scholarly journals Critical Period Plasticity Is Disrupted in the Barrel Cortex of Fmr1 Knockout Mice

Neuron ◽  
2010 ◽  
Vol 65 (3) ◽  
pp. 385-398 ◽  
Author(s):  
Emily G. Harlow ◽  
Sally M. Till ◽  
Theron A. Russell ◽  
Lasani S. Wijetunge ◽  
Peter Kind ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Critical Period ◽  
Barrel Cortex

Development of Intrinsic Properties and Excitability of Layer 2/3 Pyramidal Neurons During a Critical Period for Sensory Maps in Rat Barrel Cortex

2004 ◽  
Vol 92 (1) ◽  
pp. 144-156 ◽  
Author(s):  
Miguel Maravall ◽  
Edward A. Stern ◽  
Karel Svoboda
Keyword(s):  
Critical Period ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Membrane Properties ◽  
Sensory Maps ◽  
Layer 2 ◽  
Whole Cell Recordings ◽  
Passive Membrane Properties

The development of layer 2/3 sensory maps in rat barrel cortex (BC) is experience dependent with a critical period around postnatal days (PND) 10–14. The role of intrinsic response properties of neurons in this plasticity has not been investigated. Here we characterize the development of BC layer 2/3 intrinsic responses to identify possible sites of plasticity. Whole cell recordings were performed on pyramidal cells in acute BC slices from control and deprived rats, over ages spanning the critical period (PND 12, 14, and 17). Vibrissa trimming began at PND 9. Spiking behavior changed from phasic (more spike frequency adaptation) to regular (less adaptation) with age, such that the number of action potentials per stimulus increased. Changes in spiking properties were related to the strength of a slow Ca2+-dependent afterhyperpolarization. Maturation of the spiking properties of layer 2/3 pyramidal neurons coincided with the close of the critical period and was delayed by deprivation. Other measures of excitability, including I-f curves and passive membrane properties, were affected by development but unaffected by whisker deprivation.

scholarly journals The olfactory critical period is determined by activity-dependent Sema7A/PlxnC1 signaling within glomeruli

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Nobuko Inoue ◽  
Hirofumi Nishizumi ◽  
Rumi Ooyama ◽  
Kazutaka Mogi ◽  
Katsuhiko Nishimori ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Knockout Mice ◽  
Critical Period ◽  
Olfactory Sensory Neurons ◽  
Early Exposure ◽  
Signaling Molecule ◽  
Tufted Cells ◽  
Olfactory Imprinting ◽  
Activity Dependent ◽  
Positive Quality

In mice, early exposure to environmental odors affects social behaviors later in life. A signaling molecule, Semaphorin 7A (Sema7A), is induced in the odor-responding olfactory sensory neurons. Plexin C1 (PlxnC1), a receptor for Sema7A, is expressed in mitral/tufted cells, whose dendrite-localization is restricted to the first week after birth. Sema7A/PlxnC1 signaling promotes post-synaptic events and dendrite selection in mitral/tufted cells, resulting in glomerular enlargement that causes an increase in sensitivity to the experienced odor. Neonatal odor experience also induces positive responses to the imprinted odor. Knockout and rescue experiments indicate that oxytocin in neonates is responsible for imposing positive quality on imprinted memory. In the oxytocin knockout mice, the sensitivity to the imprinted odor increases, but positive responses cannot be promoted, indicating that Sema7A/PlxnC1 signaling and oxytocin separately function. These results give new insights into our understanding of olfactory imprinting during the neonatal critical period.

scholarly journals Cellular and Synaptic Phenotype Compensations Limit Circuit Disruption in Fmr1-KO Mouse Layer 4 Barrel Cortex but Fail to Prevent Deficits in Information Processing

2018 ◽  
Author(s):  
Aleksander P.F. Domanski ◽  
Sam A. Booker ◽  
David J.A. Wyllie ◽  
John T.R. Isaac ◽  
Peter C. Kind
Keyword(s):  
Sensory Processing ◽  
Knockout Mice ◽  
Barrel Cortex ◽  
Fragile X ◽  
Neuronal Function ◽  
Sensory Hypersensitivity ◽  
Layer 4 ◽  
Network Simulations ◽  
Sensory Encoding ◽  
Critical Process

AbstractSensory hypersensitivity is a common and debilitating feature of neurodevelopmental disorders such as Fragile X Syndrome (FXS). However, how developmental changes in neuronal function ultimately culminate in the network dysfunction that underlies sensory hypersensitivities is not known. To address this, we studied the layer 4 barrel cortex circuit in Fmr1 knockout mice, a critical sensory processing circuit in this mouse model of FXS. By systematically studying cellular and synaptic properties of layer 4 neurons and combining with cellular and network simulations, we explored how the array of phenotypes in Fmr1 knockout produce circuit pathology during development that result in sensory processing dysfunction. We show that many of the cellular and synaptic pathologies in Fmr1 knockout mice are antagonistic, mitigating circuit dysfunction, and hence can be regarded as compensatory to the primary pathology. Despite this compensation, the layer 4 network in the Fmr1 knockout exhibits significant alterations in spike output in response to ascending thalamocortical input that we show results in impaired sensory encoding. We suggest that it is this developmental loss of layer 4 sensory encoding precision that drives subsequent developmental alterations in layer 4 – layer 2/3 connectivity and plasticity observed in the Fmr1 knockout, and is a critical process producing sensory hypersensitivity.

