Striatal Extracts from Patients with Parkinson's Disease Promote Dopamine Neuron Growth in Mesencephalic Cultures

Carvey, Paul M.; Ptak, Louis R.; Nath, Sarah T.; Sierens, Diane K.; Mufson, Elliott J.; Goetz, Christopher G.; Klawans, Harold L.

doi:10.1006/exnr.1993.1049

Cited by 47 publications

(16 citation statements)

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“…with changes in indices of CA neuron growth (16, 17, ' 9 . 20, Assessment of striatal trophic activity 40 h after addition of [27][28][29][30][31]. the extracts to mesencephalic cultures revealed that in ulcro The reductions in striatal DA and its metabolite DOPAC are cocaine exposure reduced, by 61 %, the number of NSEir neurons consistent with several recent reports.…”

Section: Da Dopac Str Cbsupporting

confidence: 74%

“…media die rapidly. Several laboratories (21)(22)(23)(24)(25)(26), including ours The plates were air dried, dehydrated, and then scored for the (16,17,19,20,(27)(28)(29)(30)(31), have demonstrated that the addition of number of NSE neurons by a n observer blinded to treatment striatal extracts containing trophic activity directed at mesencehistory. Using a phase-contrast, inverted microscope Fluovert phalic neurons reduces this ncuronal death rate and stimulates (Leitz, Leipsig, Germany) the center strip of each well was the growth of DA neurons.…”

Section: Da Dopac Str Cbmentioning

confidence: 99%

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Effect of Cocaine in Early Gestation on Striatal Dopamine and Neurotrophic Activity

et al. 1993

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ABSTRACT. Prenatal exposure to the dopaminc (DA) agonist cocaine, even if limited to early gestation, is associated with impaired developmental outcome in the human infant. \Ye investigated the possible role of neurotrophic factors in this process by evaluating 4-to 6-d-old New Zealand \\'bite rabbit pups ( n = 14) born to cocaineexposed does (30 mg/kg/d s.c. from days 7 to 15 of a 32-d gestation) and control does (sterile H20). Cocaine esposure reduced striatal dopamine by 46% (t = 2.31; p < 0.05) and striatal 3,4-dihydrosyphenyl acetic acid by 49% (t = 2.44; p < 0.05). The number of neuron-specific enolase immunoreactive neurons in mesencephalic cultures incubated with striatal estracts from pups esposed to cocaine was reduced by 61% relative to the effect of striatal estracts from control pups (t = 4.84; p < 0.01). The present results suggest that the reduction in striatal dopamine observed may result from a cocaine-induced decrease in striatal trophic activity. (Pediatr Res 34: 389-392, 1993) Abbreviations DA, doparnine DOPAC, 3,4-dihydrosyphenyl acetic acid E, embryonic P, postnatal IIBSS, Ilanks' balanced salt solution TBS, Tris-buffered saline NSE, neuron-specific enolase NSEir, NSE immu~:oreactive Prenatal exposure to the DA agollist cocaine is associated with impaired developmental outcome in the human infant (1-9). Reported observations include a broad spectrum of abnormalities. However, variability in study methodology, patient populations, and dose, duration, and gestational timing of cocaine exposure prevent a clear understanding of the specific relationship of cocaine to the type and severity of impairment. Mechanisms that may be responsible for the altered developmental outcorne after prenatal cocaine exposure remain elusive. Although speculated, the role of neurotransmitters has not been thorcughly investigated in the human infant. However, recent studies of the DA system of maturing rodents after in lrtcro

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Section: Da Dopac Str Cbsupporting

confidence: 74%

Section: Da Dopac Str Cbmentioning

confidence: 99%

Effect of Cocaine in Early Gestation on Striatal Dopamine and Neurotrophic Activity

et al. 1993

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“…Some studies have further provided evidence that these targetderived neurotrophic activities increase in the Parkinsonian brain or after toxic lesion (Carvey et al, 1993;Carvey et al, 1996). The present findings put some limitations on these reports.…”

Section: Discussioncontrasting

confidence: 53%

Spatial and temporal growth factor influences on developing midbrain dopaminergic neurons

