The abnormal distribution of mossy fiber bundles and morphological abnormalities in hippocampal formation of dreherJ ( ) mouse

Sekiguchi, Masaki; Abe, Hiroshi; Nagato, Yasukazu; Tanaka, Osamu; Guo, Huiling; Nowakowski, Richard S.

doi:10.1016/0165-3806(95)00195-6

Cited by 13 publications

(9 citation statements)

References 9 publications

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“…Similar cytoarchitectonic abnormalities have been reported in other mutant mice (e.g., dreher, Hld mice) (Nowakowski and Davis, 1985;Nowakowski, 1986Nowakowski, , 1988Sekiguchi et al, 1992Sekiguchi et al, , 1996, and, in some respects, these previously reported abnormalities are similar to those observed in the Pit1 dw-J homozygous mouse. For example, ectopic granule cells such as those found in the molecular layer of the dentate gyrus and ectopic pyramidal cells in the hippocampus have also been found in NZB/BINJ and dreher mutant mice (Nowakowski, 1986(Nowakowski, , 1988Sekiguchi et al, 1992).…”

Section: Discussionsupporting

confidence: 72%

“…However, there is also a key difference between our findings in the Pit1 dw-J homozygous hippocampus and the previous findings. In other mutants the hippocampal abnormalities were typically confined to area CA3 of the hippocampus (Nowakowski and Davis, 1985;Nowakowski, 1986Nowakowski, , 1988Sekiguchi et al, 1992Sekiguchi et al, , 1996, whereas in the Pit1 dw-J Snell dwarf hippocampus the ectopic pyramidal cells are also located in all areas of CA1-CA3. In any event, it is possible that hormonal abnormalities or hormone receptor abnormalities play a role in the production of some of the common phenotypes that these animals share.…”

Section: Discussionmentioning

confidence: 94%

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Cerebellar microfolia and other abnormalities of neuronal growth, migration, and lamination in thePit1dw-Jhomozygote mutant mouse

et al. 1998

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The Snell dwarf mouse (Pit1 dw-J homozygote) has a mutation in the Pit1 gene that prevents the normal formation of the anterior pituitary. In neonates and adults there is almost complete absence of growth hormone (GH), prolactin (PRL), thyroxin (T 4 ), and thyroid-stimulating hormone (TSH). Since these hormones have been suggested to play a role in normal development of the central nervous system (CNS), we have investigated the effects of the Pit1 dw-J mutation on the cerebellum and hippocampal formation. In the cerebellum, there were abnormalities of both foliation and lamination. The major foliation anomalies were 1) changes in the relative size of specific folia and also the proportional sizes of the anterior vs posterior cerebellum; and 2) the presence of between one and three microfolia per half cerebellum. The microfolia were all in the medial portion of the hemisphere in the caudal part of the cerebellum. Each microfolium was just rostral to a normal fissure and interposed between the fissure and a normal gyrus. Lamination abnormalities included an increase in the number of single ectopic granule cells in the molecular layer in both cerebellar vermis (86%) and hemisphere (40%) in comparison with the wild-type mouse. In the hippocampus of the Pit1 dw-J homozygote mouse, the number of pyramidal cells was decreased, although the width of the pyramidal cell layer throughout areas CA1-CA3 appeared to be normal, but less densely populated than in the wild-type mouse. Moreover, the number of granule cells that form the granule cell layer was decreased from the wild-type mouse and some ectopic granule cells (occurring both as single cells and as small clusters) were observed in the innermost portion of the molecular layer. The abnormalities observed in the Pit1 dw-J homozygote mouse seem to be caused by both direct and indirect effects of the deficiency of TSH (or T 4 ), PRL, or GH rather than by a direct effect of the deletion of Pit1.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 94%

Cerebellar microfolia and other abnormalities of neuronal growth, migration, and lamination in thePit1dw-Jhomozygote mutant mouse

et al. 1998

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“…Lmx1a is also expressed in the otic vesicle, cerebellum and neural crest cells [4], [8]. Extensive studies have looked at the role of this gene in the development of the brain, and in particular the cytoarchitecture of the cerebellum [4], [5], [9], [10], [11], [12], but only a few studies have focused on the role of Lmx1a in morphogenesis of the developing inner ear [13], [14] and for those studies Lmx1a dr-J was the Lmx1a allele analysed.…”

