Showing papers by "Richard Lathe published in 2009"
TL;DR: The data reveal that the time when ERs might be activated in the brain is limited to the first 8 postnatal days, and the importance of aromatase has to be reconsidered as the alternative estrogen, 3βAdiol, is important in neuronal function in the postnatal brain.
Abstract: This study reports on the spatiotemporal dynamics of the expression of estrogen receptors (ERs) in the mouse central nervous system (CNS) during the early postnatal and the peripubertal period. At postnatal day 7 (P7), neurons with strong nuclear immunostaining for both ERα and ERβ1 were widely distributed throughout the brain. Sucrose density gradient sedimentation followed by western blotting supported the histochemical evidence for high levels of both ERs at P7. Over the following 2 days, there was a rapid downregulation of ERs. At P9, ERα expression was visible only in the hypothalamic area. Decline in ERβ1 expression was slower than that of ERα, and ERα-negative, ERβ1-positive cells were observed in the dentate gyrus and walls of third ventricle. Between P14 and P35, ERs were undetectable except for the hypothalamic area. As before P7, the ovary does not produce estrogen but does produce 5α-androstane-3β, 17β-diol (3βAdiol), an estrogenic metabolite of dihydrotestosterone, we examined the effects of high levels of 3βAdiol in the postnatal period. We used CYP7B1 knockout mice which cannot hydroxylate and inactivate 3βAdiol. The brains of these mice are abnormally large with reduced apoptosis. In the early postnatal period, there was 1-week delay in the timing of the reduction in ER expression in the brain. These data reveal that the time when ERs might be activated in the brain is limited to the first 8 postnatal days. In addition, the importance of aromatase has to be reconsidered as the alternative estrogen, 3βAdiol, is important in neuronal function in the postnatal brain.
42 citations
TL;DR: Though the nucleic acid patterns were generally identical in scrapie-infected versus control brain, some rare bands were differentially displayed and implicate specific host RNAs in the pathoetiology of the TSEs.
22 citations
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TL;DR: References H A P P É , F. & J U S T, M.A .
Abstract: References H A P P É , F. (1999) ‘Autism: Cognitive Deficit or Cognitive Style?’, Trends in Cognitive Science 3: 216–22. K A NA, R .K . , K E L L E R , T.A . , C H E R K A S S K Y, V. L . , M I N S H E W, N. J. & J U S T, M.A . (2006) ‘Sentence Comprehension in Autism: Thinking in Pictures with Decreased Functional Connectivity’, Brain 129: 2484–93. L O P E Z , B. , L E E K A M, S .R . & A RT S , G.R . (2008) ‘How Central is Central Coherence? Preliminary Evidence on the Link between Conceptual and Perceptual Processing in Children with Autism’, Autism 12 (2): 159–71. TAG E R-F L U S B E R G, H . & J O S E P H, R .M. (2003) ‘Identifying Neurocognitive Phenotypes in Autism’, Philosophical Transactions of the Royal Society of London, Series B 358: 303–14.
14 citations
TL;DR: Abnormally large, heavy brain with a decreased number of apoptotic cells in CYP7B1 knockout mice and an increase in the number of mitochondria are observed in knockout mice.
Abstract: Abnormally large, heavy brain with a decreased number of apoptotic cells in CYP7B1 knockout mice
3 citations