scholarly journals Laminar Specificity of Local Circuits in Barrel Cortex of Ephrin-A5 Knockout Mice

2000 ◽  
Vol 20 (15) ◽  
pp. RC88-RC88 ◽  
Author(s):  
N. Harumi Yabuta ◽  
Amy K. Butler ◽  
Edward M. Callaway
Keyword(s):  
Knockout Mice ◽  
Barrel Cortex ◽  
Local Circuits ◽  
Laminar Specificity

scholarly journals Onecut-2 knockout mice fail to thrive during early postnatal period and have altered patterns of gene expression in small intestine

2010 ◽  
Vol 42 (1) ◽  
pp. 115-125 ◽  
Author(s):  
Mary R. Dusing ◽  
Elizabeth A. Maier ◽  
Bruce J. Aronow ◽  
Dan A. Wiginton
Keyword(s):  
Gene Expression ◽  
Knockout Mice ◽  
Critical Period ◽  
Postnatal Period ◽  
Double Knockout ◽  
Temporal Regulation ◽  
Liver And Pancreas ◽  
In Utero Development ◽  
Knockout Allele

Ablation of the mouse genes for Onecut-2 and Onecut-3 was reported previously, but characterization of the resulting knockout mice was focused on in utero development, principally embryonic development of liver and pancreas. Here we examined postnatal development of these Onecut knockout mice, especially the critical period before weaning. Onecut-3 knockout mice develop normally during this period. However, Onecut-2 knockout mice fail to thrive, lagging behind their littermates in size and weight. By postnatal day (d)19, they are consistently 25–30% smaller. Onecut-2 knockout mice also have a much higher level of mortality before weaning, with only ∼70% survival. Interestingly, Onecut-2 knockout mice that are heterozygous for the Onecut-3 knockout allele are diminished even further in their ability to thrive. They are ∼50–60% as large as their normal-sized littermates at d19, and less than half of these mice survive to weaning. As reported previously, the Onecut-2/Onecut-3 double knockout is a perinatal lethal. Microarray technology was used to determine the effect of Onecut-2 ablation on gene expression in duodenum, whose epithelium has among the highest levels of Onecut-2. A subset of intestinally expressed genes showed dramatically altered patterns of expression. Many of these genes encode proteins associated with the epithelial membrane, including many involved in transport and metabolism. Previously, we reported that Onecut-2 was critical to temporal regulation of the adenosine deaminase gene in duodenum. Many of the genes with altered patterns of expression in Onecut-2 knockout mouse duodenum displayed changes in the timing of gene expression.

scholarly journals Effects of enriched housing on the neuronal morphology of mice that lack zinc transporter 3 (ZnT3) and vesicular zinc

2019 ◽  
Author(s):  
Brendan B. McAllister ◽  
Sarah E. Thackray ◽  
Brenda Karina Garciá de la Orta ◽  
Elise Gosse ◽  
Purnoor Tak ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Knockout Mice ◽  
Environmental Enrichment ◽  
Basolateral Amygdala ◽  
Barrel Cortex ◽  
Zinc Transporter ◽  
Neuronal Morphology ◽  
Spine Density ◽  
Dendritic Length ◽  
Dendritic Spine Density

ABSTRACTIn the central nervous system, certain neurons store zinc within the synaptic vesicles of their axon terminals. This vesicular zinc can then be released in an activity-dependent fashion as an intercellular signal. The functions of vesicular zinc are not entirely understood, but evidence suggests that it is important for some forms of experience-dependent plasticity in the brain. The ability of neurons to store and release vesicular zinc is dependent on expression of the vesicular zinc transporter, ZnT3. Here, we examined the neuronal morphology of mice that lack ZnT3. Brains were collected from mice housed under standard laboratory conditions and from mice housed in enriched environments – large, multilevel enclosures with running wheels, numerous objects and tunnels, and a greater number of cage mates. Golgi-Cox staining was used to visualize neurons for analysis of dendritic length and dendritic spine density. Neurons were analyzed from the barrel cortex, striatum, basolateral amygdala, and hippocampus (CA1). ZnT3 knockout mice, relative to wild type mice, exhibited increased basal dendritic length in the layer 2/3 pyramidal neurons of barrel cortex, independently of housing condition. Environmental enrichment decreased apical dendritic length in these same neurons and increased dendritic spine density on striatal medium spiny neurons. Elimination of ZnT3 did not modulate any of the effects of enrichment. Our results provide no evidence that vesicular zinc is required for the experience-dependent changes that occur in response to environmental enrichment. They are consistent, however, with recent reports suggesting increased cortical volume in ZnT3 knockout mice.

scholarly journals Environmental Enrichment Rescues Visually-Mediated Behavior in Ten-m3 Knockout Mice During an Early Critical Period

2020 ◽  
Vol 14 ◽  
Author(s):  
James Blok ◽  
Dylan A. Black ◽  
Justin Petersen ◽  
Atomu Sawatari ◽  
Catherine A. Leamey
Keyword(s):  
Knockout Mice ◽  
Critical Period ◽  
Environmental Enrichment
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