Interaction between nerve growth factor and GM1 monosialoganglioside in preventing cortical choline acetyltransferase and high affinity choline uptake decrease after lesion of the nucleus basalis

Patre, Pier Luigi Di; Casamenti, Fiorella; Cenni, A.; Pepeu, Giancarlo

doi:10.1016/0006-8993(89)91585-0

Cited by 75 publications

(19 citation statements)

References 30 publications

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“…In our experiments GM1 administered for 21 days at twice as large a dose attenuates neither the contralateral nor the ipsilateral decrease in the number of NBM ChAT-immunoreactive 190 F. Casamenti et al neurons and cortical ChAT activity in the 18-month-old lesioned rats, a finding consistent with previous observations (Casamenti et a!., 1990;Stephens et al, 1987). Furthermore, in our experiments no synergism occurs between NGF and GM1, whereas a potentiation of NGF effects on ChAT activity has been described in young lesioned rats Di Patre et al, 1989). Nevertheless, GM1 also significantly attenuates the decrease in cortical ChAT activity if administered for a week before the lesion.…”

Section: Discussionsupporting

confidence: 92%

“…However, little or no decrease in ChAT occurs in the contralateral cortex of young rats following a unilateral injection of ibotenate into the NBM Di Patre et al, 1989). The statistically significant decrease in cortical ChAT activity and the disappearance of NBM ChAT-immunoreactive neurons observed in the opposite hemisphere of 18-month-old rats indicate increased vulnerability, and reduced capability of recovery of the cholinergic neurons in aging rats.…”

Section: Discussionmentioning

confidence: 81%

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Effect of nerve growth factor and GM1 ganglioside on the recovery of cholinergic neurons after a lesion of the nucleus basalis in aging rats

Casamenti

Scali

Giovannelli

et al. 1994

J Neural Transm Gen Sect

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A unilateral ibotenic acid lesion was placed in the nucleus basalis magnocellularis of 3- and 18-month-old rats. In the lesioned aging rats, the number of choline acetyltransferase-immunoreactive neurons of the nucleus basalis magnocellularis was markedly reduced in the ipsilateral side and to a lesser extent in the contralateral side. Twenty-one days after the lesion, the activity of choline acetyltransferase in the ipsilateral cortex was reduced by 40% in both groups of rats and by 24% in the contralateral frontal cortex of the aging rats. Intracerebroventricular administration of nerve growth factor (10 micrograms twice a week) to aging lesioned rats for 3 weeks after surgery resulted in a complete recovery in the number of choline acetyltransferase-immunoreactive neurons in the nucleus basalis of both sides, and choline acetyltransferase activity in the contralateral cortex, with little effect on the ipsilateral cortex. No potentiation was seen after the concurrent administration of GM1 ganglioside and nerve growth factor. Complete recovery in cortical choline acetyltransferase activity was only observed in the lesioned rats treated with nerve growth factor for 1 week before and 3 weeks after lesioning. Nerve growth factor treatment, both after the lesion, and before and after the lesion, improved the passive avoidance performance disrupted by the lesion. In young lesioned rats daily intraperitoneal administration of GM1 (30 mg/kg) for 21 days after surgery promoted both the recovery of choline acetyltransferase activity and passive avoidance performance. In aging rats GM1, even at a dose twice as large, failed to reverse the biochemical and morphological deficits and behavioral impairment induced by the lesion. Only when GM1 administration was started 3 days before the lesion, were a complete recovery in choline acetyltransferase activity in the contralateral cortex and a partial recovery in the ipsilateral cortex obtained. Our results indicate that nerve growth factor and, to some extent, GM1 facilitate the recovery of the cholinergic neurons after a lesion of the nucleus basalis in aging rats, but their efficacy is reduced. The lower efficacy of GM1 as compared to NGF might be due to the different routes of administration used.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 81%

Effect of nerve growth factor and GM1 ganglioside on the recovery of cholinergic neurons after a lesion of the nucleus basalis in aging rats

Casamenti

Scali

Giovannelli

et al. 1994

J Neural Transm Gen Sect

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“…The finding that ganglioside GM1 is able to facilitate the neurotrophic effects of BDNF is in accord with previous studies demonstrating that GMl enhances the neurotrophic actions of exogenous NGF in vitro (Ferrari et al, 1983;Katoh-Semba et al, 1984;Leon et al, 1984;Doherty et al, 1985;Skaper et al, 1985) and in vivo (Vantini et al, 1988;Cuello et al, 1989;Di Patre et al, 1989). In these latter cases GMl on its own had no BDNF (or other neurotrophic) activity.…”

supporting

confidence: 92%

“…These sialic acid-containing glycosphingolipids are differentially regulated during development (Rosner and Rahmann, 1987) and have been proposed to play a critical role in central nervous system growth and function (Ando, 1983;Ledeen, 1985). The monosialoganglioside GM1 in particular has been described to potentiate the trophic effects of NGF in several in vitro (Ferrari et al, 1983;KatohSemba et al, 1984;Leon et al, 1984;Doherty et al, 1985;Skaper et al, 1985) and in vivo (Vantini et al, 1988;Cuello et al, 1989;Di Patre et al, 1989) models. To determine if GM1 could also facilitate the actions of BDNF, the above experiments were performed in the co-presence of BDNF and GM1.…”

