral phenomena has not been shown. Here we show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocaine-induced dendritic spine formation by using either localized TrkB knockout or viral-mediated expression of a dominant negative, kinase-dead TrkB mutant. Interestingly, augmenting wild-type TrkB expression after chronic cocaine self-administration reverses the sustained increase in dendritic spine density, an effect mediated by TrkB signaling pathways that converge on extracellular regulated kinase. Loss of TrkB function after cocaine self-administration, however, leaves spine density intact but markedly enhances the motivation for cocaine, an effect mediated by specific loss of TrkB signaling through phospholipase Cgamma1 (PLCγ1). Conversely, overexpression of PLCγ1 both reduces the motivation for cocaine and reverses dendritic spine density, suggesting a potential target for the treatment of addiction in chronic users. Together, these findings indicate that BDNF-TrkB signaling both mediates and reverses cocaine-induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.

Lamina-Specific Reductions in Dendritic Spine Density in the Prefrontal Cortex of Subjects With Schizophrenia

2005 ◽  
Vol 162 (6) ◽  
pp. 1200-1202 ◽  
Author(s):  
Nutan Kolluri ◽  
Zhuoxin Sun ◽  
Allan R. Sampson ◽  
David A. Lewis
Keyword(s):  
Prefrontal Cortex ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density

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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