Sensory Deprivation Alters Aggrecan and Perineuronal Net Expression in the Mouse Barrel Cortex

McRae, Paulette A.; Rocco, Mary M.; Kelly, Gail M.; Brumberg, Joshua C.; Matthews, Russell T.

doi:10.1523/jneurosci.5425-06.2007

Cited by 235 publications

(255 citation statements)

References 49 publications

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“…A major redistribution of ␣1 subunits from synaptic to extrasynaptic locations on the cell membrane appears unlikely, because we observed no significant changes in rise times (40). Our finding of increased ␣1 subunit functionality does not rule out additional contributions to altered IPSC properties through presynaptic mechanisms, such as altered structure of presynaptic terminals or the selective loss of specific types of presynaptic inhibitory neurons (12,(40)(41)(42)(43)(44)(45). Interestingly, we do not observe changes in IPSCs in RS cells from whisker-deprived mice (42).…”

Section: Long-term Sensory Deprivation Causes a Switch In Functional contrasting

confidence: 57%

Long-term sensory deprivation selectively rearranges functional inhibitory circuits in mouse barrel cortex

Rudolph

Huntsman

2009

Proc. Natl. Acad. Sci. U.S.A.

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Long-term whisker removal alters the balance of excitation and inhibition in rodent barrel cortex, yet little is known about the contributions of individual cells and synapses in this process. We studied synaptic inhibition in four major types of neurons in live tangential slices that isolate layer 4 in the posteromedial barrel subfield. Voltage-clamp recordings of layer 4 neurons reveal that fast decay of synaptic inhibition requires ␣1-containing GABAA receptors. After 7 weeks of deprivation, we found that GABA A-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the inhibitory lowthreshold-spiking (LTS) cell recorded in deprived barrels exhibited faster decay kinetics and larger amplitudes in whisker-deprived barrels than those in nondeprived barrels in age-matched controls. This was not observed in other cell types. Additionally, IPSCs recorded in LTS cells from deprived barrels show a marked increase in zolpidem sensitivity. To determine if the faster IPSC decay in LTS cells from deprived barrels indicates an increase in ␣1 subunit functionality, we deprived ␣1(H101R) mutant mice with zolpidem-insensitive ␣1-containing GABA A receptors. In these mice and matched wild-type controls, IPSC decay kinetics in LTS cells were faster after whisker removal; however, the deprivation-induced sensitivity to zolpidem was reduced in ␣1(H101R) mice. These data illustrate a change of synaptic inhibition in LTS cells via an increase in ␣1-subunit-mediated function. Because ␣1 subunits are commonly associated with circuitspecific plasticity in sensory cortex, this switch in LTS cell synaptic inhibition may signal necessary circuit changes required for plastic adjustments in sensory-deprived cortex.interneurons ͉ networks ͉ plasticity S ynaptic inhibition is involved in sensory processing at the very first stage of cortical integration in layer 4 of the rodent primary somatosensory (barrel) cortex (1). Both feedforward and feedback inhibition from local circuit inhibitory neurons regulates the integration of thalamic and intracortical inputs (2, 3). Inhibitory neurons are distinguished from each other by action potential firing properties, morphology, and biochemical expression (4, 5). Cortical inhibitory neurons are largely separated into two functional circuits that are thought to carry out two intertwined yet separate functions in sensory processing (6). Fast-spiking (FS) cells are either basket cells or chandelier cells and express parvalbumin (4). They are readily activated by thalamic afferents and are the primary mediator of thalamocortical feedforward inhibition, and recurrent synaptic inhibition onto FS cells is very fast (6, 7). Low-threshold-spiking (LTS) cells express varying combinations of somatostatin, vasoactive intestinal peptide, and cholecystokinin (4), are weakly activated by thalamic afferents, and contribute to intracortical inhibitory transmission, and recurrent synaptic inhibition onto LTS cells decays slowly (7,8).In cortex and other regions, an emerging feature in brain networks is the ''G...

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Section: Long-term Sensory Deprivation Causes a Switch In Functional contrasting

confidence: 57%

Long-term sensory deprivation selectively rearranges functional inhibitory circuits in mouse barrel cortex

Rudolph

Huntsman

2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Experiments using a nonselective blocker of voltage-gated sodium channels, but not transgenic models with compromised glutamate release, clearly inhibited PNN formation (Reimers et al, 2007). Similar observations have also been reported in the visual cortex and barrel cortices (Dityatev et al, 2007;McRae et al, 2007). Dark rearing in newborn cats prolongs the critical period in the visual cortex with a concomitant decrease in aggrecan immunostaining (Hockfield et al, 1990;Lander et al, 1997;Pizzurusso et al, 2002), but in developing chicks light deprivation did not prevent PNN formation (Gati et al, 2010).…”

Section: Activity-dependent Regulation Of Pnn Formationmentioning

confidence: 56%

“…Interestingly, after 30 days of normal activity postwhisker trimming, there is a further reduction in aggrecan-positive PNN levels, implying that experience in first 30 days of life is critical. The decrease appears to be specific to aggrecan, but not other PNN markers, localized specifically around PV-expressing cells (McRae et al, 2007). Sensory deprivation of facial vibrissae in rat barrel cortex also reduced the number of WFA-labeled PNNs (Nakamura et al, 2009).…”

