PCPA reduces both monoaminergic afferents and nonmonoaminergic synapses in the cerebral cortex

Chen, Ling; Hamaguchi, Kayoko; Ogawa, Megumu; Hamada, Shin; Okado, Nobuo

doi:10.1016/0168-0102(94)90014-0

Cited by 65 publications

(25 citation statements)

References 11 publications

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“…At the cellular level, several previous in vitro and in vivo studies suggest that extracellular 5-HT levels may affect synaptic density or neurite branching and elongation in nonserotoninergic cortical neurons (Chubakov et al, 1986;Haydon et al, 1987;Okado et al, 1989, Sikich et al, 1990Okado et al, 1993;Chen et al, 1994;Niitsu et al, 1995;Yan et al, 1997). The results of our quantitative electron microscopic study provide no evidence of enhanced extracellular 5-HT exerting either a positive or a negative effect on synapse formation.…”

Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htcontrasting

confidence: 43%

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

et al. 2001

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Thalamocortical neurons innervating the barrel cortex in neonatal rodents transiently store serotonin (5-HT) in synaptic vesicles by expressing the plasma membrane serotonin transporter (5-HTT) and the vesicular monoamine transporter (VMAT2). 5-HTT knock-out (ko) mice reveal a nearly complete absence of 5-HT in the cerebral cortex by immunohistochemistry, and of barrels, both at P7 and adulthood. Quantitative electron microscopy reveals that 5-HTT ko affects neither the density of synapses nor the length of synaptic contacts in layer IV. VMAT2 ko mice, completely lacking activity-dependent vesicular release of monoamines including 5-HT, also show a complete lack of 5-HT in the cortex but display largely normal barrel fields, despite sometimes markedly reduced postnatal growth. Transient 5-HTT expression is thus required for barrel pattern formation, whereas activity-dependent vesicular 5-HT release is not.

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Section: Possible Mechanisms Of Serotonin-induced Alterations In 5-htcontrasting

confidence: 43%

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

et al. 2001

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“…have suggested that 5-HT depletion produced by administration of selective neurotoxins (5,7-dihydroxytryptamine, 5,7-DHT and p-chloroamphetamine, PCA) or synthesis inhibitor (p-chlorophenylalanine, PCPA) may lead to morphological changes. PCPA treatment reduced the number of cortical synapses (Chen et al, 1994) and loss of synaptic markers such as MAP2 and synaptophysin was also observed after PCA administration, associated with decreases in S100␤ immunoreactivity (Azmitia et al, 1995). These data suggest that 5-HT may have effects on adult neuronal plasticity, in agreement with the observations performed in invertebrate preparations (Baker et al, 1993;Haydon et al, 1984;Zhang et al, 1997).…”

supporting

confidence: 84%

Serotonin depletion in the adult rat produces differential changes in highly polysialylated form of neural cell adhesion molecule and tenascin-C immunoreactivity

Brezun

Daszuta

1999

J. Neurosci. Res.

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Levels of immunoreactivity for highly polysialylated neural cell adhesion molecule (PSA-NCAM), NCAM, and tenascin-C (TN-C), were examined in the basal ganglia regions and hypothalamic nuclei of adult rats after serotonergic (5-HT) lesions induced by 5,7-dihydroxytryptamine injections in the dorsal and medial raphe nuclei. Decreases in the density of serotonin fibers were associated with no changes in NCAM and general decreases in PSA-NCAM staining, the time-course of changes being selective for each region. Taken that the confocal analysis indicated that serotonin neurons do not express PSA-NCAM and that similar decreases in PSA-NCAM staining were observed after inhibition of 5-HT synthesis induced by parachlorophenylalanine administration, these results suggest that 5-HT may reduce adhesion by acting on PSA-NCAM expression in its environment, and thus facilitate plasticity in adult brain. Two months after the neurotoxin lesions, a normalization of PSA-NCAM staining was associated with a partial restoration in 5-HT fiber density in the nucleus accumbens and the supraoptic nucleus, suggesting that PSA-NCAM may facilitate sprouting of 5-HT fibers. Since a similar normalization was also detected in the suprachiasmatic nucleus, which remained deprived of serotonin fibers, negative factors are likely to be involved in regeneration processes. Indeed, increases in glial fibrillary acidic protein (GFAP) followed by increases in TN-C were observed in these areas, suggesting that the secretion of TN-C by astrocytes may have negative consequences on the sprouting of 5-HT fibers. Finally, the lack of changes in striatal PSA-NCAM or TN-C staining observed after selective lesions of the dopaminergic pathway induced by intranigral injections of 6-hydroxydopamine indicates that 5-HT has a selective and critical role in adult brain plasticity.

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“…In any event, there is experimental support to the view that 5-HT may be critically involved, through a glial mechanism, in the maintenance and plasticity of synaptic connections in the adult brain (Azmitia et al, 1995;Chen et al, 1994;Wilson et al, 1998). This is of particular interest because it allows the assumption that corticosterone/5-HT interactions in the raphe nuclei may play important roles in synaptic reorganizations that might occur in the SCN over the 24-h cycle.…”

Section: Serotoninergic Fibers As Potential Relays For Corticosteronementioning

confidence: 90%

Glucocorticoids up-regulate the expression of glial fibrillary acidic protein in the rat suprachiasmatic nucleus

Maurel

Sage

Mekaouche

et al. 2000

Glia

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PCPA reduces both monoaminergic afferents and nonmonoaminergic synapses in the cerebral cortex

Cited by 65 publications

References 11 publications

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

Barrel Pattern Formation Requires Serotonin Uptake by Thalamocortical Afferents, and Not Vesicular Monoamine Release

Serotonin depletion in the adult rat produces differential changes in highly polysialylated form of neural cell adhesion molecule and tenascin-C immunoreactivity

Glucocorticoids up-regulate the expression of glial fibrillary acidic protein in the rat suprachiasmatic nucleus

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