Toxins Affecting the Cholinergic System

Hörtnagl, Heide; Hanin, Israel

doi:10.1007/978-3-642-85117-9_9

Cited by 7 publications

(4 citation statements)

References 211 publications

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“…Although there exist many tools to induce more or less durable cholinergic dysfunctions in the brain (e.g. Hortnagl and Hanin, 1992), two technical approaches have been favoured because the compounds on which they rely are able to induce true and irreversible degeneration of cholinergic neurons. The first of these compounds is commonly termed AF64A (or ECMA for ethylcholine mustard aziridinium) and consists of a nitrogen mustard derivative of choline which is highly similar to choline and is assumed to exert its specific neurotoxic effects in two steps (Hortnagl and Hanin, 1992).…”

Section: Cholinergic Denervation Paradigmsmentioning

confidence: 99%

The Fimbria-Fornix/Cingular Bundle Pathways: A Review of Neurochemical and Behavioural Approaches Using Lesions and Transplantation Techniques

Cassel

Duconseille

Jeltsch

et al. 1997

Progress in Neurobiology

104

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Section: Cholinergic Denervation Paradigmsmentioning

confidence: 99%

The Fimbria-Fornix/Cingular Bundle Pathways: A Review of Neurochemical and Behavioural Approaches Using Lesions and Transplantation Techniques

Cassel

Duconseille

Jeltsch

et al. 1997

Progress in Neurobiology

104

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“…A unique genetic model lacking L ‐isoaspartyl methyltransferase, which is responsible for converting the isomerization of aspartic residues in β‐amyloid protein, was generated to elucidate the pathogenesis of sporadic senile dementia of Alzheimer's type (Ikegaya et al, 2001). Excitotoxic reagents, cholinergic neurotoxin AF64A (Walsh et al, 1984) and glutamatergic toxin ibotenic acid (Hortnagl and Hanin, 1994), and cholinergic immunotoxin 192IgG‐saporin (Roßner, 1997) were used to destroy specific neurons. Transection of nerve connections and electrolytic lesions of brain tissues have been used as devastating surgical methods to destroy brain functions.…”

Section: Discussionmentioning

confidence: 99%

Animal model of dementia induced by entorhinal synaptic damage and partial restoration of cognitive deficits by BDNF and carnitine

Ando

Kobayashi

Waki

et al. 2002

J of Neuroscience Research

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A rat dementia model with cognitive deficits was generated by synapse-specific lesions using botulinum neurotoxin (BoNTx) type B in the entorhinal cortex. To detect cognitive deficits, different tasks were needed depending upon the age of the model animals. Impaired learning and memory with lesions were observed in adult rats using the Hebb-Williams maze, AKON-1 maze and a continuous alternation task in T-maze. Cognitive deficits in lesioned aged rats were detected by a continuous alternation and delayed non-matching-to-sample tasks in T-maze. Adenovirus-mediated BDNF gene expression enhanced neuronal plasticity, as revealed by behavioral tests and LTP formation. Chronic administration of carnitine over time pre-and post-lesions seemed to partially ameliorate the cognitive deficits caused by the synaptic lesion. The carnitine-accelerated recovery from synaptic damage was observed by electron microscopy. These results demonstrate that the BoNTx-lesioned rat can be used as a model for dementia and that cognitive deficits can be alleviated in part by BDNF gene transfer or carnitine administration.

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“…Previous experiments showed that ganglioside treatment (AGF2) may improve RAM learning performance in rats given an intraventricular injection of either AF64A (Emerich and Walsh 1990), a cholinergic neurotoxin (e.g., Hörtnagl and Hanin 1992), or colchicine, a neurotoxin inducing cholinergic damage of more limited extent (Emerich and Walsh 1991). In these experiments, the AGF2-treated rats with lesions presented improved RAM performances as compared to their nontreated counterparts, but this improvement did not withstand the introduction of a delay in the testing procedure.…”

Section: Septohippocampal Lesions and Gm1 Treatmentmentioning

confidence: 90%

Behavioral effects of GM1 ganglioside treatment and intrahippocampal septal grafts in rats with fimbria-fornix lesions

1997

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The monosialoganglioside GM1 is a compound with neurotrophic properties found to foster functional recovery in various paradigms of brain damage. The present experiment examined whether systemic treatment with GM1 may facilitate behavioral recovery in rats with fimbria-fornix lesions and intrahippocampal grafts rich in cholinergic neurons. Among 68 Long-Evans female rats, 46 sustained a bilateral electrolytic lesion of the fimbria and the dorsal fornix and 22 were sham-operated. Fourteen days later, half the lesioned rats were subjected to intrahippocampal grafts of a fetal septal cell suspension. Starting a few hours after lesion surgery and over a 2-month period, half the rats of each surgical treatment group received a daily injection of GM1 (30 mg/kg i.p.), the other half being injected with saline as a control. All rats were subsequently tested for locomotor activity and radial maze learning. The lesions induced locomotor hyperactivity and impaired learning performances in both an uninterrupted and an interrupted radial maze testing procedure. In all rats with surviving grafts, the grafts had provided the hippocampus with a new and dense organotypic acetylcholinesterase-positive innervation pattern which did not differ between saline- and GM1-treated subjects. The scores/performances of the rats that had received only the grafts or only the GM1 treatment did not differ significantly from those of their respective lesion-only counterparts. However, in the radial-arm maze task, the grafted rats given GM1 showed improved learning performances as compared with their saline-treated counterparts: they used more efficient visit patterns under the uninterrupted testing conditions and made fewer errors under the interrupted ones. The results suggest that GM1 treatment or intrahippocampal grafts used separately do not attenuate the lesion-induced behavioral deficits measured in this experiment. However, when GM1 treatment and grafts are used conjointly, both may interact in a manner allowing part of these deficits to be attenuated.

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Toxins Affecting the Cholinergic System

Cited by 7 publications

References 211 publications

The Fimbria-Fornix/Cingular Bundle Pathways: A Review of Neurochemical and Behavioural Approaches Using Lesions and Transplantation Techniques

The Fimbria-Fornix/Cingular Bundle Pathways: A Review of Neurochemical and Behavioural Approaches Using Lesions and Transplantation Techniques

Animal model of dementia induced by entorhinal synaptic damage and partial restoration of cognitive deficits by BDNF and carnitine

Behavioral effects of GM1 ganglioside treatment and intrahippocampal septal grafts in rats with fimbria-fornix lesions

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