Section: Pharmacological Modulation Of Bdnf Neuroprotective Effects Bmentioning

confidence: 97%

Brain‐derived neurotrophic factor selectively rescues mesencephalic dopaminergic neurons from 2,4,5‐trihydroxyphenylalanine‐induced injury

Skaper

Negro

Facci

et al. 1993

J of Neuroscience Research

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Brain-derived neurotrophic factor (BDNF) supports the survival of sensory neurons as well as retinal ganglion cells, basal forebrain cholinergic neurons, and mesencephalic dopaminergic neurons in vitro. Here we examined the ability of BDNF to confer protection on cultured dopaminergic neurons against the neurotoxic effects of 6-hydroxyDOPA (TOPA or 2,4,5-trihydroxyphenylalanine), a metabolite of the dopamine pathway suggested to participate in the pathology of Parkinson's disease. Cells prepared from embryonic day 14-15 rat mesencephalon were maintained with 10-50 ng/ml BDNF for 7 days prior to addition of TOPA (10-30 microM) for 24 hr. In BDNF-treated cultures, the extensive loss (> 90%) of tyrosine hydroxylase immunopositive cells was virtually (< 10%) eliminated, while the equally drastic loss (> 90%) of the overall cell population was limited to only a 25-30% recovery. Furthermore, the monosialoganglioside GM1 (1-10 microM), although inactive alone, acted synergistically with subthreshold amounts of BDNF to rescue tyrosine hydroxylase-positive cells against TOPA neurotoxicity. These results add impetus to exploring the therapeutic potential of gangliosides and BDNF in Parkinson's disease.

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“…Recent studies indicate that nerve growth factor may protect hippocampal CA1 pyramidal neurons against ischemic injury in both gerbils 29 and rats. 30 Because GM1 potentiates the action of neuronotrophic factors both in vitro 31 " 33 and in vivo, 33 " 35 we cannot exclude a potentiation of endogenous neuronotrophic factors as contributing to the action of siagoside in reducing neuronal damage after ischemia.…”

mentioning

confidence: 99%

Protective effects of a monosialoganglioside derivative following transitory forebrain ischemia in rats.

Seren

Rubini

Lazzaro

et al. 1990

Stroke

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We evaluated the effects of treatment with the inner ester derivative of the monosialoganglioside GM1 on cortical electroencephalographic activity and hippocampal CA1 morphology after transitory, near-complete cerebral ischemia in rats. Ischemia was induced by the four-vessel occlusion method, and we studied only the 58 rats that showed amino acid neurotransmission plays an important role. Neurons selectively vulnerable to an ischemic episode receive prominent excitatory amino acid transmitter inputs, and ablation of these pathways reduces ischemia-induced neuronal loss. In addition, the extracellular concentrations of glutamate and aspartate -potential neurotoxins both in vitro and in vivo -increase during ischemia. A current hypothesis is that excessive accumulation of glutamate or related compounds, via specific postsynaptic receptors, cause neuronal overactivation, triggering a cascade of cellular events that ultimately lead to cell death. 1 A corollary to the above hypothesis is that agents capable of antagonizing specific excitatory amino acid receptor-related recognition sites or postreceptor effects may be of potential therapeutic value. In particular, great attention has recently been focused on Af-methyl-D-aspartate (NMDA) receptor antago-

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Interaction between nerve growth factor and GM1 monosialoganglioside in preventing cortical choline acetyltransferase and high affinity choline uptake decrease after lesion of the nucleus basalis

Cited by 75 publications

References 30 publications

Effect of nerve growth factor and GM1 ganglioside on the recovery of cholinergic neurons after a lesion of the nucleus basalis in aging rats

Effect of nerve growth factor and GM1 ganglioside on the recovery of cholinergic neurons after a lesion of the nucleus basalis in aging rats

Brain‐derived neurotrophic factor selectively rescues mesencephalic dopaminergic neurons from 2,4,5‐trihydroxyphenylalanine‐induced injury

Protective effects of a monosialoganglioside derivative following transitory forebrain ischemia in rats.

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