scholarly journals Lateralized expression of cortical perineuronal nets during maternal experience is dependent on MECP2

2019 ◽  
Author(s):  
Billy Y.B. Lau ◽  
Dana E. Layo ◽  
Brett Emery ◽  
Matthew Everett ◽  
Anushree Kumar ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Plasticity ◽  
Adult Female ◽  
Social Contexts ◽  
Gabaergic Neurons ◽  
Perineuronal Nets ◽  
Critical Periods ◽  
Early Postnatal Development ◽  
Female Mice ◽  
Maternal Experience

Cortical neuronal circuits along the sensorimotor pathways are shaped by experience during critical periods of heightened plasticity in early postnatal development. After closure of critical periods, measured histologically by the formation and maintenance of extracellular matrix structures called perineuronal nets (PNNs), the adult mouse brain exhibits restricted plasticity and maturity. Mature PNNs are typically considered to be stable structures that restrict synaptic plasticity on cortical parvalbumin+ GABAergic neurons. Changes in environment (i.e. novel behavioral training) or social contexts (i.e. motherhood) are known to elicit synaptic plasticity in relevant neural circuitry. However, little is known about concomitant changes in the PNNs surrounding the cortical parvalbumin+ GABAergic neurons. Here, we show novel changes in PNN density in the primary somatosensory cortex (SS1) of adult female mice after maternal experience, using systematic microscopy analysis of a whole brain region. On average, PNNs were increased in the right barrel field and decreased in the left forelimb regions. Individual mice had left hemisphere dominance in PNN density. Using adult female mice deficient in methyl-CpG-binding protein 2 (MECP2), an epigenetic regulator involved in regulating experience-dependent plasticity, we found that MECP2 is critical for this precise and dynamic expression of PNN. Adult naïve Mecp2-heterozygous females (Het) had increased PNN density in specific subregions in both hemispheres before maternal experience. The laterality in PNN expression seen in naïve Het was lost after maternal experience, suggesting possible intact mechanisms for plasticity. Together, our results identify subregion and hemisphere-specific alterations in PNN expression in adult females, suggesting extracellular matrix plasticity as a possible neurobiological mechanism for adult behaviors in rodents.

Perineuronal Nets in the Superior Olivary Complex

2018 ◽  
pp. 420-444 ◽  
Author(s):  
Markus Morawski ◽  
Mandy Sonntag
Keyword(s):  
Experimental Data ◽  
Extracellular Matrix ◽  
Synaptic Plasticity ◽  
Neuronal Excitability ◽  
Auditory Brainstem ◽  
Specific Form ◽  
Superior Olivary Complex ◽  
Perineuronal Nets ◽  
Neuronal Somata ◽  
Main Components

This chapter addresses perineuronal nets in the superior olivary complex, a collection of nuclei in the auditory brainstem that are involved in the processing of sound source location. Perineuronal nets, a specific form of extracellular matrix, are believed to control synaptic plasticity. They surround neuronal somata and dendrites of specific types of neurons, among which are many neurons of the superior olivary complex. The chapter describes the distribution of perineuronal nets in the superior olivary complex, focusing on controversial results and discussing underlying reasons. In addition, it considers the development of perineuronal nets and highlights differences between the main components of perineuronal nets, including the proteoglycans aggrecan, brevican, and neurocan. Finally, it introduces current concepts on the function of perineuronal nets that are specifically based on experimental data collected in the superior olivary complex and point to a contribution of perineuronal nets to synaptic transmission and neuronal excitability.

scholarly journals Alteration of Extracellular Matrix Molecules and Perineuronal Nets in the Hippocampus of Pentylenetetrazol-Kindled Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Hiroshi Ueno ◽  
Shunsuke Suemitsu ◽  
Shinji Murakami ◽  
Naoya Kitamura ◽  
Kenta Wani ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Plasticity ◽  
Neural Circuit ◽  
Perineuronal Nets ◽  
Cellular Mechanisms ◽  
Kindling Model ◽  
Ptz Kindling ◽  
Extracellular Matrix Molecules ◽  
Model Mouse ◽  
Wisteria Floribunda

