Ultrastructural localization of reelin in the cortex in post-mortem human brain

Roberts, Rosalinda C.; Xu, Leyan; Roche, Joy K.; Kirkpatrick, Brian

doi:10.1002/cne.20408

Cited by 52 publications

(42 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings are in agreement with previous ultrastructural findings of Reelin-immunoreactivity in small axon terminals and unmyelinated axons in the post-mortem human neocortex (Roberts et al, 2005), as well as in smooth cisterns of the axon of Cajal-Retzius cells during development (Derer et al, 2001). …”

Section: The Reelin Signaling Pathway In the Developing And Adult Brainsupporting

confidence: 93%

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Knuesel

2010

Progress in Neurobiology

View full text Add to dashboard Cite

show abstract

Section: The Reelin Signaling Pathway In the Developing And Adult Brainsupporting

confidence: 93%

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Knuesel

2010

Progress in Neurobiology

View full text Add to dashboard Cite

show abstract

“…Although reelin is abundantly expressed in the postnatal brain (Pesold et al, 1998;Roberts et al, 2005;RamosMoreno et al, 2006), its functional role remains enigmatic. We have shown previously that reelin enhances tetanusinduced LTP in CA1 by activating apoER2 and VLDLR and hypothesized a potential role of reelin signaling in modulating synaptic transmission and plasticity (Weeber et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Differential Reelin-Induced Enhancement of NMDA and AMPA Receptor Activity in the Adult Hippocampus

Qiu¹,

Zhao²,

Korwek³

et al. 2006

J. Neurosci.

166

161

View full text Add to dashboard Cite

The developmental lamination of the hippocampus and other cortical structures requires a signaling cascade initiated by reelin and its receptors, apoER2 (apolipoprotein E receptor 2) and VLDLR (very-low-density lipoprotein receptor). However, the functional significance of continued reelin expression in the postnatal brain remains poorly understood. Here, we show that reelin application to adult mice hippocampal slices leads to enhanced glutamatergic transmission mediated by NMDA receptors (NMDARs) and AMPA receptors (AMPARs) through distinct mechanisms. Application of recombinant reelin enhanced NMDAR-mediated currents through postsynaptic mechanisms, as revealed by the variance-mean analysis of synaptic NMDAR currents, assessment of spontaneous miniature events, and the levels of NMDAR subunits at synaptic surface. In comparison, nonstationary fluctuation analysis of miniature AMPAR currents and quantification of synaptic surface proteins revealed that reelin-induced enhancement of AMPAR responses was mediated by increased AMPAR numbers. Reelin enhancement of synaptic NMDAR currents was abolished when receptor-associated protein (RAP) or the Src inhibitor 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo[3,4-d]-pyrimidine (PP1) was bath applied and was abrogated by includingPP1 in the recording electrodes. In comparison, including RAP or an inactive PP1 analog PP3 in the recording electrode was without effect. Interestingly, the increased AMPAR response after reelin application was not blocked by PP1 but was blocked by the phosphoinositide-3Ј kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride]. Furthermore, reelin-induced, PI3K-dependent AMPAR surface insertion was also observed in cultured hippocampal neurons. Together, these results reveal a differential functional coupling of reelin signaling with NMDAR and AMPAR function and define a novel mechanism for controlling synaptic strength and plasticity in the adult hippocampus.

show abstract

“…All sections were cut on a vibratome at a thickness of 60 microns. Vibratomes have been shown to distort histology less than do methods that involve freezing, and allow more sensitive (albeit specific) detection of immunoreactivity (Kung et al, 1998;Roberts and Knickman, 2002;Roberts et al, 2005).…”

Section: Methodsmentioning

confidence: 98%

DISC1 immunoreactivity at the light and ultrastructural level in the human neocortex

Kirkpatrick

Cascella

et al. 2006

J of Comparative Neurology

Self Cite

101

View full text Add to dashboard Cite

Disrupted-In-Schizophrenia 1 (DISC1) is one of two genes that straddle the chromosome 1 breakpoint of a translocation associated with an increased risk of schizophrenia. DISC1 has been identified in the brain of various mammalian species, but no previous immunocytochemical studies have been conducted in human neocortex. We examined DISC1 immunoreactivity in frontal and parietal cortex (BA 4, 9, 39, and 46) in normal human brain. At the light microscopic level, immunolabeling was prominent in the neuropil, in multiple populations of cells, and in the white matter. At the ultrastructural level, staining was prominent in structures associated with synaptic function. Immunolabeled axon terminals comprised 8% of all terminals and formed both asymmetric and symmetric synapses. Labeled axon terminals formed synapses with labeled spines and dendrites; in some, only the postsynaptic density (PSD) of the postsynaptic structure was labeled. The most common configuration, however, was an unlabeled axon terminal forming an asymmetric synapse with a spine that had immunoreactivity deposited on the PSD and throughout the spine. The presence of DISC1 in multiple types of synapses suggests the involvement of DISC1 in corticocortical as well as thalamocortical connections. Staining was also present in ribosomes, parts of the chromatin, in dendritic shafts, and on some microtubules. Labeling was absent from the Golgi apparatus and multivesicular bodies, which are associated with protein excretion. These anatomical localization data suggest that DISC1 participates in synaptic activity and microtubule function, and are consistent with the limited data on its adult function.

show abstract

Ultrastructural localization of reelin in the cortex in post-mortem human brain

Cited by 52 publications

References 65 publications

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

Differential Reelin-Induced Enhancement of NMDA and AMPA Receptor Activity in the Adult Hippocampus

DISC1 immunoreactivity at the light and ultrastructural level in the human neocortex

Contact Info

Product

Resources

About