Dissociating Barrel Development and Lesion-Induced Plasticity in the Mouse Somatosensory Cortex

Rebsam, Alexandra; Seif, Isabelle; Gaspar, Patricia

doi:10.1523/jneurosci.4191-04.2005

Cited by 53 publications

(44 citation statements)

References 28 publications

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“…We also combined PCPA and ␣MT injections. PCPA treatments in mouse pups have been found previously to cause a 80 -50% decrease of brain 5-HT levels (Rebsam et al, 2005;Dailly et al, 2006). Anti-serotonin immunoreactivity showed a reduction of serotonin-immunolabeled axons after PCPA injections (Fig.…”

Section: Neurotransmitter Phenotypementioning

confidence: 60%

“…Our data failed to show an increase in cell death in the cerebral cortex. However, these pharmacological treatments are not specific and may cause only partial monoamine depletion [80% reduction of 5-HT in the cortex (Dailly et al, 2006); 50% in the whole brain (Rebsam et al, 2005)]. To avoid any confounding effect of pharmacological treatment, we used mice lacking the transcription factor Pet-1.…”

Section: Inhibition Of Monoamine Synthesismentioning

confidence: 99%

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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.

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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.

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Section: Neurotransmitter Phenotypementioning

confidence: 60%

Section: Inhibition Of Monoamine Synthesismentioning

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.

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“…MAO A KO mice display permanent alterations in layer IV of the primary somatosensory cortex (S1); the thalamocortical axons and the granular neurons form a homogeneous band instead of being clustered into barrels (23). Restoration of MAO A function in the forebrain transgenic mice should therefore result in a restoration or similarity of cortical structure between wild and forebrain transgenic mice, compared with MAO A KO.…”

Section: Mao a Substrates 5-ht Ne And Da Decreased And Mao A Metabomentioning

confidence: 99%

“…Neonatal administration of the tryptophan hydroxylase inhibitor parachlorophenylalanine reduced 5-HT and partly restored the capacity to form cortical barrels (17). Restoration of the barrel field can be accomplished before postnatal day 7 (22,23). These studies suggest the neuronal developmental stage is critically important for the aggressive behavior in adulthood in both human and mice, prompting us to create a transgenic mouse that would restore the somatosensory cortex structure in the early developmental period and alleviate the aggressive behavior in the adult male mouse.…”

mentioning

confidence: 99%

Forebrain-specific Expression of Monoamine Oxidase A Reduces Neurotransmitter Levels, Restores the Brain Structure, and Rescues Aggressive Behavior in Monoamine Oxidase A-deficient Mice

Chen

Cases

Rebrin

et al. 2007

Journal of Biological Chemistry

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Previous studies have established that abrogation of monoamine oxidase (MAO) A expression leads to a neurochemical, morphological, and behavioral specific phenotype with increased levels of serotonin (5-HT), norepinephrine, and dopamine, loss of barrel field structure in mouse somatosensory cortex, and an association with increased aggression in adults. Forebrain-specific MAO A transgenic mice were generated from MAO A knock-out (KO) mice by using the promoter of calcium-dependent kinase II␣ (CaMKII␣). The presence of human MAO A transgene and its expression were verified by PCR of genomic DNA and reverse transcription-PCR of mRNA and Western blot, respectively. Significant MAO A catalytic activity, autoradiographic labeling of 5-HT, and immunocytochemistry of MAO A were found in the frontal cortex, striatum, and hippocampus but not in the cerebellum of the forebrain transgenic mice. Also, compared with MAO A KO mice, lower levels of 5-HT, norepinephrine, and DA and higher levels of MAO A metabolite 5-hydroxyindoleacetic acid were found in the forebrain regions but not in the cerebellum of the transgenic mice. These results suggest that MAO A is specifically expressed in the forebrain regions of transgenic mice. This forebrain-specific differential expression resulted in abrogation of the aggressive phenotype. Furthermore, the disorganization of the somatosensory cortex barrel field structure associated with MAO A KO mice was restored and became morphologically similar to wild type. Thus, the lack of MAO A in the forebrain of MAO A KO mice may underlie their phenotypes.This study shows that a forebrain-specific expression of monoamine oxidase (MAO) 3 A is able to restore the disorganized somatosensory cortex barrel field structure and an aggressive behavior seen in MAO A KO mice. MAO A and B are outer membrane mitochondrial enzymes responsible for the metabolic degradation of biogenic amines in humans (1, 2). MAO A prefers serotonin (5-HT) and norepinephrine (NE) as substrates, whereas MAO B prefers phenylethylamine (PEA) and benzylamine (1-5). Dopamine (DA), tyramine, and tryptamine are common substrates for both forms. MAO A and B are encoded by different genes (6, 7) closely linked on the X chromosome (8). Both isoenzymes are widely present in most brain regions (9). MAO A gene deficiency in a Dutch family shows borderline mental retardation and impulsive aggression (10, 11). A promoter region was associated with high or low MAO A promoter activity (12). Individuals with low MAO A promoter activity who are maltreated in early childhood have increased risk for antisocial behavior as adults (13,14). These results indicated that the interaction of the gene and the environment of early childhood predispose the adult behavior. Functional magnetic resonance imaging in healthy human volunteers shows that the low expression variant, associated with increased risk of violent behavior, correlated with pronounced limbic volume reductions, hyper-responsive amygdala during emotional arousal, and diminished reactivity of r...