Engele

1998

J. Neurosci. Res.

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Despite the large number of growth factors shown to affect dopaminergic cell survival and differentiation in vitro, presently little is known about the role these growth factors play during normal in vivo development of dopaminergic neurons. To address this issue, glia and neurons of both the mesencephalic home region as well as the striatal and cortical target areas have been screened for effects on dopaminergic cell survival in serum-free dissociated cell cultures of the embryonic day (E) 15 and E17 rat mesencephalon. In E15 mesencephalic cultures, the number of surviving tyrosine hydroxylase-immunoreactive dopaminergic neurons maximally increased 2.6-fold with medium conditioned by glia of the E15-E20 mesencephalon, the E17-E20 striatum, or the E20 cortex. In marked contrast, all glial-conditioned media (CM) failed to affect dopaminergic cell survival in E17 mesencephalic cultures. Similarly, E17 dopaminergic cell survival was not affected by CM derived from striatal or mesencephalic neurons. This absence of survival-promoting effects was not due to a general lack of sensitivity of the late embryonic dopaminergic neurons to growth factors. Basal survival of cultured E17 dopaminergic neurons declined with PD98059 (20 microM), a potent inhibitor of growth factor-activated microtubule-associated protein (MAP) kinase cascade. Moreover, irrespective of the age of the cultured mesencephalic tissue, dopaminergic growth factors with potential autocrine functions such as brain-derived neurotrophic factor (BDNF; 50 ng/ml) and glial cell line-derived neurotrophic factor (GDNF; 10 ng/ml) promoted dopaminergic cell survival 1.5- to 1.9-fold. These findings suggest that dopaminergic cell survival is predominantly affected by, as yet unknown, growth factors derived from mesencephalic, cortical, and striatal glia during early embryonic development, and by autocrine-acting growth factors during late developmental stages.

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“…Jaeger and collaborators (1989) demonstrated that the majority of nigral neurons require the presence of caudateiputamen target tissues for survival in vitro, and it has long been known that striatal extracts derived from animals with chemical or mechanical lesions of the nigrostriatal pathway will stimulate the growth and survival of fetal dopaminergic neurons in vitro (Tomozawa and Appel, 1986;Prochiantz et al, 1991;Lo et al, 1990;Carvey et al, 1989). Carvey and collaborators have also recently shown that striatal extracts, but not cerebellar extracts, from Parkinsonian patients could stimulate survival of ventral mesencephalic dopaminergic neurons in culture (Carvey et al, 1993). In addition, one of the members of the neurotrophin family, brain-derived neurotrophic factor (BDNF), has been shown to have trophic effects on mesencephalic dopaminergic neurons (Hyman et al, 1991;Knusel et al, 1991;Conner and Varon, 1992;Beck et al, 1992).…”

mentioning

confidence: 96%

Glial cell line‐derived neurotrophic factor supports survival of injured midbrain dopaminergic neurons

Bowenkamp

Hoffman

Gerhardt

et al. 1995

J of Comparative Neurology

279

128

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Glial cell-lined derived neurotrophic factor (GDNF) has been shown to promote survival of developing mesencephalic dopaminergic neurons in vitro. In order to determine if there is a positive effect of GDNF on injured adult midbrain dopaminergic neurons in situ, we have carried out experiments in which a single dose of GDNF was injected into the substantia nigra following a unilateral lesion of the nigrostriatal system. Rats were unilaterally lesioned by a single stereotaxic injection of 6-hydroxydopamine (6-OHDA; 9 micrograms/4 microliters normal saline with 0.02% ascorbate) into the medial forebrain bundle and tested weekly for apomorphine-induced (0.05 mg/kg s.c.) contralateral rotation behavior. Rats that manifested > 300 turns/hour received a nigral injection of 100 micrograms GDNF, or cytochrome C as a control, 4 weeks following the 6-OHDA lesion. Rotation behavior was quantified weekly for 5 weeks after GDNF. Rats were subsequently anesthetized, transcardially perfused, and processed for tyrosine hydroxylase immunohistochemistry. It was found that 100 micrograms GDNF decreased apomorphine-induced rotational behavior by more than 85%. Immunohistochemical studies revealed that tyrosine hydroxylase immunoreactivity was equally reduced in the striatum ipsilateral to the lesion in both cytochrome C and GDNF-injected animals. In contrast, large increments in tyrosine hydroxylase immunoreactivity were observed in the substantia nigra of animals treated with 100 micrograms of GDNF, with a significant increase in numbers of tyrosine hydroxylase-immunoreactive cell bodies and neurites as well as a small increase in the cell body area of these neurons. The results suggest that GDNF can maintain the dopaminergic neuronal phenotype in a number of nigral neurons following a unilateral nigrostriatal lesion in the rat.

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Striatal Extracts from Patients with Parkinson's Disease Promote Dopamine Neuron Growth in Mesencephalic Cultures

Cited by 47 publications

References 0 publications

Effect of Cocaine in Early Gestation on Striatal Dopamine and Neurotrophic Activity

Effect of Cocaine in Early Gestation on Striatal Dopamine and Neurotrophic Activity

Spatial and temporal growth factor influences on developing midbrain dopaminergic neurons

Glial cell line‐derived neurotrophic factor supports survival of injured midbrain dopaminergic neurons

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