Interactions between TrkB Signaling and Serotonin Excess in the Developing Murine Somatosensory Cortex: A Role in Tangential and Radial Organization of Thalamocortical Axons

Vitalis, Tania; Cases, Olivier; Gillies, Katy; Hanoun, Naı̈ma; Hamon, Michel; Seif, Isabelle; Gaspar, Patrícia; Kind, Peter C.; Price, David J.

doi:10.1523/jneurosci.22-12-04987.2002

Cited by 42 publications

(32 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…7G) and have normal levels of 5-HT. Mice lacking both trkB and MAOA display high levels of brain 5-HT, similar to those found in the MAOA KO mice (Vitalis et al, 2002b). Interestingly a rescue of cell death in the cortex of the trkB-MAOA DKO mice was noted during the P0 -P4 period (Fig.…”

Section: The Neuroprotectant Effect Of 5-ht Is Independent Of Trkb Sisupporting

confidence: 72%

See 1 more Smart Citation

Developmental Cell Death Is Enhanced in the Cerebral Cortex of Mice Lacking the Brain Vesicular Monoamine Transporter

Stankovski¹,

Alvarez²,

Ouimet

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

Neurotransmitters have emerged as important players in the control of programmed cell death in the cerebral cortex. We report that genetic depletion of serotonin, dopamine, and norepinephrine in mice lacking the vesicular monoamine transporter (VMAT2 KO mice) causes an increase in cell death in the superficial layers of the cingulate and retrosplenial cortices during early postnatal life (postnatal days 0 -4). Electron microscopy and terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling indicated that this represents a form of apoptosis. Caspase-3 and -9 are over activated in the VMAT2 KO cortex and Bcl-X L is downregulated, whereas the apoptosis-inducing factor caspase-8 and FasL/FasR pathway are not involved. Partial inhibition of serotonin or/and catecholamine synthesis by pharmacological treatments or genetic reduction of serotonin neuron number in mice lacking the transcription factor Pet-1 (pheochromocytoma 12 E26 transformation-specific) did not modify the cell death ratios in the cerebral cortex. However, when monoamine oxidase type A was invalidated in the VMAT2 KO background (VMAT2-MAOA DKO mice), increases in 5-HT levels coincided with a reduction of cell death and a normalization of Bcl-X L expression. trkB signaling is not implicated in the anti-apoptotic effects of MAOA inhibition because BDNF mRNA levels were unchanged in VMAT2-MAOA DKO mice and because the massive cell death in the cerebral cortex of trkB KO mice is also reverted by genetic invalidation of the MAOA gene. Finally the broad 5-HT 2 receptor agonist (Ϫ)-2,5-dimethoxy-4-iodoamphetamine hydrochloride prevented the increase in cell death of VMAT2 KO mice. Altogether, these results suggest that high levels of serotonin, acting through 5-HT 2 receptors, have neuroprotective action on cortical neurons by controlling Bcl-X L mRNA levels and that this action is independent of trkB signaling.

show abstract

Section: The Neuroprotectant Effect Of 5-ht Is Independent Of Trkb Sisupporting

confidence: 72%

“…Mouse lines were maintained on a mixed C57BL/6/129Sv genetic background enriched in C3H/HeJ. For VMAT2, MAOA, trkB, and Pet-1 genotyping, we used the same primers as described previously, respectively, by Fon et al (1997), Vitalis et al (2002b), and Hendricks et al (2003). Some pharmacological experiments were made on Swiss mice.…”

Section: Methodsmentioning

confidence: 99%

Developmental Cell Death Is Enhanced in the Cerebral Cortex of Mice Lacking the Brain Vesicular Monoamine Transporter

Stankovski¹,

Alvarez²,

Ouimet

et al. 2007

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…One vital trophic substance in CNS-conditioned medium responsible for the maintenance of thalamic neurons is brain-derived neurotrophic factor (BDNF). Four independent sets of data imply that transported cortexderived BDNF plays a role in the survival of VB neurons: (1) BDNF mRNA is undetectable in the VB between G15.5 and P15, and VB neurons are BDNF responsive (Baquet et al, 2004); (2) the thalamus of the preweanling expresses p75 and trk during the period of postnatal neuronogenesis, and this expression wanes by P21 when this production is virtually complete; (3) inactivation of trkB, the high-affinity receptor for BDNF, results in increased cell death in VB (Vitalis et al, 2002); and (4) conversely, injection of BDNF into cortex on P2 enhances the survival of thalamic neurons (Lotto et al, 2001). …”

