Dendritic spine morphogenesis and plasticity

Lippman, Jocelyn J.; Dunaevsky, Anna

doi:10.1002/neu.20149

Cited by 125 publications

(99 citation statements)

References 91 publications

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“…The biochemical properties of the KLHL1 protein are consistent with those of known actin-organizing proteins, and the primary location of actin fibers in dendrites is in postsynaptic spines (Rao and Craig, 2000;Ethell and Pasquale, 2005;Lippman and Dunaevsky, 2005). We hypothesize from this that KLHL1 may be involved in cross-linking the actin cytoskeleton that determines the shape and dynamics of the dendritic spine head.…”

Section: Discussionsupporting

confidence: 56%

Targeted Deletion of a SingleSca8Ataxia Locus Allele in Mice Causes Abnormal Gait, Progressive Loss of Motor Coordination, and Purkinje Cell Dendritic Deficits

He¹,

Benzow

et al. 2006

J. Neurosci.

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Spinocerebellar ataxia type 8 (SCA8) patients typically have a slowly progressive, adult-onset ataxia. SCA8 is dominantly inherited and is caused by large CTG repeat expansions in the untranslated antisense RNA of the Kelch-like 1 gene (KLHL1), but the molecular mechanism through which this expansion leads to disease is still unknown. To more fully characterize the underlying molecular mechanisms involved in SCA8, we developed a mouse model in which Klhl1 is deleted in either all tissues or is deleted specifically in Purkinje cells only. We found that mice that are either homozygous or heterozygous for the Klhl1 deletion have significant gait abnormalities at an early age and develop a significant loss of motor coordination by 24 weeks of age. This loss progresses more rapidly in homozygous knock-outs. Mice with Klhl1 specifically deleted in only Purkinje cells had a loss of motor coordination that was almost identical to the total-tissue deletion mice. Finally, we found significant Purkinje cell dendritic deficits, as measured by the thickness of the molecular layer, in all mice in which Klhl1 was deleted (both total and Purkinje cell-specific deletions) and an intermediate reduction in molecular layer thickness in mice with reduced levels of Klhl1 expression (heterozygous deletions). The results from this mouse model show that even a partial loss of Klhl1 function leads to degeneration of Purkinje cell function and indicates that loss of KLHL1 activity is likely to play a significant part in the underlying pathophysiology of SCA8.

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Section: Discussionsupporting

confidence: 56%

Targeted Deletion of a SingleSca8Ataxia Locus Allele in Mice Causes Abnormal Gait, Progressive Loss of Motor Coordination, and Purkinje Cell Dendritic Deficits

He¹,

Benzow

et al. 2006

J. Neurosci.

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“…NMDA receptors in the brain of neonates, on the other hand, has been reported to inhibit nerve cell migration and the development of dendrites and realignment of synaptic junctions. 24,25) We demonstrated in the present study that neonatal PCP treatment on postnatal days 7, 9 and 11 (once a day at 10 mg/kg, s.c.) in mice enhanced susceptibility to PCP, a behavioral abnormality related positive symptom of schizophrenia, 26,27) impaired spatial working memory and social interaction behaviors in adulthood compared to saline-treated control mice. To examine whether such behavioral changes are due to PCP treatment during neurodevelopment, adult mice were treated with PCP (10 mg/kg, s.c.) 3 times every second day and subjected to the social interaction test.…”

