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Joshua C Brumberg - One of the best experts on this subject based on the ideXlab platform.
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the impact of development and Sensory Deprivation on dendritic protrusions in the mouse barrel cortex
Cerebral Cortex, 2015Co-Authors: Chiachien Chen, Adesh Bajnath, Joshua C BrumbergAbstract:Dendritic protrusions (spines and filopodia) are structural indicators of synapses that have been linked to neuronal learning and memory through their morphological alterations induced by development and experienced-dependent activities. Although previous studies have demonstrated that depriving Sensory experience leads to structural changes in neocortical organization, the more subtle effects on dendritic protrusions remain unclear, mostly due to focus on only one specific cell type and/or age of manipulation. Here, we show that Sensory Deprivation induced by whisker trimming influences the dendritic protrusions of basilar dendrites located in thalamocortical recipient lamina (IV and VI) of the mouse barrel cortex in a layer-specific manner. Following 1 month of whisker trimming after birth, the density of dendritic protrusions increased in layer IV, but decreased in layer VI. Whisker regrowth for 1 month returned protrusion densities to comparable level of age-matched controls in layer VI, but not in layer IV. In adults, chronic Sensory Deprivation led to an increase in protrusion densities in layer IV, but not in layer VI. In addition, chronic pharmacological blockade of N-methyl-d-aspartate receptors (NMDARs) increased protrusion density in both layers IV and VI, which returned to the control level after 1 month of drug withdrawal. Our data reveal that different cortical layers respond to chronic Sensory Deprivation in different ways, with more pronounced effects during developmental critical periods than adulthood. We also show that chronically blocking NMDARs activity during developmental critical period also influences the protrusion density and morphology in the cerebral cortex.
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organization of myelin in the mouse somatoSensory barrel cortex and the effects of Sensory Deprivation
Developmental Neurobiology, 2013Co-Authors: Kyrstle Barrera, Philip Chu, Jason Abramowitz, Robert Steger, Raddy L Ramos, Joshua C BrumbergAbstract:In rodents, the barrel cortex is a specialized area within the somatoSensory cortex that processes signals from the mystacial whiskers. We investigated the normal development of myelination in the barrel cortex of mice, as well as the effects of Sensory Deprivation on this pattern. Deprivation was achieved by trimming the whiskers on one side of the face every other day from birth. In control mice, myelin was not present until postnatal day 14 and did not show prominence until postnatal day 30; adult levels of myelination were reached by the end of the second postnatal month. Unbiased stereology was used to estimate axon density in the interbarrel septal region and barrel walls as well as the barrel centers. Myelin was significantly more concentrated in the interbarrel septa/barrel walls than in the barrel centers in both control and Sensory-deprived conditions. Sensory Deprivation did not impact the onset of myelination but resulted in a significant decrease in myelinated axons in the barrel region and decreased the amount of myelin ensheathing each axon. Visualization of the oligodendrocyte nuclear marker Olig2 revealed a similar pattern of myelin as seen using histochemistry, but with no significant changes in Olig2+ nuclei following Sensory Deprivation. Consistent with the anatomical results showing less myelination, local field potentials revealed slower rise times following trimming. Our results suggest that myelination develops relatively late and can be influenced by Sensory experience.
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Sensory Deprivation differentially impacts the dendritic development of pyramidal versus non-pyramidal neurons in layer 6 of mouse barrel cortex
Brain Structure and Function, 2012Co-Authors: Chiachien Chen, Danny Tam, Joshua C BrumbergAbstract:Early postnatal Sensory experience can have profound impacts on the structure and function of cortical circuits affecting behavior. Using the mouse whisker-to-barrel system we chronically deprived animals of normal Sensory experience by bilaterally trimming their whiskers every other day from birth for the first postnatal month. Brain tissue was then processed for Golgi staining and neurons in layer 6 of barrel cortex were reconstructed in three dimensions. Dendritic and somatic parameters were compared between Sensory-deprived and normal Sensory experience groups. Results demonstrated that layer 6 non-pyramidal neurons in the chronically deprived group showed an expansion of their dendritic arbors. The pyramidal cells responded to Sensory Deprivation with increased somatic size and basilar dendritic arborization but overall decreased apical dendritic parameters. In sum, Sensory Deprivation impacted on the neuronal architecture of pyramidal and non-pyramidal neurons in layer 6, which may provide a substrate for observed physiological and behavioral changes resulting from whisker trimming.
Rainer Klinke - One of the best experts on this subject based on the ideXlab platform.
