Isthmic origin of neurons of the rat substantia nigra

Marchand, R.; Poirier, Louis

doi:10.1016/0306-4522(83)90300-7

Cited by 96 publications

(51 citation statements)

References 12 publications

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“…A thin rim of Th-positive cells was observed in the ventral midbrain. These cells are thought to originate from the neuroepithelium lining the ventricular space and to migrate ventrally by interacting with radial glia cells (Hanaway et al, 1971;Marchand and Poirier, 1983;Shults et al, 1990;Kawano et al, 1995;Hall et al, 2003). In line with this, we observed Development 131 (5) Research article Pitx3 is essential for early development of the substantia nigra Th-positive neurons in close contact with fibrillous structures in paraffin wax sections (data not shown).…”

Section: Early Development Of Mesda Neurons In Ak Micesupporting

confidence: 72%

Early developmental failure of substantia nigra dopamine neurons in mice lacking the homeodomain genePitx3

et al. 2004

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The mesencephalic dopamine (mesDA) system is involved in the control of movement and behavior. The expression of Pitx3 in the brain is restricted to the mesDA system and the gene is induced relatively late, at E11.5, a time when tyrosine hydroxylase (Th) gene expression is initiated. We show here that, in the Pitx3-deficient aphakia(ak) mouse mutant, the mesDA system is malformed. Owing to the developmental failure of mesDA neurons in the lateral field of the midbrain,mesDA neurons are not found in the SNc and the projections to the caudate putamen are selectively lost. However, Pitx3 is expressed in all mesDA neurons in control animals. Therefore, mesDA neurons react specifically to the loss of Pitx3. Defects of motor control where not seen in the ak mice,suggesting that other neuronal systems compensate for the absence of the nigrostriatal pathway. However, an overall lower activity was observed. The results suggest that Pitx3 is specifically required for the formation of the SNc subfield at the onset of dopaminergic neuron differentiation.

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Section: Early Development Of Mesda Neurons In Ak Micesupporting

confidence: 72%

Early developmental failure of substantia nigra dopamine neurons in mice lacking the homeodomain genePitx3

et al. 2004

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“…Similarities between the dopamine-containing neurons and cerebellar granule cells are not obvious, however. They have different perikaryal, dendritic, and axonal morphologies; they express different neurotransmitters; and they arise from different parts of the germinal epithelium during embryogenesis (see Marchand and Poirier, 1983). The critical commonality is likely to be subtle.…”

Section: Discussionmentioning

confidence: 99%

“…There is no evidence that neurons of the nigral complex undergo major waves of migration postnatally. According to Marchand and Poirier (1983), they migrate in medial and lateral groups during embryonic days E15-18. However, other postnatal defects in cellcell interactions could lead to the dopamine defect in the weaver brain.…”

Section: Discussionmentioning

confidence: 99%

Expression of the weaver gene in dopamine-containing neural systems is dose-dependent and affects both striatal and nonstriatal regions

Roffler-Tarlov¹,

Graybiel²

1986

J. Neurosci.

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In an earlier report we presented evidence pointing to a differential effect of the mutant gene weaver on the dopamine-containing fiber systems innervating the striatum. In mice homozygous for the weaver mutation, there is a severe loss of dopamine in the caudoputamen, the main target of the nigrostriatal system. By contrast, dopamine is entirely conserved in the nucleus accumbens, a target of the mesolimbic system, and is moderately affected in the olfactory tubercle. The present study shows that these defects in dopamine are gene dose-dependent, that they are established by the end of the first month of life, and that the losses are permanent and not progressive. As in homozygous weavers, the greatest defects in striatal dopamine in heterozygous weavers occur in the dorsolateral caudoputamen and the lateral olfactory tubercle.The abnormalities in the striatal dopamine content of weaver mice are not accompanied by abnormalities in the turnover of dopamine, judging from measurements of the dopamine metabolite dihydroxyphenylacetic acid. Norepinephrine content is also normal in each striatal region. No deficits in striatal dopamine occur in mice homozygous for the mutant genes staggerer and Purkinje cell degeneration, which, like the weaver mutation, result in ataxia and cerebellar pathology.A survey of nonstriatal regions in the weaver mice showed that the effects of the weaver gene on the dopamine-containing innervation of the forebrain are not confined to striatal targets but also extend to the septum and the hypothalamus. By contrast, dopamine in the frontal cortex, the amygdala, the olfactory bulb, and the retina is entirely spared. The pattern and extent of loss of dopamine in the weaver forebrain is thus regionand system-specific. In confirmation of our initial findings, a ca. 30% depletion of dopamine occurs in the weaver midbrain, the region containing the cell bodies of origin of the mesostriatal dopamine systems. A comparison of histofluorescent sections through weaver and control midbrains revealed a reduction of catecholamine-containing neurons in the pars compacta of the weaver animals.These results point to a subpopulation of dopamine-containing neurons as primary targets of the weaver gene or as being closely associated with such primary targets. As a gene-dose effect has also been shown for the cerebellar granule cell loss in the weaver, the mutant gene must have at least 2 cellular Received Jan. 7, 1986; revised Apr. 30, 1986; accepted May 5, 1986. This work was supported by National Institutes of Health targets. We suggest that the cerebellar and mesostriatal pathologies may be linked by a common molecular mechanism.Two defects, one obvious and the other well hidden, are known to be present in the brains of mice that carry the autosomal recessive gene weaver. This mutation results in an atrophy of the cerebellum that is so severe in homozygous weavers that it can be detected after a glance at the intact brain. As was first reported by Sidman et al. in 1965, this macroscopic defect reflects an...