The pathophysiological processes leading to epilepsy are poorly understood. Understanding the molecular and cellular mechanisms involved in the onset of epilepsy is crucial for drug development. Epileptogenicity is thought to be associated with changes in synaptic plasticity; however, whether extracellular matrix molecules—known regulators of synaptic plasticity—are altered during epileptogenesis is unknown. To test this, we used a pentylenetetrazole- (PTZ-) kindling model mouse to investigate changes to hippocampal parvalbumin- (PV-) positive neurons, extracellular matrix molecules, and perineuronal nets (PNNs) after the last kindled seizure. We found an increase in Wisteria floribunda agglutinin- (WFA-) and Cat-315-positive PNNs and a decrease in PV-positive neurons not surrounded by PNNs, in the hippocampus of PTZ-kindled mice compared to control mice. Furthermore, the expression of WFA- and Cat-315-positive molecules increased in the extracellular space of PTZ-kindled mice. In addition, consistent with previous studies, astrocytes were activated in PTZ-kindled mice. We propose that the increase in PNNs after kindling decreases neuroplasticity in the hippocampus and helps maintain the neural circuit for recurrent seizures. This study shows that possibility of changes in extracellular matrix molecules due to astrocyte activation is associated with epilepticus in PTZ-kindled mice.

scholarly journals Effects of chronic exposure to bisphenol A in adult female mice on social behavior, vasopressin system, and estrogen membrane receptor (GPER1)

2021 ◽  
Vol 65 (s1) ◽  
Author(s):  
Brigitta Bonaldo ◽  
Antonino Casile ◽  
Martina Bettarelli ◽  
Stefano Gotti ◽  
GianCarlo Panzica ◽  
...  
Keyword(s):  
Body Weight ◽  
Social Behavior ◽  
Bisphenol A ◽  
Adult Female ◽  
Chronic Exposure ◽  
Corn Oil ◽  
Chemical Exposure ◽  
Hormonal Changes ◽  
Critical Periods ◽  
Female Mice

Bisphenol A (BPA), an organic synthetic compound found in some plastics and epoxy resins, is classified as an endocrine disrupting chemical. Exposure to BPA is especially dangerous if it occurs during specific “critical periods” of life, when organisms are more sensitive to hormonal changes (i.e., intrauterine, perinatal, juvenile or puberty periods). In this study, we focused on the effects of chronic exposure to BPA in adult female mice starting during pregnancy. Three months old C57BL/6J females were orally exposed to BPA or to vehicle (corn oil). The treatment (4 µg/kg body weight/day) started the day 0 of pregnancy and continued throughout pregnancy, lactation, and lasted for a total of 20 weeks. BPA-treated dams did not show differences in body weight or food intake, but they showed an altered estrous cycle compared to the controls. In order to evidence alterations in social and sociosexual behaviors, we performed the Three-Chamber test for sociability, and analyzed two hypothalamic circuits (well-known targets of endocrine disruption) particularly involved in the control of social behavior: the vasopressin and the oxytocin systems. The test revealed some alterations in the displaying of social behavior: BPA-treated dams have higher locomotor activity compared to the control dams, probably a signal of high level of anxiety. In addition, BPA-treated dams spent more time interacting with no-tester females than with no-tester males. In brain sections, we observed a decrease of vasopressin immunoreactivity (only in the paraventricular and suprachiasmatic nuclei) of BPA-treated females, while we did not find any alteration of the oxytocin system. In parallel, we have also observed, in the same hypothalamic nuclei, a significant reduction of the membrane estrogen receptor GPER1 expression.