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hearing after congenital deafness central auditory plasticity and Sensory Deprivation
Cerebral Cortex, 2002Co-Authors: Andrej Kral, Jochen Tillein, Silvia Heid, R. Hartmann, Rainer KlinkeAbstract:The congenitally deaf cat suffers from a degeneration of the inner ear. The organ of Corti bears no hair cells, yet the auditory afferents are preserved. Since these animals have no auditory experience, they were used as a model for congenital deafness. Kittens were equipped with a cochlear implant at different ages and electrostimulated over a period of 2.0–5.5 months using a monopolar single-channel compressed analogue stimulation strategy (VIENNAtype signal processor). Following a period of auditory experience, we investigated cortical field potentials in response to electrical biphasic pulses applied by means of the cochlear implant. In comparison to naive unstimulated deaf cats and normal hearing cats, the chronically stimulated animals showed larger cortical regions producing middle-latency responses at or above 300 µV amplitude at the contralateral as well as the ipsilateral auditory cortex. The cortex ipsilateral to the chronically stimulated ear did not show any signs of reduced responsiveness when stimulating the ‘untrained’ ear through a second cochlear implant inserted in the final experiment. With comparable duration of auditory training, the activated cortical area was substantially smaller if implantation had been performed at an older age of 5–6 months. The data emphasize that young Sensory systems in cats have a higher capacity for plasticity than older ones and that there is a sensitive period for the cat’s auditory system.
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hearing after congenital deafness central auditory plasticity and Sensory Deprivation
Cerebral Cortex, 2002Co-Authors: Andrej Kral, Jochen Tillein, Silvia Heid, R. Hartmann, Rainer KlinkeAbstract:The congenitally deaf cat suffers from a degeneration of the inner ear. The organ of Corti bears no hair cells, yet the auditory afferents are preserved. Since these animals have no auditory experience, they were used as a model for congenital deafness. Kittens were equipped with a cochlear implant at different ages and electrostimulated over a period of 2.0–5.5 months using a monopolar single-channel compressed analogue stimulation strategy (VIENNAtype signal processor). Following a period of auditory experience, we investigated cortical field potentials in response to electrical biphasic pulses applied by means of the cochlear implant. In comparison to naive unstimulated deaf cats and normal hearing cats, the chronically stimulated animals showed larger cortical regions producing middle-latency responses at or above 300 µV amplitude at the contralateral as well as the ipsilateral auditory cortex. The cortex ipsilateral to the chronically stimulated ear did not show any signs of reduced responsiveness when stimulating the ‘untrained’ ear through a second cochlear implant inserted in the final experiment. With comparable duration of auditory training, the activated cortical area was substantially smaller if implantation had been performed at an older age of 5–6 months. The data emphasize that young Sensory systems in cats have a higher capacity for plasticity than older ones and that there is a sensitive period for the cat’s auditory system.
Tansu Celikel - One of the best experts on this subject based on the ideXlab platform.
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proteomic landscape of the primary somatoSensory cortex upon Sensory Deprivation
GigaScience, 2017Co-Authors: Koen Kole, Paul H E Tiesinga, Rik G H Lindeboom, Marijke P Baltissen, Pascal W T C Jansen, Michiel Vermeulen, Tansu CelikelAbstract:: Experience-dependent plasticity (EDP) powerfully shapes neural circuits by inducing long-lasting molecular changes in the brain. Molecular mechanisms of EDP have been traditionally studied by identifying single or small subsets of targets along the biochemical pathways that link synaptic receptors to nuclear processes. Recent technological advances in large-scale analysis of gene transcription and translation now allow systematic observation of thousands of molecules simultaneously. Here we employed label-free quantitative mass spectrometry to address experience-dependent changes in the proteome after Sensory Deprivation of the primary somatoSensory cortex. Cortical column- and layer-specific tissue samples were collected from control animals, with all whiskers intact, and animals whose C-row whiskers were bilaterally plucked for 11-14 days. Thirty-three samples from cortical layers (L) 2/3 and L4 spanning across control, deprived, and first- and second-order spared columns yielded at least 10 000 peptides mapping to ∼5000 protein groups. Of these, 4676 were identified with high confidence, and >3000 were found in all samples. This comprehensive database provides a snapshot of the proteome after whisker Deprivation, a protocol that has been widely used to unravel the synaptic, cellular, and network mechanisms of EDP. Complementing the recently made available transcriptome for identical experimental conditions (see the accompanying article by Kole et al.), the database can be used to (i) mine novel targets whose translation is modulated by Sensory organ use, (ii) cross-validate experimental protocols from the same developmental time point, and (iii) statistically map the molecular pathways of cortical plasticity at a columnar and laminar resolution.