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“…Rat DA midbrain neurons are generated on days 12 -15 of gestation and migrate to the SNc and VTA shortly thereafter (Specht et al, 1981,Marchand and Poirier, 1983,Voorn et al, 1988. These neurons have been shown to differentiate biochemically when they are still morphologically immature (Specht et al, 1981).…”

Section: Fetal Periodmentioning

confidence: 99%

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

2007

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We have combined anatomical and functional methodologies to provide a comprehensive analysis of the properties of nicotinic acetylcholine receptors (nAChRs) on developing dopamine (DA) neurons. Double-labeling in situ hybridization was used to examine the expression of nAChR subunit mRNAs within developing midbrain DA neurons. As brain maturation progressed there was a change in the pattern of subunit mRNA expression within DA neurons, such that α3 and α4 subunits declined and α6 mRNA increased. Although there were strong similarities in subunit mRNA expression in substantia nigra (SNc) and ventral tegmental area (VTA), there was higher expression of α4 mRNA in SNc than VTA at gestational day (G)15, and of α5, α6 and β3 mRNAs during postnatal development. Using a superfusion neurotransmitter release paradigm to functionally characterize nicotine-stimulated release of [ 3 H]DA from striatal slices, the properties of the nAChRs on DA terminals were also found to change with age. Functional nAChRs were detected on striatal terminals at G18. There was a decrease in maximal release in the first postnatal week, followed by an increase in nicotine efficacy and potency during the second and third postnatal weeks. In the transition from adolescence (postnatal days (P) 30 and 40) to adulthood, there was a complex pattern of functional maturation of nAChRs in ventral, but not dorsal, striatum. In males, but not females, there were significant changes in both nicotine potency and efficacy during this developmental period. These findings suggest that nAChRs may play critical functional roles throughout DA neuronal maturation. Keywords adolescent; fetal; nicotine; sex; striatum; maternal smoking Maternal smoking during pregnancy has been correlated with a number of adverse outcomes in the offspring (Lichtensteiger et al., 1988,Lichtensteiger andSchlumpf, 1993), including cognitive deficits that are often manifested in early childhood as attention deficit hyperactivity disorder (ADHD) (Millberger et al., 1996). Though the underlying neurobiological mechanism * Correspondence to: Dr. Layla Azam Department of Biology, University of Utah 257 South 1400 East Salt Lake City, UT 84112 Tel.: (801) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ,Pliszka et al., 1996,Castellanos, 1997. In animal studies, maternal nicotine exposure produces sexdependent alterations in the development of DA neurochemical markers (Fung, 1988,Fung, 1989,Ribary and Lichtensteiger, 1989,Lichtensteiger and Schlumpf, 1993,Muneoka et al., 1997, and induces hyperactivity in the offspring, which is believed...

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Isthmic origin of neurons of the rat substantia nigra

Cited by 96 publications

References 12 publications

Early developmental failure of substantia nigra dopamine neurons in mice lacking the homeodomain genePitx3

Early developmental failure of substantia nigra dopamine neurons in mice lacking the homeodomain genePitx3

Expression of the weaver gene in dopamine-containing neural systems is dose-dependent and affects both striatal and nonstriatal regions

Developmental regulation of nicotinic acetylcholine receptors within midbrain dopamine neurons

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