Monoaminergic afferents to cortex modulate structural plasticity in the barrelfield of the mouse

Osterheld-Haas, M.C.; Loos, H. Van der; Hornung, Jean‐Pierre

doi:10.1016/0165-3806(94)90196-1

Cited by 59 publications

(30 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, the maturation of the barrelfield and its plasticity are concomitant, suggesting that the two processes are linked (Woolsey and Wann, 1976). To test this hypothesis, a number of authors have tried to uncouple these phenomena (Vongdokmai, 1980;Osterheld-Haas et al, 1994). However, these results can be questioned because the delay in barrel emergence was limited and the experimental paradigms that were used implied a general delay of brain maturation.…”

Section: Introductionmentioning

confidence: 95%

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

Rebsam

Seif²,

Gaspar³

2005

J. Neurosci.

View full text Add to dashboard Cite

In the mouse somatosensory cortex, thalamocortical axons (TCAs) corresponding to individual whiskers cluster into restricted barrel domains during the first days of life. If whiskers are lesioned before that time, the cortical space devoted to the afferents from the damaged whisker shrinks and becomes occupied by thalamocortical afferents from neighboring unlesioned whiskers. This plasticity ends by postnatal day 3 (P3) to P4 when barrels emerge. To test whether TCA development and lesion-induced plasticity are linked, we used monoamine oxidase A knock-out (MAOA-KO) mice in which normal TCA development is halted by an excess of serotonin. Normal TCA development can be restored when serotonin levels are lowered by parachlorophenylalanine (PCPA). By varying the time of PCPA administration, we found that barrel development can be reinitiated until P11, although the emergence of TCA clusters becomes gradually slower and less complete. In mice in which barrels emerge 3 d later than the normal schedule, at P6 instead of P3, we examined lesion-induced plasticity. We find a progressive decline of the lesion-induced plasticity and a closure at P3, similar to normal mice, showing that this plasticity is not influenced by an excess of serotonin levels. Thus, in MAOA-KO mice, the emergence of barrel patterning can be delayed without a concomitant delay in lesion-induced plasticity, and the cortical space devoted to one whisker representation cannot be modified by the periphery once patterning is imprinted in the subcortical relays. We conclude that the closure of the lesioninduced plasticity period in the barrelfield is probably not determined at the cortical level.

show abstract

Section: Introductionmentioning

confidence: 95%

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

Rebsam

Seif²,

Gaspar³

2005

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…These results indicate that with normal 5-HT levels, glutamate-and NMDA-dependent mechanisms appear sufficient to instruct barrel formation. However, the importance of 5-HT for barrel formation may be more subtle, as shown by the reduced barrel size and by the modification of the critical period (Osterheld-Haas et al, 1994) induced by 5-HT deprivation. Therefore, a possible involvement of 5-HT1B receptors for the plasticity of the barrels requires further investigation.…”

Section: Possible Effects Of the 5-ht1b Receptor Activation On The Bamentioning

confidence: 99%

Activity-Dependent Presynaptic Effect of Serotonin 1B Receptors on the Somatosensory Thalamocortical Transmission in Neonatal Mice

et al. 2002

View full text Add to dashboard Cite

The disruptive effect of excessive serotonin (5-HT) levels on the development of cortical sensory maps is mediated by 5-HT1B receptors, as shown in barrelless monoamine oxidase A knockout mice, in which the additional inactivation of 5-HT1B receptors restores the barrels. However, it is unclear whether 5-HT1B receptors mediate their effect on barrel formation by a trophic action or an activity-dependent effect.To test for a possible effect of 5-HT1B receptors on activity, we studied the influence of 5-HT on the thalamocortical (TC) synaptic transmission in layer IV cortical neurons. In TC slices of postnatal day 5 (P5)-P9 neonate mice, we show that 5-HT reduces monosynaptic TC EPSCs evoked by low-frequency internal capsule stimulation and relieves the short-term depression of the EPSC evoked by high-frequency stimulation. We provide evidence that 5-HT decreases the presynaptic release of glutamate: 5-HT reduces similarly the AMPA-kainate and NMDA components and the paired pulse depression of TC EPSCs. We show also that 5-HT1B receptors mediate exclusively the effect of 5-HT: first, the effect of 5-HT on the TC EPSC is correlated with the transient expression of 5-HT1B receptor mRNAs in the ventrobasal thalamic nucleus during postnatal development; second, it is mimicked by a 5-HT1B agonist; third, 5-HT has no effect in 5-HT1B receptor knock-out mice. Our results show that in the developing barrel field of the neonatal mice, 5-HT1B receptors mediate an activitydependent regulation of the TC EPSC that could favor the propagation of high-frequency TC activity.

show abstract

“…Surprisingly, perinatal 5-HT deficiency only induces a reduction of barrel field organization without altering its general organization [177,207,208]. Nevertheless, further studies need to be carried since early reduction of 5-HT during embryonic development induces the emergence of altered behaviour [153].…”

Section: Serotonin and Axonal Development Within The Cerebral Cortexmentioning

confidence: 99%

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

Vitalis¹,

Verney²

2017

Serotonin - A Chemical Messenger Between All Types of Living Cells

View full text Add to dashboard Cite

The mammalian cerebral cortex is critical for sensory and motor integrations and, for higher-order cognitive functions. The construction of mammalian cortical circuits involves the coordinated interplay between cellular processes such as proliferation, migration and differentiation of neural and glial cell subtypes followed by accurate connectivity evolving in complexity in primates. Alteration in cortical development may induce the emergence of various pathological traits and behaviours. Among the large array of factors that regulate the assembly of cortical circuits, serotonin (5-HT) plays important role as a developmental signal that impacts on a broad diversity of cellular processes. 5-HT plays distinct roles during specific sensitive periods and is produced from various sources depending on the perinatal stage. Its roles are mediated by more than fourteen 5-HT receptors that are all G-protein coupled receptors except the ionotropic 5-HT type 3A receptor (5-HT 3A ) mediating rapid neuronal activation. Importantly, 5-HT metabolism and signalling are influenced by numerous epigenetic and genetic factors, including nutrition and gut microbiota, perinatal stress, infection and inflammation. In this review, we will recapitulate some evidences showing that dysregulation of 5-HT homeostasis and 5-HT 3A signalling impairs distinct steps of cortical circuit formation leading to the predisposition of the onset of various psychiatric diseases.

show abstract

Monoaminergic afferents to cortex modulate structural plasticity in the barrelfield of the mouse

Cited by 59 publications

References 67 publications

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

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

Activity-Dependent Presynaptic Effect of Serotonin 1B Receptors on the Somatosensory Thalamocortical Transmission in Neonatal Mice

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

Contact Info

Product

Resources

About