Differential effects of AMPA receptor activation on survival and neurite integrity during neuronal development

Manzini, M. Chiara; Joseph, Donald J.; MacDermott, Amy B.; Mason, Carol A.

doi:10.1016/j.mcn.2007.03.010

Cited by 6 publications

(3 citation statements)

References 66 publications

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“…Methods for isolation and purification of murine and rat CGNs were as previously described [91],[92]. CGNs were purified from P5 mouse pups, resuspended in serum-free medium (SFM) and plated at a density of 2.5×10 6 cells/well, six-well plate) with poly-L-ornithine (0.01%; Sigma) and mouse laminin (20 µg/ml; Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

et al. 2013

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Section: Methodsmentioning

confidence: 99%

Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

et al. 2013

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“…This protocol is based on modifications of procedures that have been described in the past 3,7,11 . There are several important points to note as discussed below.…”

Section: Discussionmentioning

confidence: 99%

Isolation and Culture of Post-Natal Mouse Cerebellar Granule Neuron Progenitor Cells and Neurons

Lee

Greene

Mason

et al. 2009

JoVE

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The cerebellar cortex is a well described structure that provides unique opportunities for studying neuronal properties and development 1,2 . Of the cerebellar neuronal types (granule cells, Purkinje cells and inhibitory interneurons), granule neurons are by far the most numerous and are the most abundant type of neurons in the mammalian brain. In rodents, cerebellar granule neurons are generated during the first two post-natal weeks from progenitor cells in the outermost layer of the cerebellar cortex, the external granule layer (EGL). The protocol presented here describes techniques to enrich and culture granule neurons and their progenitor cells from post-natal mouse cerebellum. We will describe procedures to obtain cultures of increasing purity 3,4, which can be used to study the differentiation of proliferating progenitor cells into granule neurons 5,6 . Once the progenitor cells differentiate, the cultures also provide a homogenous population of granule neurons for experimental manipulation and characterization of phenomena such as synaptogenesis, glutamate receptor function 7 , interaction with other purified cerebellar cells 8,9 or cell death 7 . ProtocolPart 1: Setting up (1-2 days before dissection) (Not shown on video)

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“…Methods for isolation and purification of murine and rat CGNs were as previously described [91,92]. CGNs were purified from P5 mouse pups, resuspended in serum-free medium (SFM) and plated at a density of 2.5610 6 cells/well, six-well plate) with poly-Lornithine (0.01%; Sigma) and mouse laminin (20 mg/ml; Invitrogen).…”

Section: Cgn Purificationmentioning

confidence: 99%

Correction: Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

Cao¹,

Rioult-Pedotti²,

Migani³

et al. 2013

PLoS Biol

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Angelman syndrome (AS) is a neurodevelopment disorder characterized by severe cognitive impairment and a high rate of autism. AS is caused by disrupted neuronal expression of the maternally inherited Ube3A ubiquitin protein ligase, required for the proteasomal degradation of proteins implicated in synaptic plasticity, such as the activity-regulated cytoskeletalassociated protein (Arc/Arg3.1). Mice deficient in maternal Ube3A express elevated levels of Arc in response to synaptic activity, which coincides with severely impaired long-term potentiation (LTP) in the hippocampus and deficits in learning behaviors. In this study, we sought to test whether elevated levels of Arc interfere with brain-derived neurotrophic factor (BDNF) TrkB receptor signaling, which is known to be essential for both the induction and maintenance of LTP. We report that TrkB signaling in the AS mouse is defective, and show that reduction of Arc expression to control levels rescues the signaling deficits. Moreover, the association of the postsynaptic density protein PSD-95 with TrkB is critical for intact BDNF signaling, and elevated levels of Arc were found to impede PSD-95/TrkB association. In Ube3A deficient mice, the BDNFinduced recruitment of PSD-95, as well as PLCc and Grb2-associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced activation of PLCc-a-calcium/calmodulin-dependent protein kinase II (CaMKII) and PI3K-Akt, but leaving the extracellular signal-regulated kinase (Erk) pathway intact. A bridged cyclic peptide (CN2097), shown by nuclear magnetic resonance (NMR) studies to uniquely bind the PDZ1 domain of PSD-95 with high affinity, decreased the interaction of Arc with PSD-95 to restore BDNF-induced TrkB/PSD-95 complex formation, signaling, and facilitate the induction of LTP in AS mice. We propose that the failure of TrkB receptor signaling at synapses in AS is directly linked to elevated levels of Arc associated with PSD-95 and PSD-95 PDZ-ligands may represent a promising approach to reverse cognitive dysfunction.

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Differential effects of AMPA receptor activation on survival and neurite integrity during neuronal development

Cited by 6 publications

References 66 publications

Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

Isolation and Culture of Post-Natal Mouse Cerebellar Granule Neuron Progenitor Cells and Neurons

Correction: Impairment of TrkB-PSD-95 Signaling in Angelman Syndrome

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