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“…The presynaptic 5-HT 1B receptors (5-HT 1B Rs) that inhibit glutamate release at the TC synapse (Laurent et al, 2002) control also barrel development (Cases et al, 1996;Salichon et al, 2001). However, several cortex-specific genetic modifications have no effect on the closure of the critical period (Lu et al, 2001;Datwani et al, 2002a;Rebsam et al, 2005;Inan et al, 2006;Iwasato et al, 2008) and the TC axon clustering (Iwasato et al, 2000;Hannan et al, 2001;Inan et al, 2006;Watson et al, 2006), suggesting that still unknown changes occur in the thalamus.…”

Section: Introductionmentioning

confidence: 99%

Early Development of the Thalamic Inhibitory Feedback Loop in the Primary Somatosensory System of the Newborn Mice

Evrard¹,

Ropert²

2009

J. Neurosci.

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Spontaneous neuronal activity plays an important role during the final development of the brain circuits and the formation of the primary sensory maps. In young rats, spindle bursts have been recorded in the primary somatosensory cortex. They are correlated with spontaneous muscle twitches and occur before active whisking. They bear similarities with the spindles recorded in adult brain that occur during early stages of sleep and rely on a thalamic feedback loop between the glutamatergic nucleus ventroposterior medialis (nVPM) and the GABAergic nucleus reticularis thalami (nRT). However, whether a functional nVPM-nRT loop exists in newborn rodents is unknown. We studied the reciprocal synaptic connections between nVPM and nRT in thalamic acute slices from mice from birth [postnatal day 0 (P0)] until P9. We first demonstrated that nVPM-to-nRT EPSCs could be distinguished from corticothalamic EPSCs by their inhibition by 5-HT attributable to the transient expression of functional presynaptic serotonin 1B receptors. The nVPM-to-nRT EPSCs and nRT-to-nVPMIPSCs were both detected the first day after birth; their amplitude near 2 nS was relatively stable until P5. At P6 -P7, there was a rapid and simultaneous increase of both nVPM-to-nRT EPSCs and nRT-to-nVPM IPSCs that reached 8 and 9 nS, respectively. Our results show that the thalamic synapses implicated in spindle activity are functional shortly after birth, suggesting that they could already generate spindles during the first postnatal week. Our results also suggest an inhibitory action of 5-HT on the spindle bursts of the newborn mice.

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Dissociating Barrel Development and Lesion-Induced Plasticity in the Mouse Somatosensory Cortex

Cited by 53 publications

References 28 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

Forebrain-specific Expression of Monoamine Oxidase A Reduces Neurotransmitter Levels, Restores the Brain Structure, and Rescues Aggressive Behavior in Monoamine Oxidase A-deficient Mice

Early Development of the Thalamic Inhibitory Feedback Loop in the Primary Somatosensory System of the Newborn Mice

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