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transcriptional mapping of the primary somatoSensory cortex upon Sensory Deprivation
GigaScience, 2017Co-Authors: Koen Kole, Yutaro Komuro, Jan Provaznik, Jelena Pistolic, Vladimir Benes, Paul H E Tiesinga, Tansu CelikelAbstract:: Experience-dependent plasticity (EDP) is essential for anatomical and functional maturation of Sensory circuits during development. Although the principal synaptic and circuit mechanisms of EDP are increasingly well studied experimentally and computationally, its molecular mechanisms remain largely elusive. EDP can be readily studied in the rodent barrel cortex, where each "barrel column" preferentially represents deflections of its own principal whisker. Depriving select whiskers while sparing their neighbours introduces competition between barrel columns, ultimately leading to weakening of intracortical, translaminar (i.e., cortical layer (L)4-to-L2/3) feed-forward excitatory projections in the deprived columns. The same synapses are potentiated in the neighbouring spared columns. These experience-dependent alterations of synaptic strength are thought to underlie somatoSensory map plasticity. We used RNA sequencing in this model system to uncover cortical-column and -layer specific changes on the transcriptome level that are induced by altered Sensory experience. Column- and layer-specific barrel cortical tissues were collected from juvenile mice with all whiskers intact and mice that received 11-12 days of long whisker (C-row) Deprivation before high-quality RNA was purified and sequenced. The current dataset entails an average of 50 million paired-end reads per sample, 75 base pairs in length. On average, 90.15% of reads could be uniquely mapped to the mm10 reference mouse genome. The current data reveal the transcriptional changes in gene expression in the barrel cortex upon altered Sensory experience in juvenile mice and will help to molecularly map the mechanisms of cortical plasticity.
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transcriptional mapping of the primary somatoSensory cortex upon Sensory Deprivation
GigaScience, 2017Co-Authors: Koen Kole, Yutaro Komuro, Jan Provaznik, Jelena Pistolic, Vladimir Benes, Paul H E Tiesinga, Tansu CelikelAbstract:Experience-dependent plasticity (EDP) is essential for anatomical and functional maturation of Sensory circuits during development. Although the principal synaptic and circuit mechanisms of EDP are increasingly well studied experimentally and computationally, its molecular mechanisms remain largely elusive. EDP can be readily studied in the rodent barrel cortex, where each "barrel column" preferentially represents deflections of its own principal whisker. Depriving select whiskers while sparing their neighbours introduces competition between barrel columns, ultimately leading to weakening of intracortical, translaminar (i.e., cortical layer (L)4-to-L2/3) feed-forward excitatory projections in the deprived columns. The same synapses are potentiated in the neighbouring spared columns. These experience-dependent alterations of synaptic strength are thought to underlie somatoSensory map plasticity. We used RNA sequencing in this model system to uncover cortical-column and -layer specific changes on the transcriptome level that are induced by altered Sensory experience. Column- and layer-specific barrel cortical tissues were collected from juvenile mice with all whiskers intact and mice that received 11-12 days of long whisker (C-row) Deprivation before high-quality RNA was purified and sequenced. The current dataset entails an average of 50 million paired-end reads per sample, 75 base pairs in length. On average, 90.15% of reads could be uniquely mapped to the mm10 reference mouse genome. The current data reveal the transcriptional changes in gene expression in the barrel cortex upon altered Sensory experience in juvenile mice and will help to molecularly map the mechanisms of cortical plasticity.
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Modulation of spike timing by Sensory Deprivation during induction of cortical map plasticity
Nature neuroscience, 2004Co-Authors: Tansu Celikel, Vanessa A Szostak, Daniel E. FeldmanAbstract:Deprivation-induced plasticity of Sensory cortical maps involves long-term potentiation (LTP) and depression (LTD) of cortical synapses, but how Sensory Deprivation triggers LTP and LTD in vivo is unknown. Here we tested whether spike timing-dependent forms of LTP and LTD are involved in this process. We measured spike trains from neurons in layer 4 (L4) and layers 2 and 3 (L2/3) of rat somatoSensory cortex before and after acute whisker Deprivation, a manipulation that induces whisker map plasticity involving LTD at L4-to-L2/3 (L4-L2/3) synapses. Whisker Deprivation caused an immediate reversal of firing order for most L4 and L2/3 neurons and a substantial decorrelation of spike trains, changes known to drive timing-dependent LTD at L4-L2/3 synapses in vitro. In contrast, spike rate changed only modestly. Thus, whisker Deprivation is likely to drive map plasticity by spike timing-dependent mechanisms.