Section: Introductionmentioning

confidence: 99%

Mutanlallemand (mtl) and Belly Spot and Deafness (bsd) Are Two New Mutations of Lmx1a Causing Severe Cochlear and Vestibular Defects

et al. 2012

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Mutanlallemand (mtl) and Belly Spot and Deafness (bsd) are two new spontaneous alleles of the Lmx1a gene in mice. Homozygous mutants show head tossing and circling behaviour, indicative of vestibular defects, and they have short tails and white belly patches of variable size. The analysis of auditory brainstem responses (ABR) showed that mtl and bsd homozygotes are deaf, whereas heterozygous and wildtype littermates have normal hearing. Paint-filled inner ears at E16.5 revealed that mtl and bsd homozygotes lack endolymphatic ducts and semicircular canals and have short cochlear ducts. These new alleles show similarities with dreher (Lmx1a) mutants. Complementation tests between mtl and dreher and between mtl and bsd suggest that mtl and bsd are new mutant alleles of the Lmx1a gene. To determine the Lmx1a mutation in mtl and bsd mutant mice we performed PCR followed by sequencing of genomic DNA and cDNA. The mtl mutation is a single point mutation in the 3′ splice site of exon 4 leading to an exon extension and the activation of a cryptic splice site 44 base pairs downstream, whereas the bsd mutation is a genomic deletion that includes exon 3. Both mutations lead to a truncated LMX1A protein affecting the homeodomain (mtl) or LIM2-domain (bsd), which is critical for LMX1A protein function. Moreover, the levels of Lmx1a transcript in mtl and bsd mutants are significantly down-regulated. Hmx2/3 and Pax2 expression are also down-regulated in mtl and bsd mutants, suggesting a role of Lmx1a upstream of these transcription factors in early inner ear morphogenesis. We have found that these mutants develop sensory patches although they are misshapen. The characterization of these two new Lmx1a alleles highlights the critical role of this gene in the development of the cochlea and vestibular system.

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“…19 This deafferentation stimulates sprouting of granule cell mossy axon collaterals into the molecular layer (ML), where they are not normally found in abundance. 20,63,81 There they make aberrant synapses with dendrites of the deafferented granule cells ("reactive synaptogenesis") that are electrophysiologically functional.…”

mentioning

confidence: 99%

Role of apolipoprotein E and estrogen in mossy fiber sprouting in hippocampal slice cultures

et al. 1999

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Abstract-A role for apolipoprotein E is implicated in regeneration of synaptic circuitry after neural injury. The in vitro mouse organotypic hippocampal slice culture system shows Timm's stained mossy fiber sprouting into the dentate gyrus molecular layer in response to deafferentation of the entorhinal cortex. We show that cultures derived from apolipoprotein E knockout mice are defective in this sprouting response; specifically, they show no sprouting in the dorsal region of the dentate gyrus, yet retain sprouting in the ventral region. Dorsal but not ventral sprouting in cultures from C57Bl/6J mice is increased 75% by treatment with 100 pM 17b-estradiol; this response is blocked by both progesterone and tamoxifen.These results show that neuronal sprouting is increased by estrogen in the same region where sprouting is dependent on apolipoprotein E. Sprouting may be stimulated by estrogen through its up-regulation of apolipoprotein E expression leading to increased recycling of membrane lipids for use by sprouting neurons. Estrogen and apolipoprotein E may therefore interact in their modulation of both Alzheimer's disease risk and recovery from CNS injury.

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The abnormal distribution of mossy fiber bundles and morphological abnormalities in hippocampal formation of dreherJ ( ) mouse

Cited by 13 publications

References 9 publications

Cerebellar microfolia and other abnormalities of neuronal growth, migration, and lamination in thePit1dw-Jhomozygote mutant mouse

Cerebellar microfolia and other abnormalities of neuronal growth, migration, and lamination in thePit1dw-Jhomozygote mutant mouse

Mutanlallemand (mtl) and Belly Spot and Deafness (bsd) Are Two New Mutations of Lmx1a Causing Severe Cochlear and Vestibular Defects

Role of apolipoprotein E and estrogen in mossy fiber sprouting in hippocampal slice cultures

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