Regulation of cell survival in the developing thalamus: an in vitro analysis

Asavaritikrai, Pundit; Lotto, Beau; Anderson, Gillian; Price, David J.

doi:10.1016/s0014-4886(03)00025-6

Cited by 8 publications

(10 citation statements)

References 41 publications

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“…For VB cells, trophic substances likely come from somatosensory cortex. Survival of neonatal thalamic neurons in vitro is enhanced by cortically conditioned medium (Lotto et al, 1997;Asavaritikrai et al, 2003). One vital trophic substance in CNS-conditioned medium responsible for the maintenance of thalamic neurons is brain-derived neurotrophic factor (BDNF).…”

Section: Factors Influencing Postnatal Neuronogenesismentioning

confidence: 99%

Postnatal Generation of Neurons in the Ventrobasal Nucleus of the Rat Thalamus

Mooney¹,

Miller²

2007

J. Neurosci.

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Most CNS systems, including the trigeminal-somatosensory system, develop via a hierarchical order (from the periphery and up the neuraxis). We tested the hypothesis that development of the trigeminal system can proceed via a nonhierarchical mechanism (i.e., that neuronogenesis can occur postnatally). Preweanling rats were perfused, and brain sections were stained with cresyl violet or immunolabeled with NeuN (for neuronal counts), or processed for acetylcholinesterase (AChE) activity or p75 immunoreactivity [to identify boundaries of the ventrobasal nucleus (VB)]. Neuronal number decreased during the first postnatal week but increased 2.5-fold over the next 3 weeks. To determine whether this remarkable rise resulted from the generation of new neurons, preweanlings were given injections of bromodeoxyuridine (BrdU) on postnatal day 6 (P6) or P21. BrdU-positive VB cells were apparent on both days. Cumulative BrdU labeling showed that the cell cycle was 17.3 h on P6. Moreover, Ki-67, a protein elaborated throughout the cell cycle, was expressed by 25.8 -29.3% of all VB cells on P6 -P15, falling to 7.7% by P21. BrdU-positive VB cells coexpressed neuronal markers: NeuN, HuC/D, microtubule-associated protein 2, and a dextran placed in the somatosensory cortex. Note that postnatal neuronal generation was also evident in other thalamic nuclei (e.g., the lateral geniculate nucleus). Thus, the developing VB experiences two periods of neuronal generation. Prenatal neuronogenesis is part of hierarchical trigeminal-somatosensory development. Postnatal nonhierarchical neuronogenesis is intrathalamic and matches changes in neuromodulatory systems (exemplified by AChE activity and p75) and the arrival of corticothalamic afferents.

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Section: Factors Influencing Postnatal Neuronogenesismentioning

confidence: 99%

Postnatal Generation of Neurons in the Ventrobasal Nucleus of the Rat Thalamus

Mooney¹,

Miller²

2007

J. Neurosci.

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“…Among the epigenetic factors that may influence neocortical development, neocortical afferents provide an important contribution (Abreu‐Villaça et al, 2002; Windrem and Finlay, 1991). Neuronal afferents have been shown to regulate the survival of developing neurons in several locations of the nervous system (Linden, 1994; Oppenheim, 1991), probably through the release of trophic factors (Agerman et al, 2003; Asavaritikrai et al, 2003; Ensor et al, 2003; Radulovic et al, 2003) and/or electrical activity‐dependent processes (Jevtovic‐Todorovic et al, 2003; Mennerick and Zorumski, 2000).…”

Section: Introductionmentioning

confidence: 99%

Early callosal absence disrupts the establishment of normal neocortical structure in Swiss mice

Ribeiro‐Carvalho

Manhães

Abreu‐Villaça

et al. 2006

Intl J of Devlp Neuroscience

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In the present study, we tested the hypothesis that the ontogenetic development of the corpus callosum is relevant for the establishment of a normal neocortical structure. To that effect, neocortical morphology (thickness and neuronal density) was analyzed in adult Swiss mice rendered acallosal by midline transection at the first postnatal day (Acallosal group) and in non-manipulated mice. The neocortical thicknesses and neuronal densities of layers II+III through VI were measured in area 6 and at the 17/18a border, both of which present abundant callosal inputs, and in the relatively acallosal area 17. For the thickness measure, significant differences between Non-manipulated and Acallosal groups were only found in the areas that receive massive callosal connections. In area 6, Acallosal mice presented a reduced thickness of layer V, while at the 17/18a border, these mice presented a reduced thickness of layers II+III when compared to non-manipulated ones. No statistical difference between acallosal and non-manipulated mice was found regarding the neuronal density measure. The reduced cortical thickness associated with a comparatively normal neuronal density in neocortical regions which normally have abundant callosal connections suggest a reduction in the number of cortical neurons in acallosal mice. Altogether, the present data indicate that the input provided by callosal axons is necessary for the normal development of the neocortex.

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“…Quantification was performed with ImageQuant 5.0 software and normalized to the intensity at time point 0, which was set as 1. (30,31). The localization of ␤-catenin in thalamic neurons was compared with cortical and hippocampal cells at 7 DIV.…”

Section: Methodsmentioning

confidence: 99%

WNT Protein-independent Constitutive Nuclear Localization of β-Catenin Protein and Its Low Degradation Rate in Thalamic Neurons

Misztal

Wisniewska

Ambrozkiewicz

et al. 2011

Journal of Biological Chemistry

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Nuclear localization of ␤-catenin is a hallmark of canonical Wnt signaling, a pathway that plays a crucial role in brain development and the neurogenesis of the adult brain. We recently showed that ␤-catenin accumulates specifically in mature thalamic neurons, where it regulates the expression of the Ca v 3.1 voltage-gated calcium channel gene. Here, we investigated the mechanisms underlying ␤-catenin accumulation in thalamic neurons. We report that a lack of soluble factors produced either by glia or cortical neurons does not impair nuclear ␤-catenin accumulation in thalamic neurons. We next found that the number of thalamic neurons with ␤-catenin nuclear localization did not change when the Wnt/Dishevelled signaling pathway was inhibited by Dickkopf1 or a dominant negative mutant of Dishevelled3. These results suggest a WNT-independent cellautonomous mechanism. We found that the protein levels of APC, AXIN1, and GSK3␤, components of the ␤-catenin degradation complex, were lower in the thalamus than in the cortex of the adult rat brain. Reduced levels of these proteins were also observed in cultured thalamic neurons compared with cortical cultures. Finally, pulse-chase experiments confirmed that cytoplasmic ␤-catenin turnover was slower in thalamic neurons than in cortical neurons. Altogether, our data indicate that the nuclear localization of ␤-catenin in thalamic neurons is their cell-intrinsic feature, which was WNT-independent but associated with low levels of proteins involved in ␤-catenin labeling for ubiquitination and subsequent degradation.

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Regulation of cell survival in the developing thalamus: an in vitro analysis

Cited by 8 publications

References 41 publications

Postnatal Generation of Neurons in the Ventrobasal Nucleus of the Rat Thalamus

Postnatal Generation of Neurons in the Ventrobasal Nucleus of the Rat Thalamus

Early callosal absence disrupts the establishment of normal neocortical structure in Swiss mice

WNT Protein-independent Constitutive Nuclear Localization of β-Catenin Protein and Its Low Degradation Rate in Thalamic Neurons

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