Section: Activity-dependent Regulation Of Pnn Formationmentioning

confidence: 89%

“…The PNN has been observed surrounding the neurons throughout the CNS, including visual cortex, barrel cortex, deep cerebellar nuclei, substantia nigra, hippocampus, and spinal cord (Brauer et al, 1993;Morris and Henderson 2000;Pizzorusso et al, 2002;Carulli et al 2006;McRae et al, 2007;Brückner et al, 2008;Galtrey et al, 2008). It has also been identified in different organisms, such as mouse, rat, opossum, monkey, and human (Brückner et al, 1998b;Sayed et al, 2002;Horn et al, 2003;Hilbig et al, 2007;Schmidt et al, 2010).With the use of WFA staining, the PNN has mainly been localized to parvalbumin (PV)-positive GABAergic interneurons in the CNS, although it has also been described in other neurons, such as pyramidal neurons from parietal cortex and neurons in medial nucleus of the trapezoid body (Takahashi-Iwanaga et al, 1998;Härtig et al, 2001;Wegner et al, 2003).…”

Section: The Role Of the Pnn In Neuronsmentioning

confidence: 99%

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Extracellular matrix and perineuronal nets in CNS repair

Kwok

Dick

Wang

et al. 2011

Developmental Neurobiology

354

304

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A perineuronal net (PNN) is a layer of lattice-like matrix which enwraps the surface of the soma and dendrites, and in some cases the axon initial segments, in sub-populations of neurons in the central nervous system (CNS). First reported by Camillo Golgi more than a century ago, the molecular structure and the potential role of this matrix have only been unraveled in the last few decades. PNNs are mainly composed of hyaluronan, chondroitin sulfate proteoglycans, link proteins, and tenascin R. The interactions between these molecules allow the formation of a stable pericellular complex surrounding synapses on the neuronal surface. PNNs appear late in development co-incident with the closure of critical periods for plasticity. They play a direct role in the control of CNS plasticity, and their removal is one way in which plasticity can be re-activated in the adult CNS. In this review, we examine the molecular components and formation of PNNs, their role in maturation and synaptic plasticity after CNS injury, and the possible mechanisms of PNN action.

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“…However, none of such difference was detected with GFAP or S100 staining or in GFAP-eGFP mice. Finally, the compartmentalized expression of Cxs could be attributable to a difference in the expression of extracellular matrix and/or adhesion molecules reported to occur in the barrel cortex, as for instance the perineuronal net (McRae et al, 2007) or cadherins (Gil et al, 2002). Indeed, such compartmentalized pattern could affect the expression of astrocytic Cxs and GJC because proteoglycans (Spray et al, 1987) and cadherins (Giepmans, 2004) have been reported to control Cx expression and function.…”

Section: Discussionmentioning

confidence: 99%

Gap Junction-Mediated Astrocytic Networks in the Mouse Barrel Cortex

Houades¹,

Koulakoff²,

Ezan³

et al. 2008

J. Neurosci.

193

161

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The barrel field of the somatosensory cortex constitutes a well documented example of anatomofunctional compartmentalization and activity-dependent interaction between neurons and astrocytes. In astrocytes, intercellular communication through gap junction channels composed by connexin 43 and 30 underlies a network organization. Immunohistochemical and electrophysiological experiments were undertaken to determine the coupling properties of astrocyte networks in layer IV of the developing barrel cortex. The expression of both connexins was found to be enriched within barrels compared with septa and other cortical layers. Combination of dye-coupling experiments performed with biocytin and immunostaining with specific cell markers demonstrated that astrocytic networks do not involve neurons, oligodendrocytes or NG2 cells. The shape of dye coupling was oval in the barrel cortex whereas it was circular in layer IV outside the barrel field. Two-dimensional analysis of these coupling areas indicated that gap junctional communication was restricted from a barrel to its neighbor. Such enrichment of connexin expression and transversal restriction were not observed in a transgenic mouse lacking the barrel organization, whereas they were both observed in a double-transgenic mouse with restored barrels. Direct observation of sulforhodamine B spread indicated that astrocytes located between two barrels were either weakly or not coupled, whereas coupling within a barrel was oriented toward its center. These observations indicated a preferential orientation of coupling inside the barrels resulting from subpopulations of astrocytes with different coupling properties that contribute to shaping astrocytic networks. Such properties confine intercellular communication in astrocytes within a defined barrel as previously reported for excitatory neuronal circuits.

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Sensory Deprivation Alters Aggrecan and Perineuronal Net Expression in the Mouse Barrel Cortex

Cited by 235 publications

References 49 publications

Long-term sensory deprivation selectively rearranges functional inhibitory circuits in mouse barrel cortex

Long-term sensory deprivation selectively rearranges functional inhibitory circuits in mouse barrel cortex

Extracellular matrix and perineuronal nets in CNS repair

Gap Junction-Mediated Astrocytic Networks in the Mouse Barrel Cortex

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