Cyclooxygenase-2 expression during rat neocortical development and in Rett syndrome

Kaufmann, Walter E.; Worley, Paul F.; Taylor, Christopher V.; Bremer, Margaret E.; Isakson, Peter C.

doi:10.1016/s0387-7604(96)00047-2

Cited by 67 publications

(38 citation statements)

References 34 publications

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“…The present study also included a comparison between monozygotic twins discordant for the RTT phenotype, which confirmed our previous study demonstrating greater cortical involvement in the affected twin 24 and the relative sparing of the occipital cortex in RTT reported in several neuroanatomic and neuroimaging studies. [22][23][24]45,46 Neurobiologically, the preferential volumetric reductions in dorsal parietal GM found in this study support the hypothesis of early dendritic growth arrest in RTT, 20,27,[47][48][49] because the most affected cortical regions are among the first to develop. 27,48 On the other hand, the mild and diffuse reductions in cortical WM are most likely related to axonal pathology (ie, decreased axonal diameter and/or branching) and not to myelination abnormalities, because no changes in T2 signal intensity or other related parameters have been observed or reported in the literature.…”

Section: Discussionsupporting

confidence: 83%

Selective Cerebral Volume Reduction in Rett Syndrome: A Multiple-Approach MR Imaging Study

Carter¹,

Lanham²,

Pham³

et al. 2007

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:Previous studies have examined volumetric abnormalities in Rett syndrome (RTT), using MR imaging and focusing on selective changes. However, these studies preceded the identification of MECP2 as the gene mutated in most RTT cases. We studied regional brain volume changes as noted by MR imaging in girls with RTT who had mutations in the MECP2 gene and more or less severe clinical outcomes to further characterize the neuroanatomy of RTT and its correlations with clinical severity.

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Section: Discussionsupporting

confidence: 83%

Selective Cerebral Volume Reduction in Rett Syndrome: A Multiple-Approach MR Imaging Study

Carter¹,

Lanham²,

Pham³

et al. 2007

AJNR Am J Neuroradiol

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“…In the rodent, there is very little COX-2 expression immediately after birth. Expression then increases to achieve peak values during the third and fourth postnatal weeks before decreasing to the intermediate levels contained in adult brain (11,12). A similar pattern of expression is found for nitric oxide synthase (NOS).…”

mentioning

confidence: 73%

“…The expression pattern of COX and NOS, with a peak at approximately 1 mo, parallels cortical maturation and synaptogenesis, suggesting that they are potentially important regulators of normal neuronal development. Indeed, abnormal distribution of COX-2 has been described in human children with the neurodegenerative disease Rett syndrome (11). On the other hand, NOS and COX-2 have been shown to act synergistically to worsen ischemic brain injury (13).…”

