Prenatal Developmental Expression of Rat Brain 5-HT1A Receptor Gene Followed by PCR

Hillion, Joëlle; Milneedwards, J.B.D.; Catelon, J.; Devitry, F.; Gros, François; Hamon, Michel

doi:10.1006/bbrc.1993.1315

Cited by 41 publications

(13 citation statements)

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“…Development of the neuronal serotoninergic system occurs very early in most species, including rats and mice. In rat raphe, serotonin‐immunopositive neurons have been observed at E13 (Hendricks et al ., 2003) and 5‐HT 1A R mRNA at E12 (Hillion et al ., 1993). Furthermore, in E14 raphe primary cultures, 5‐HT 1A and 5‐HT 1B autoreceptors and the 5‐HTT are functional (Héry et al ., 1999).…”

Section: Discussionmentioning

confidence: 99%

Adaption of the serotoninergic neuronal phenotype in the absence of 5‐HT autoreceptors or the 5‐HT transporter: involvement of BDNF and cAMP

Rumajogee

Vergé

Hanoun

et al. 2004

Eur J of Neuroscience

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Serotonin 5-HT1A and 5-HT1B receptors and the 5-HT transporter are key regulators of the serotoninergic neuronal phenotype. We show here that genetic deletion of any of these elements differentially regulates 5-HT neuronal number in rostral raphe cultures from E14 mice. Serotonin neuronal number was increased by almost four-fold and 1.8-fold in cultures from 5-HT1AR-/- and 5-HT1BR-/- mice, respectively. In contrast, the lack of serotonin transporter expression was associated with a 50% decrease in 5-HT neuronal number. In raphe cultures from the rat, BDNF and cAMP have been shown to up-regulate the neuronal serotoninergic phenotype through TrkB-dependent mechanisms [Rumajogee et al. (2002) J. Neurochem., 83, 1525-1528]. Similar tyrosine kinase-dependent up-regulating effects, in the absence of serotoninergic key-elements are reported here, on both 5-HT neuronal number and neurites length. However, the extents of BDNF-triggered and cAMP-triggered effects on serotoninergic neuritic length were approximately 1.5-fold higher in 5-HT1AR-/- mutants. These findings show that the up-regulatory mechanisms triggered by BDNF on serotoninergic neuronal number and neurite extension are different and that the latter are partially linked to 5-HT, probably through 5-HT1A autoreceptors. Together, these data suggest that serotonin autoreceptors, mainly 5-HT1A but also 5-HT1B, may be responsible for a tonic auto-inhibitory effect of 5-HT itself on the serotoninergic neuronal phenotype during embryonic development, particularly marked in the absence of the 5-HT transporter.

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Section: Discussionmentioning

confidence: 99%

Adaption of the serotoninergic neuronal phenotype in the absence of 5‐HT autoreceptors or the 5‐HT transporter: involvement of BDNF and cAMP

Rumajogee

Vergé

Hanoun

et al. 2004

Eur J of Neuroscience

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“…In rats there is a peak of 5-HT 1A mRNA expression in whole brain at about gestational day 16 [Lauder et al, 1996]. Expression levels then gradually decrease until the time of birth, and then increase to adult levels during the postnatal period [Bar-Peled et al, 1991;Del Olmo et al, 1998;Hillion et al, 1993;Lauder et al, 1996]. Increased levels of 5-HT 1A receptors seen in prenatally exposed neonatal male offspring [Johns et al, 1998] could indicate that cocaine led to retarded prenatal development of these receptors in males, such that the prenatal peak was delayed until around the time of birth.…”

Section: Discussionmentioning

confidence: 99%

Developmental Effects of Prenatal Cocaine Exposure on 5-HT<sub>1A</sub> Receptors in Male and Female Rat Offspring

Johns

Lubin²,

Lieberman³

et al. 2002

Dev Neurosci

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Prenatal cocaine exposure results in behavioral abnormalities throughout development in rats, but little is known regarding the biological mechanisms underlying these abnormalities. Pregnant rats received subcutaneous twice-daily injections (1 ml/kg) of normal saline or 15 mg/kg of cocaine hydrochloride throughout gestation (gestation days 1–20). Following delivery, pups were placed with untreated surrogates. Male and female pups were killed on postnatal days 30, 60 or 120 for assessment of 5-HT_1A receptor development in the forebrain, diencephalon, midbrain and pons using radiolabel immunocytochemistry. Findings revealed gender and age differences in developmental regulation of 5-HT_1A receptors, indicating that male rats are more susceptible to long-term consequences of prenatal cocaine exposure in comparison to females. This study also demonstrates gender-specific development of serotonin (5-HT_1A) receptors across postnatal ages, demonstrating a fundamentally different pattern of development of 5-HT_1A receptors between males and females.

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“…The 5-HT 1A R transcript is detected in the rodent fetal brain at stage E12, achieves a maximum level at E15 and then progressively reduces its expression to low levels before birth (E20; Hillion et al, 1993). The expression of 5-HT 1A R coincides with the migration of young neurons to their appropriate neuronal stratum during embryonic development (Patel and Zhou, 2005).…”

Section: -Ht1ar Distribution In the Hippocampus During Development Amentioning

confidence: 99%

What Do We Really Know About 5-HT1A Receptor Signaling in Neuronal Cells?

Rojas

Fiedler

2016

Front. Cell. Neurosci.

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Serotonin (5-HT) is a neurotransmitter that plays an important role in neuronal plasticity. Variations in the levels of 5-HT at the synaptic cleft, expression or dysfunction of 5-HT receptors may alter brain development and predispose to various mental diseases. Here, we review the transduction pathways described in various cell types transfected with recombinant 5-HT1A receptor (5-HT1AR), specially contrasting with those findings obtained in neuronal cells. The 5-HT1AR is detected in early stages of neural development and is located in the soma, dendrites and spines of hippocampal neurons. The 5-HT1AR differs from other 5-HT receptors because it is coupled to different pathways, depending on the targeted cell. The signaling pathway associated with this receptor is determined by Gα isoforms and some cascades involve βγ signaling. The activity of 5-HT1AR usually promotes a reduction in neuronal excitability and firing, provokes a variation in cAMP and Ca2+, levels which may be linked to specific types of behavior and cognition. Furthermore, evidence indicates that 5-HT1AR induces neuritogesis and synapse formation, probably by modulation of the neuronal cytoskeleton through MAPK and phosphoinositide-3-kinase (PI3K)-Akt signaling pathways. Advances in understanding the actions of 5-HT1AR and its association with different signaling pathways in the central nervous system will reveal their pivotal role in health and disease.

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Prenatal Developmental Expression of Rat Brain 5-HT1A Receptor Gene Followed by PCR

Cited by 41 publications

References 0 publications

Adaption of the serotoninergic neuronal phenotype in the absence of 5‐HT autoreceptors or the 5‐HT transporter: involvement of BDNF and cAMP

Adaption of the serotoninergic neuronal phenotype in the absence of 5‐HT autoreceptors or the 5‐HT transporter: involvement of BDNF and cAMP

Developmental Effects of Prenatal Cocaine Exposure on 5-HT<sub>1A</sub> Receptors in Male and Female Rat Offspring

What Do We Really Know About 5-HT1A Receptor Signaling in Neuronal Cells?

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