Andrej Kral - One of the best experts on this subject based on the ideXlab platform.
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hearing after congenital deafness central auditory plasticity and Sensory Deprivation
Cerebral Cortex, 2002Co-Authors: Andrej Kral, Jochen Tillein, Silvia Heid, R. Hartmann, Rainer KlinkeAbstract:The congenitally deaf cat suffers from a degeneration of the inner ear. The organ of Corti bears no hair cells, yet the auditory afferents are preserved. Since these animals have no auditory experience, they were used as a model for congenital deafness. Kittens were equipped with a cochlear implant at different ages and electrostimulated over a period of 2.0–5.5 months using a monopolar single-channel compressed analogue stimulation strategy (VIENNAtype signal processor). Following a period of auditory experience, we investigated cortical field potentials in response to electrical biphasic pulses applied by means of the cochlear implant. In comparison to naive unstimulated deaf cats and normal hearing cats, the chronically stimulated animals showed larger cortical regions producing middle-latency responses at or above 300 µV amplitude at the contralateral as well as the ipsilateral auditory cortex. The cortex ipsilateral to the chronically stimulated ear did not show any signs of reduced responsiveness when stimulating the ‘untrained’ ear through a second cochlear implant inserted in the final experiment. With comparable duration of auditory training, the activated cortical area was substantially smaller if implantation had been performed at an older age of 5–6 months. The data emphasize that young Sensory systems in cats have a higher capacity for plasticity than older ones and that there is a sensitive period for the cat’s auditory system.
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hearing after congenital deafness central auditory plasticity and Sensory Deprivation
Cerebral Cortex, 2002Co-Authors: Andrej Kral, Jochen Tillein, Silvia Heid, R. Hartmann, Rainer KlinkeAbstract:The congenitally deaf cat suffers from a degeneration of the inner ear. The organ of Corti bears no hair cells, yet the auditory afferents are preserved. Since these animals have no auditory experience, they were used as a model for congenital deafness. Kittens were equipped with a cochlear implant at different ages and electrostimulated over a period of 2.0–5.5 months using a monopolar single-channel compressed analogue stimulation strategy (VIENNAtype signal processor). Following a period of auditory experience, we investigated cortical field potentials in response to electrical biphasic pulses applied by means of the cochlear implant. In comparison to naive unstimulated deaf cats and normal hearing cats, the chronically stimulated animals showed larger cortical regions producing middle-latency responses at or above 300 µV amplitude at the contralateral as well as the ipsilateral auditory cortex. The cortex ipsilateral to the chronically stimulated ear did not show any signs of reduced responsiveness when stimulating the ‘untrained’ ear through a second cochlear implant inserted in the final experiment. With comparable duration of auditory training, the activated cortical area was substantially smaller if implantation had been performed at an older age of 5–6 months. The data emphasize that young Sensory systems in cats have a higher capacity for plasticity than older ones and that there is a sensitive period for the cat’s auditory system.
Karel Svoboda - One of the best experts on this subject based on the ideXlab platform.
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experience dependent plasticity of dendritic spines in the developing rat barrel cortex in vivo
Nature, 2000Co-Authors: Balazs Lendvai, Edward A Stern, Brian E Chen, Karel SvobodaAbstract:Do changes in neuronal structure underlie cortical plasticity1,2? Here we used time-lapse two-photon microscopy3,4 of pyramidal neurons in layer 2/3 of developing rat barrel cortex5 to image the structural dynamics of dendritic spines and filopodia. We found that these protrusions were highly motile: spines and filopodia appeared, disappeared or changed shape over tens of minutes. To test whether Sensory experience drives this motility we trimmed whiskers one to three days before imaging. Sensory Deprivation markedly (∼40%) reduced protrusive motility in deprived regions of the barrel cortex during a critical period around postnatal days (P)11–13, but had no effect in younger (P8–10) or older (P14–16) animals. Unexpectedly, whisker trimming did not change the density, length or shape of spines and filopodia. However, Sensory Deprivation during the critical period degraded the tuning of layer 2/3 receptive fields. Thus Sensory experience drives structural plasticity in dendrites, which may underlie the reorganization of neural circuits.