scholarly journals Otx2-PNN Interaction to Regulate Cortical Plasticity

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Clémence Bernard ◽  
Alain Prochiantz
Keyword(s):  
Extracellular Matrix ◽  
Visual Cortex ◽  
Binocular Vision ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Inhibitory Interneurons ◽  
Perineuronal Nets ◽  
Critical Periods ◽  
Cortical Function ◽  
Parvalbumin Interneurons

The ability of the environment to shape cortical function is at its highest during critical periods of postnatal development. In the visual cortex, critical period onset is triggered by the maturation of parvalbumin inhibitory interneurons, which gradually become surrounded by a specialized glycosaminoglycan-rich extracellular matrix: the perineuronal nets. Among the identified factors regulating cortical plasticity in the visual cortex, extracortical homeoprotein Otx2 is transferred specifically into parvalbumin interneurons and this transfer regulates both the onset and the closure of the critical period of plasticity for binocular vision. Here, we review the interaction between the complex sugars of the perineuronal nets and homeoprotein Otx2 and how this interaction regulates cortical plasticity during critical period and in adulthood.

The development of perineuronal nets around parvalbumin gabaergic neurons in the medial prefrontal cortex and basolateral amygdala of rats.

2017 ◽  
Vol 131 (4) ◽  
pp. 289-303 ◽  
Author(s):  
Kathryn D. Baker ◽  
Arielle R. Gray ◽  
Rick Richardson
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Basolateral Amygdala ◽  
Gabaergic Neurons ◽  
Perineuronal Nets

scholarly journals Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction

2021 ◽  
pp. 1-16
Author(s):  
Wei Wei ◽  
Yinghua Liu ◽  
Chunling Dai ◽  
Narjes Baazaoui ◽  
Yunn-Chyn Tung ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Early Development ◽  
Neurodegenerative Disorder ◽  
Synaptic Dysfunction ◽  
Early Postnatal Development ◽  
Wild Type Female

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance. Cognitive dysfunction and loss of neuronal plasticity are known to begin decades before the clinical diagnosis of the disease. The important influence of congenital genetic mutations on the early development of AD provides a novel opportunity to initiate treatment during early development to prevent the Alzheimer-like behavior and synaptic dysfunction. Objective: To explore strategies for early intervention to prevent Alzheimer’s disease. Methods: In the present study, we investigated the effect of treatment during early development with a ciliary neurotrophic factor (CNTF) derived peptidergic compound, P021 (Ac-DGGLAG-NH2) on cognitive function and synaptic plasticity in 3xTg-AD transgenic mouse model of AD. 3xTg-AD and genetic background-matched wild type female mice were treated from birth to postnatal day 120 with P021 in diet or as a control with vehicle diet, and cognitive function and molecular markers of neuroplasticity were evaluated. Results: P021 treatment during early development prevented cognitive impairment and increased expressions of pCREB and BDNF that activated downstream various signaling cascades such as PLC/PKC, MEK/ERK and PI3K/Akt, and ameliorated synaptic protein deficit in 4-month-old 3xTg-AD mice. Conclusion: These findings indicate that treatment with the neurotrophic peptide mimetic such as P021 during early development can be an effective therapeutic strategy to rescue synaptic deficit and cognitive impairment in familial AD and related tauopathies.

scholarly journals The Extracellular Matrix Molecule Hyaluronic Acid Regulates Hippocampal Synaptic Plasticity by Modulating Postsynaptic L-Type Ca2+ Channels

Neuron ◽  
2010 ◽  
Vol 67 (1) ◽  
pp. 116-128 ◽  
Author(s):  
Gaga Kochlamazashvili ◽  
Christian Henneberger ◽  
Olena Bukalo ◽  
Elena Dvoretskova ◽  
Oleg Senkov ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Synaptic Plasticity ◽  
Matrix Molecule ◽  
Hippocampal Synaptic Plasticity ◽  
Extracellular Matrix Molecule ◽  
Ca2 Channels
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