Section: Discussionsupporting

confidence: 52%

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

Nakatani-Pawlak

Yamaguchi²,

Tatsumi

et al. 2009

Biological & Pharmaceutical Bulletin

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N-Methyl-D-aspartate (NMDA)-type glutamic acid receptors play a critical role in excitatory synaptic transmission, synaptic plasticity and neuronal development in the central nervous system. During the developmental stage from week 25 of gestation to birth in humans, elongation and branching of axons and dendrites of nerve cells, synapse formation, myelination and realignment of nerve pathways (neural circuits) for acquiring higher neural function actively proceed, and this stage corresponds to postnatal weeks 1 through 2 in mice.1) It is generally recognized that non-synapse-mediated intercellular glutamic acid is largely involved in this process of nerve development. Stimulation of NMDA receptors facilitated radial migration of the cortical plate of excitatory nerve cells 2) and the selective blockade of NMDA receptors disturbed neuronal migration in the cerebral cortex.3)It has been reported that rats injected subcutaneously (s.c.) with phencyclidine (PCP), a noncompetitive NMDA receptor antagonist, at 10 mg/kg once a day during the postnatal development stage (postnatal days 7, 9 and 11) exhibit an increase in spontaneous motor activity, impairment of prepulse inhibition and behavioral changes in respect of learning and cognition after attaining maturation.4-7) When rats neonatally administered PCP were examined for any changes in the binding capacity of NMDA receptors and g-aminobutyrate A (GABA A ) receptors at maturity by autoradiography using In the present study, we investigated brain function from the behavioral, anatomical and neurochemical viewpoints in mice injected with PCP at 10 mg/kg on postnatal days 7, 9 and 11. Especially, we focused on changes in social interaction in PCP-treated mice, and examined the effects of clozapine, an atypical antipsychotic drug, D-cycloserine, an NMDA receptor partial agonist, flumazenil, a benzodiazepine receptor antagonist, and SHC50911, a GABA B receptor antagonist on social interaction deficits in PCP-treated mice. Of note, as far as we are aware, this is the first experimental demonstration that neonatal PCP treatment in mice results in increased sensitivity to PCP, and impaired social interaction behaviors in adulthood, which are accompanied by a decrease in the number of GABAergic interneurons and spine density in the frontal cortex and hippocampus, and abnormal monoamine metabolism in the brain. Neonatal PCP treatment in mice could be regarded as a neurodevelopmental animal model for schizophrenia. MATERIALS AND METHODSMethods. Animals Male mice aged 13 weeks old and female mice aged 13 weeks old Crlj:CD1 (ICR) were mated, and male offspring were used on postnatal day 7. Animals were maintained in a room controlled at 23°C and 55% humidity with a 12-h lighting cycle (lights on: 6:00 a.m.), and 12 ventilations/h. Animals had free access to solid feed (CRF-1; Oriental Yeast Co., Ltd., Tokyo, Japan) from feed- Kakuma-machi, Kanazawa 920-1192, Japan: b Nihon Bioresearch Inc.; 6-104 Majima, Fukuju-cho, Hashima, Gifu 501-6251, Japan: c Narabyouri Research Co.,...

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“…They concentrate and compartmentalise biochemical signals such as Ca 2+ , and synaptic protein machinery such as neurotransmitter receptors, providing the synaptic specificity required for plasticity. [29][30][31][32] In addition to regulating the number of synaptic AMPARs by trafficking, changes in synaptic strength correlate with corresponding changes in dendritic spine size, and possibly shape. [33][34][35][36][37][38] LTD stimuli result in spine shrinkage and retraction, 35,38 whereas LTP leads to the formation of new spines, or the growth of existing ones.…”

Section: Linking Ampar Trafficking With Spine Morphogenesismentioning

confidence: 99%

AMPA receptor trafficking pathways and links to dendritic spine morphogenesis

Hanley

2008

Cell Adhesion & Migration

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Dendritic spine morphogenesis and plasticity

Cited by 125 publications

References 91 publications

Targeted Deletion of a SingleSca8Ataxia Locus Allele in Mice Causes Abnormal Gait, Progressive Loss of Motor Coordination, and Purkinje Cell Dendritic Deficits

Targeted Deletion of a SingleSca8Ataxia Locus Allele in Mice Causes Abnormal Gait, Progressive Loss of Motor Coordination, and Purkinje Cell Dendritic Deficits

Neonatal Phencyclidine Treatment in Mice Induces Behavioral, Histological and Neurochemical Abnormalities in Adulthood

AMPA receptor trafficking pathways and links to dendritic spine morphogenesis

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