Section: Factors Influencing Postnatal Neuronogenesismentioning

confidence: 99%

“…These include serotonin (Fujimiya et al, 1986;Bennett-Clarke et al, 1991;Bruning and Liangos, 1997), glutamate (Spreafico et al, 1994), acetylcholine (Kristt, 1983;Broide et al, 1995Broide et al, , 1996, and neurotrophins (Crockett et al, 2000;Vitalis et al, 2002). The latter two are of particular interest because they are important for the development of NSCs in the adult (Li et al, 2001;Hosomi et al, 2003;Cooper-Kuhn et al, 2004;Giuliani et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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

Mooney¹,

Miller²

2007

J. Neurosci.

View full text Add to dashboard Cite

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.

show abstract

“…Reduced expression of BDNF modifies synaptic plasticity resulting in specific alterations in spatial learning and memory processes, anxiety-related behavior, and motor activity in the knockout mouse model (McAllister et al, 1999;Kernie et al, 2000;Carter et al, 2002;Tyler et al, 2002;Yamada et al, 2002). However, targeted inactivation of the BDNF receptor, TrkB, leads to neuronal loss and cortical degenerative changes (Vitalis et al, 2002;Xu et al, 2000). In addition, BDNF mediates the effects of repeated stress exposure and longterm antidepressant treatment on neurogenesis and neuronal survival in the hippocampus (D'Sa and Duman, 2002;Rasmusson et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Interaction between BDNF Val66Met and Dopamine Transporter Gene Variation Influences Anxiety-Related Traits

Hünnerkopf

Strobel²,

Gutknecht

et al. 2007

Neuropsychopharmacol

117

View full text Add to dashboard Cite

The involvement in neural plasticity and the mediation of effects of repeated stress exposure and long-term antidepressant treatment on hippocampal neurogenesis supports a critical role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of affective and other stress-related disorders. A previously reported valine to methionine substitution at amino-acid position 66 (BDNF Val66Met) seems to account for memory disturbance and hippocampal dysfunction. In the present study, we evaluated the impact of the BDNF Val66Met polymorphism on individual differences in personality traits in a sample of healthy volunteers in relation to other common gene variants thought to be involved in the pathophysiology of affective disorders, such as the serotonin transporter promoter polymorphism (5-HTTLPR) and a variable number of tandem repeat polymorphism of the dopamine transporter gene (DAT VNTR). Personality traits were assessed using the NEO personality inventory (NEO-PI-R) and Tridimensional Personality Questionnaire (TPQ). There was a significant DAT VNTR-dependent association between NEO-PI-R Neuroticism and the BDNF Val66Met polymorphism. Among individuals with at least one copy of the DAT 9-repeat allele, carriers of the BDNF Met allele exhibited significantly lower Neuroticism scores than noncarriers. This interaction was also observed for TPQ Harm Avoidance, a personality dimension related to Neuroticism. Our results support the notion that allelic variation at the BDNF locusFin interaction with other gene variantsFinfluences anxietyand depression-related personality traits.

show abstract

Interactions between TrkB Signaling and Serotonin Excess in the Developing Murine Somatosensory Cortex: A Role in Tangential and Radial Organization of Thalamocortical Axons

Cited by 42 publications

References 50 publications

Developmental Cell Death Is Enhanced in the Cerebral Cortex of Mice Lacking the Brain Vesicular Monoamine Transporter

Developmental Cell Death Is Enhanced in the Cerebral Cortex of Mice Lacking the Brain Vesicular Monoamine Transporter

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

Interaction between BDNF Val66Met and Dopamine Transporter Gene Variation Influences Anxiety-Related Traits

Contact Info

Product

Resources

About