mentioning

confidence: 99%

Cyclooxygenase-2 Activity Following Traumatic Brain Injury in the Developing Rat

et al. 2007

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Cyclooxygenase (COX) is the rate-limiting enzyme in the production of prostaglandins. COX-2, the predominant COX isoform in brain, is induced by synaptic activity. COX-2-generated prostaglandins are important regulators for a range of activities under physiologic conditions. However, under pathologic conditions, COX-2 activity can produce reactive oxygen species and toxic prostaglandin metabolites that can exacerbate brain injury. In this study, we examine the developmental production of COX-2 and test the ability of a COX-2 inhibitor, SC58125, to attenuate traumatic brain injury in developing rats. We show that constitutive COX-2 concentration is low (0.5-fold adult concentration) during the first postnatal week and then increases to 3-fold of adult levels between days 14 -60. Controlled cortical impact (CCI) at postnatal day (PND) 17, but not PND 7, caused an additional 3-fold increase in COX-2 content and was associated with an increase in the COX-2 product PGE 2 . Treatment with the COX-2 inhibitor SC58125 in PND17 rats exposed to CCI attenuated the rise in PGE 2 but did not attenuate lesion volume or improve performance in the Morris water maze. C OX is the rate-limiting enzyme in the production of prostaglandins from arachidonic acid. There are two COX isoforms, COX-1 and COX-2. COX-1 is a constitutive isoform produced in many tissues including stomach, kidneys, blood vessels, and platelets. COX-2 is an inducible isoform found in inflammatory cells and brain; it is the predominant isoform in brain. In brain, COX-2 is induced by synaptic activity and COX-2-generated prostaglandins are important physiologic regulators for a range of activities including local cerebral blood flow and learning. The recent controversy surrounding the association of stroke and COX-2 inhibitors in otherwise healthy patients reinforces the notion that COX-2 has an important role in cerebrovascular homeostasis. On the other hand, overexpression of COX-2 can be harmful. Under pathologic conditions including trauma, ischemia, and chronic neurodegenerative conditions, COX-2 activity is up-regulated, producing reactive oxygen species and toxic prostaglandin metabolites that worsen injury [reviewed in (1)]. Accordingly, experimental models of ischemic brain injury show less damage in rodents treated with COX-2 inhibitors and in COX-2 knock out mice.Both COX-1 (2) and COX-2 are increased after traumatic brain injury (3-5). However, treatment using COX-2 inhibitors in models of traumatic brain injury have led to contradictory results, with some showing a benefit to therapy (6 -9) and others showing harm or no benefit (3,10).COX-2 in the immature brain is developmentally regulated. In the rodent, there is very little COX-2 expression immediately after birth. Expression then increases to achieve peak values during the third and fourth postnatal weeks before decreasing to the intermediate levels contained in adult brain (11,12). A similar pattern of expression is found for nitric oxide synthase (NOS). NOS, like COX, is an important...

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“…Dendritic growth initially follows genetic dictates but later becomes modified by levels and patterns of activity (Bartlett and Banker, 1984) in both developing (Kossel et al, 1995;Segal, 1995) and mature systems in response to numerous manipulations, including denervation (Parnavelas et al, 1974), long-term potentiation (LTP) (Buchs and Muller, 1996;Sorra and Harris, 1998), and environmental stimulation (Comery et al, 1996;Jones et al, 1997). With each developmental stage, the expression of a set of dendritic proteins (Petit et al, 1988;Kaufmann et al, 1997), neurotransmitters and growth factors that influence the progression of dendritic development changes. Spines are very dynamic structures; their size, shape and number change throughout life.…”

Section: How Do Dendritic Arbourisations Develop In Down Syndrome Bramentioning

confidence: 99%

On dendrites in Down syndrome and DS murine models: a spiny way to learn

Benavides-Piccione

Ballesteros-Yáñez

Lagrán

et al. 2004

Progress in Neurobiology

122

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Since the discovery in the 1970s that dendritic abnormalities in cortical pyramidal neurons are the most consistent pathologic correlate of mental retardation, research has focused on how dendritic alterations are related to reduced intellectual ability. Due in part to obvious ethical problems and in part to the lack of fruitful methods to study neuronal circuitry in the human cortex, there is little data about the microanatomical contribution to mental retardation. The recent identification of the genetic bases of some mental retardation associated alterations, coupled with the technology to create transgenic animal models and the introduction of powerful sophisticated tools in the field of microanatomy, has led to a growth in the studies of the alterations of pyramidal cell morphology in these disorders. Studies of individuals with Down syndrome, the most frequent genetic disorder leading to mental retardation, allow the analysis of the relationships between cognition, genotype and brain microanatomy. In Down syndrome the crucial question is to define the mechanisms by which an excess of normal gene products, in interaction with the environment, directs and constrains neural maturation, and how this abnormal development translates into cognition and behaviour. In the present article we discuss mainly Down syndrome-associated dendritic abnormalities and plasticity and the role of animal models in these studies. We believe that through the further development of such approaches, the study of the microanatomical substrates of mental retardation will contribute significantly to our understanding of the mechanisms underlying human brain disorders associated with mental retardation. #

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Cyclooxygenase-2 expression during rat neocortical development and in Rett syndrome

Cited by 67 publications

References 34 publications

Selective Cerebral Volume Reduction in Rett Syndrome: A Multiple-Approach MR Imaging Study

Selective Cerebral Volume Reduction in Rett Syndrome: A Multiple-Approach MR Imaging Study

Cyclooxygenase-2 Activity Following Traumatic Brain Injury in the Developing Rat

On dendrites in Down syndrome and DS murine models: a spiny way to learn

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