Region and lamina-specific distribution of extracellular matrix proteoglycans, hyaluronan and tenascin-R in the mouse hippocampal formation

Brückner, Gert; Grosche, Jens; Hartlage‐Rübsamen, Maike; Schmidt, Sandra; Schachner, Melitta

doi:10.1016/s0891-0618(03)00036-x

Cited by 103 publications

(92 citation statements)

References 88 publications

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“…The impairment of LTP stabilization at later time points in mouse CA2, and the lack of long-term synaptic potentiation entirely in rat CA2, has many possible molecular causes: (1) A 1 adenosine receptors, which inhibit LTP consolidation (Arai et al, 1990;de Mendonca and Ribeiro, 1990) and/or synaptic transmission in general (Mitchell et al, 1993) are abundant in CA2 (Ochiishi et al, 1999); (2) extracellular matrix proteins, thought to play a role in restricting plasticity (Pizzorusso et al, 2002), are high in CA2 (Yamamoto et al, 1988;Bruckner et al, 2003); (3) oligodendrocytes (Berger and Frotscher, 1994) and astrocytes (Yamamoto et al, 1988) are distinct in CA2; (4) calbindin, a calcium binding protein more commonly found in inhibitory interneurons, is present in CA2 pyramidal cells (Leranth and Ribak, 1991;Toth and Freund, 1992) and can regulate synaptic plasticity (Chard et al, 1995); (5) STEP, a phosphatase that can dephosphorylate and inactivate ERK in response to NMDA receptor activation (Paul et al, 2003) and prevents LTP induction by inhibiting NMDA receptor function (Pelkey et al, 2002), is enriched in CA2 (Fig. 1) and (Boulanger et al, 1995); and (6) CA2 neurons have a different complement of integrin subunits than those in CA3 and CA1, particularly in their lack of the ␤5 integrin subunit (Pinkstaff et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

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Synaptic Plasticity (and the Lack Thereof) in Hippocampal CA2 Neurons

Zhao¹,

Choi²,

Obrietan³

et al. 2007

J. Neurosci.

163

232

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The hippocampus is critical for some forms of memory and spatial navigation, but previous research has mostly neglected the CA2, a unique region situated between CA3 and CA1. Here, we show that CA2 pyramidal neurons have distinctive physiological characteristics that include an unprecedented synaptic stability. Although basal synaptic currents in CA1 and CA2 are quite similar, synaptic plasticity including long-term potentiation and long-term depression is absent or less likely to be induced with conventional methods of stimulation in CA2. We also find that CA2 neurons have larger leak currents and more negative resting membrane potentials than CA1 neurons, and consequently, more current is required for action potential generation in CA2 neurons. These data suggest that the molecular "conspiracy against plasticity" in CA2 makes it functionally distinct from the other hippocampal CA regions. This work provides critical insight into hippocampal function and may lead to an understanding of the resistance of CA2 to damage from disease, trauma, and hypoxia.

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Section: Discussionmentioning

confidence: 99%

“…Molecularly, CA2 can be clearly delineated from its neighboring CA regions by expression patterns of some genes (Zhao et al, 2001;Lein et al, 2004Lein et al, , 2005. Also, some extracellular matrix components and oligodendrocytes are found in greater abundance there than in CA1 and CA3 (Berger and Frotscher, 1994;Bruckner et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Synaptic Plasticity (and the Lack Thereof) in Hippocampal CA2 Neurons

Zhao¹,

Choi²,

Obrietan³

et al. 2007

J. Neurosci.

163

232

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“…4). Moreover, hyaluronan-containing pericellular extracellular matrix depositions enclosing somata of individual neural cell bodies, also known as perineuronal nets [35], could clearly be observed in wild type mice (Fig. 4A, C), while they were difficult to identify in quadruple KO mice, although staining for aggrecan (Fig.…”

Section: Quadruple Ko Mice Have An Altered Hyaluronan Deposition Patternmentioning

confidence: 98%

Extracellular matrix alterations in brains lacking four of its components

Rauch

Zhou

Roos

2005

Biochemical and Biophysical Research Communications

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The organization of the brain extracellular matrix appears to be based on aggregates of hyaluronan and proteoglycans, connected by oligomeric glycoproteins. Mild phenotypical consequences were reported from several mouse strains lacking components of this matrix such as neurocan, brevican, tenascin-R and tenascin-C. To further challange the flexibility of the extracellular matrix network of the brain, mice lacking all four brain extracellular matrix molecules were generated, which were found to be viable and fertile. Analysis of the brains of one month old quadruple KO mice revealed increased protein levels of fibulin-1 and fibulin-2. Histochemical analysis showed an unusual parenchymal deposition of these fibulins. The quadruple KO mice displayed also obvious changes in the pattern of deposition of hyaluronan.Further, an almost quadruple knock out like extracellular environment was noticed in the brains of triple knock out mice lacking both tenascins and brevican, since these brains had strongly reduced levels of neurocan.

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“…For example, a key component of the extracellular matrix, a chondroitin sulfate proteoglycan that increases during development and is regulated by visual experience (Lander et al 1997), is highly enriched in CA2 (Bruckner et al 2003). Interestingly, destruction of this matrix has been reported to "reactivate" plasticity at ages extending beyond most critical periods (Pizzorusso et al 2006) and to increase dendritic spine motility (Oray et al 2004).…”

Section: Area Ca2 Looking Forwardmentioning

confidence: 99%

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

2012

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The search for molecules that restrict synaptic plasticity in the brain has focused primarily on sensory systems during early postnatal development, as critical periods for inducing plasticity in sensory regions are easily defined. The recent discovery that Schaffer collateral inputs to hippocampal area CA2 do not readily support canonical activity-dependent long-term potentiation (LTP) serves as a reminder that the capacity for synaptic modification is also regulated anatomically across different brain regions. Hippocampal CA2 shares features with other similarly "LTP-resistant" brain areas in that many of the genes linked to synaptic function and the associated proteins known to restrict synaptic plasticity are expressed there. Add to this a rich complement of receptors and signaling molecules permissive for induction of atypical forms of synaptic potentiation, and area CA2 becomes an ideal model system for studying specific modulators of brain plasticity. Additionally, recent evidence suggests that hippocampal CA2 is instrumental for certain forms of learning, memory, and social behavior, but the links between CA2-enriched molecules and putative CA2-dependent behaviors are only just beginning to be made. In this review, we offer a detailed look at what is currently known about the synaptic plasticity in this important, yet largely overlooked component of the hippocampus and consider how the study of CA2 may provide clues to understanding the molecular signals critical to the modulation of synaptic function in different brain regions and across different stages of development.

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Region and lamina-specific distribution of extracellular matrix proteoglycans, hyaluronan and tenascin-R in the mouse hippocampal formation

Cited by 103 publications

References 88 publications

Synaptic Plasticity (and the Lack Thereof) in Hippocampal CA2 Neurons

Synaptic Plasticity (and the Lack Thereof) in Hippocampal CA2 Neurons

Extracellular matrix alterations in brains lacking four of its components

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

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