Medium-sized neurofilament protein related to maturation of a subset of cortical neurons

Hornung, Jean-Pierre; Riederer, Beat M.

doi:10.1002/(sici)1096-9861(19991122)414:3<348::aid-cne5>3.0.co;2-h

Cited by 49 publications

(17 citation statements)

References 46 publications

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“…Antiserum against NFh labeled neither type of neurons. This may be due to heavy phosphorylation of the corresponding neurofilaments which masks the epitopes for the antiserum (Riederer, 1996;Hornung and Riederer, 1999). Altogether the results of neurofilament immunohistochemistry support the similarity of lobe neurons and those near the lobes and the dissimilarity of paragriseal cells.…”

Section: Discussionsupporting

confidence: 52%

Histological and immunocytochemical characterization of neurons located in the white matter of the spinal cord of the pigeon

Necker

2004

Journal of Chemical Neuroanatomy

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Section: Discussionsupporting

confidence: 52%

Histological and immunocytochemical characterization of neurons located in the white matter of the spinal cord of the pigeon

Necker

2004

Journal of Chemical Neuroanatomy

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“…The markers we used were intermediate neurofilaments (NF-M), which are typical structures of the neuronal cytoskeleton. In the neocortex of all species examined, the antibodies labeled pyramidal cells (Hayes and Lewis, 1992;Hornung and Riederer, 1999). In barrel cortex, layer IV, NF-M also labeled star pyramidal-like cells.…”

Section: Whisker Trimming Induced Downregulation Of Perisomatic Gabaementioning

confidence: 90%

Major Effects of Sensory Experiences on the Neocortical Inhibitory Circuits

Jiao¹,

Zhang²,

Yanagawa³

et al. 2006

J. Neurosci.

151

164

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During postnatal development, sensory experiences play critical roles in the refinement of cortical connections. However, both the process of postnatal experience-dependent maturation of neocortical inhibitory networks and its underlying mechanisms remain elusive. Here, we examined the differential properties of intracortical inhibitory networks of layer IV in "sensory-spared" and "sensorydeprived" cortices of glutamate acid decarboxylase 67 (GAD67)-green fluorescent protein (GFP) (⌬neo) and wild-type mouse. Our results showed that row D whisker trimming (WT) begun at postnatal day 7 (P7), but not after P15, induced a robust reduction of parvalbumin (PV) expression, measured by the PV/GFP ratio and PV cell densities, in the deprived barrels. WT also induced a robust reduction in the number of inhibitory perisomatic varicosities and synaptic GAD65/67 immunoreactivities in spiny neurons of the deprived barrels. Although the GAD65/67 expressions in interneurons were also downregulated in the deprived barrels, the GFP expression remained unchanged. Patch-clamp recording from spiny cells showed a 1.5-fold reduction of intracortical evoked IPSCs (eIPSCs) in deprived versus spared cortices. The reduction in eIPSCs occurred via changes in presynaptic properties and unitary IPSC amplitudes. Miniature IPSCs showed subtle but significant differences between the two experimental conditions. In addition, properties of the IPSCs in deprived barrels resemble those of IPSCs recorded in immature brains (P7). Together, these results suggest that the properties of local intracortical inhibitory networks are modified by sensory experiences. Perisomatic inhibition mediated by PV-positive basket cells is pruned by sensory deprivation.

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“…Newly born male Wistar rats (UNIFESP-EPM, São Paulo, Brazil) were maintained in controlled environmental conditions (light/dark cycle of 12 h, 07:00-19:00 h; room temperature of [22][23][24] • C) with their respective mothers. The age of the animals was determined starting from the day of birth (P0).…”

Section: Induction Of Status Epilepticusmentioning

confidence: 99%

“…Neurofilaments are the main cytoskeletal components of neurons. They participate in the formation and stabilization of axonal/dendritic architecture and are associated with cellular differentiation (24). Because developmental changes of neuronal morphology are able to influence the neocortical electrophysiologic maturation (25), the increased neurofilament immunoreactivity observed in treated animals suggests an altered maturation process in neocortical neurons.…”

Section: Early Changes In Neocortical Maturationmentioning

confidence: 99%

Disruption of Cortical Development as a Consequence of Repetitive Pilocarpine‐induced Status Epilepticus in Rats

et al. 2005

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Summary: Purpose:The aim of the present study was to observe possible cortical abnormalities after repetitive pilocarpineinduced status epilepticus (SE) in rats during development.Methods: Wistar rats received intraperitoneal injection of pilocarpine hydrochloride 2% (380 mg/kg) at P7, P8, and P9. All experimental rats displayed SE after pilocarpine injections. Rats were killed at P10 and P35, and immunocytochemistry procedures were performed on 50-µm vibratome sections, by using antibodies against nonphosphorylated neurofilament (SMI-311), parvalbumin (PV), calbindin (CB), calretinin (CR), and glutamate decarboxylase (GAD-65). Selected sections were used for the TUNEL method and double-labeling experiments, with different mixtures of the same markers. Results:The major findings of the present work were (a) altered intracortical circuitry development; (b) anticipation of PV immunoreactivity in neocortical interneurons; (c) increased GAD-65 immunoreactivity; and (d) reduced neocortical apoptotic process.Conclusions: From these results, we suggest that previously healthy brain, without genetic abnormalities, might develop an "acquired" disruption of cortical development whose evolution reproduces some characteristics of the childhood epilepsies associated with cognitive impairment. Key Words: Immature brain-Early insult-Apoptosis-Neocortex-Interneurons.In humans, the incidence of seizures is higher in the first year of life and decreases until adulthood (1,2). Although most of the early-life seizures are inherently benign, symptomatic febrile or hypoxic seizures are present in the history of many patients with temporal lobe epilepsy (TLE) and are believed to be associated with an underlying progressive epileptogenic process (3). Despite increasing knowledge of basic epileptology, the role of early-life seizures in the development of TLE remains an open question.In rats, neonatal seizures induce a range of hippocampal changes, such as glia activation and cytokine increase (4), altered glutamate and γ -aminobutyric acid (GABA)(A)-receptor gene immunoreactivity (5), persistent changes in intrinsic properties of CA1 cells (6), long-term behavioral deficits (7), and reduced hippocampal neurogenesis (8). Nevertheless, several studies have shown that the immature brain is resistant to seizure-induced hippocampal neuronal cell loss (9-12) and synaptic reorganization (11,13,14). Despite hippocampal resistance to neuronal Address correspondence and reprint requests to Dr. A. V. Silva at Lab Neurologia Experimental UNIFESP-EPM, Rua Botucatú, 862, CEP 04023-900 São Paulo, SP, Brazil. E-mail: valotta.nexp@epm.br damage during early development, Santos and colleagues (15,16) recently demonstrated that multiple episodes of pilocarpine-induced status epilepticus (SE) in developing rats (P7-P9) led to progressive neocortical/hippocampal epileptiform activity, persistent in vitro hyperexcitability, increased hippocampal/thalamic apoptosis, and severe cognitive impairment in adulthood.In contrast to adult rats that develop hippocam...

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Medium-sized neurofilament protein related to maturation of a subset of cortical neurons

Cited by 49 publications

References 46 publications

Histological and immunocytochemical characterization of neurons located in the white matter of the spinal cord of the pigeon

Histological and immunocytochemical characterization of neurons located in the white matter of the spinal cord of the pigeon

Major Effects of Sensory Experiences on the Neocortical Inhibitory Circuits

Disruption of Cortical Development as a Consequence of Repetitive Pilocarpine‐induced Status Epilepticus in Rats

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