Adolescent bisphenol-A exposure decreases dendritic spine density: Role of sex and age

Mastoparan-7 (Mas-7), an analogue of the peptide mastoparan, which is derived from wasp venom, is a direct activator ofPertussis toxin-(PTX-) sensitive G proteins. Mas-7 produces several biological effects in different cell types; however, little is known about how Mas-7 influences mature hippocampal neurons. We examined the specific role of Mas-7 in the development of dendritic spines, the sites of excitatory synaptic contact that are crucial for synaptic plasticity. We report here that exposure of hippocampal neurons to a low dose of Mas-7 increases dendritic spine density and spine head width in a time-dependent manner. Additionally, Mas-7 enhances postsynaptic density protein-95 (PSD-95) clustering in neurites and activatesGαosignaling, increasing the intracellular Ca2+concentration. To define the role of signaling intermediates, we measured the levels of phosphorylated protein kinase C (PKC), c-Jun N-terminal kinase (JNK), and calcium-calmodulin dependent protein kinase IIα(CaMKIIα) after Mas-7 treatment and determined that CaMKII activation is necessary for the Mas-7-dependent increase in dendritic spine density. Our results demonstrate a critical role forGαosubunit signaling in the regulation of synapse formation.

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

Neural Plasticity ◽

10.1155/2012/976164 ◽

2012 ◽

Vol 2012 ◽

pp. 1-9 ◽

Cited By ~ 19

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.

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Bisphenol-A exposure during adolescence leads to enduring alterations in cognition and dendritic spine density in adult male and female rats

Hormones and Behavior ◽

10.1016/j.yhbeh.2014.12.007 ◽

2015 ◽

Vol 69 ◽

pp. 89-97 ◽

Cited By ~ 34

Author(s):

Rachel E. Bowman ◽

Victoria Luine ◽

Samantha Diaz Weinstein ◽

Hameda Khandaker ◽

Sarah DeWolf ◽

...

Keyword(s):

Bisphenol A ◽

Adult Male ◽

Dendritic Spine ◽

Female Rats ◽

Spine Density ◽

Male And Female ◽

Dendritic Spine Density ◽

Male And Female Rats

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Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.

Behavioral Neuroscience ◽

10.1037/a0025959 ◽

2012 ◽

Vol 126 (1) ◽

pp. 175-185 ◽

Cited By ~ 75

Author(s):

Tehila Eilam-Stock ◽

Peter Serrano ◽

Maya Frankfurt ◽

Victoria Luine

Keyword(s):

Bisphenol A ◽

Adult Male ◽

Dendritic Spine ◽

Male Rats ◽

Spine Density ◽

Dendritic Spine Density

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Repeated intermittent administration of (R)-ketamine during juvenile and adolescent stages prevents schizophrenia-relevant phenotypes in adult offspring after maternal immune activation: a role of TrkB signaling

European Archives of Psychiatry and Clinical Neuroscience ◽

10.1007/s00406-021-01365-6 ◽

2022 ◽

Author(s):

Yunfei Tan ◽

Yuko Fujita ◽

Yaoyu Pu ◽

Lijia Chang ◽

Youge Qu ◽

...

Keyword(s):

Cognitive Deficits ◽

Immune Activation ◽

Dendritic Spine ◽

Poly I:C ◽

Adult Offspring ◽

Spine Density ◽

Intermittent Administration ◽

Maternal Immune Activation ◽

Dendritic Spine Density

AbstractMaternal immune activation (MIA) plays a role in the etiology of schizophrenia. MIA by prenatal exposure of polyinosinic:polycytidylic acid [poly(I:C)] in rodents caused behavioral and neurobiological changes relevant to schizophrenia in adult offspring. We investigated whether the novel antidepressant (R)-ketamine could prevent the development of psychosis-like phenotypes in adult offspring after MIA. We examined the effects of (R)-ketamine (10 mg/kg/day, twice weekly for 4 weeks) during juvenile and adolescent stages (P28–P56) on the development of cognitive deficits, loss of parvalbumin (PV)-immunoreactivity in the medial prefrontal cortex (mPFC), and decreased dendritic spine density in the mPFC and hippocampus from adult offspring after prenatal poly(I:C) exposure. Furthermore, we examined the role of TrkB in the prophylactic effects of (R)-ketamine. Repeated intermittent administration of (R)-ketamine during juvenile and adolescent stages significantly blocked the development of cognitive deficits, reduced PV-immunoreactivity in the prelimbic (PrL) of mPFC, and decreased dendritic spine density in the PrL of mPFC, CA3 and dentate gyrus of the hippocampus from adult offspring after prenatal poly(I:C) exposure. Furthermore, pretreatment with ANA-12 (TrkB antagonist: twice weekly for 4 weeks) significantly blocked the beneficial effects of (R)-ketamine on cognitive deficits of adult offspring after prenatal poly(I:C) exposure. These data suggest that repeated intermittent administration of (R)-ketamine during juvenile and adolescent stages could prevent the development of psychosis in adult offspring after MIA. Therefore, (R)-ketamine would be a potential prophylactic drug for young subjects with high-risk for psychosis.

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