Disease relevance of Ethylcholine aziridinium

• A 25 min anoxia, or an intracerebroventricular bilateral 2 nmol dose of ethylcholine aziridinium (AF-64A), administered postnatally to male rat pups, elicited on further development of these behavioural disorders, which are partly related to central cholinergic hypofunction [1].
• Using a repeated acquisition procedure in a three-panel runway apparatus, the effects of minaprine on the impairment of working memory produced by scopolamine, ethylcholine aziridinium ion (AF64A) or cerebral ischemia were investigated in rats [2].
• Relatively selective lesions produced by bilateral 50 nl microinjections of 75 pmol of the cholinergic neurotoxin ethylcholine mustard aziridinium ion (AF64A) resulted in a significant reduction in the threshold of myoclonic and facial-forelimb clonic seizures but not tonic seizures when PTZ was infused 7 days later [3].
• Ethylcholine mustard aziridinium ion lesions of the rat cortex result in retrograde degeneration of basal forebrain cholinergic neurons: implications for animal models of neurodegenerative disease [4].
• The cholinotoxin ethylcholine mustard aziridinium ion (AF64A) was diluted in artificial perilymph to concentrations ranging from 10-100 microM, injected unilaterally into the bulla of chinchillas, and allowed to passively diffuse across the round window membrane [5].

Psychiatry related information on Ethylcholine aziridinium

• 1. The effect of alpha-sialyl cholesterol (alpha-SC; alpha-D-N-acetylneuraminyl cholesterol) on disturbances of the central cholinergic system induced by ethylcholine mustard aziridinium ion (AF64A) and by scopolamine were studied by means of a step-down passive avoidance response and locomotor activities in mice [6].
• The amnesia models were produced by bilateral intracerebroventricular injection of ethylcholine aziridinium ion (AF64A), a selective cholinotoxin, in rats [7].

High impact information on Ethylcholine aziridinium

• Neuronal apoptosis was induced by either staurosporine or the neurotoxin ethylcholine aziridinium (AF64A) with a delayed occurrence of apoptotic cell death (within 72 h) [8].
• Role of glucocorticoids in the cholinergic degeneration in rat hippocampus induced by ethylcholine aziridinium (AF64A) [9].
• We show that neurons lacking gelsolin (gsn(-/-)) have enhanced apoptosis following exposure to staurosporine, thapsigargin, or the cholinergic toxin ethylcholine aziridinium (AF64A) [10].
• Intracerebroventricular administration of ethylcholine aziridinium (AF64A) caused cholinergic damage in the septum, and glial lesions in the lateral septal nucleus and in the lateral zones of the hippocampus [11].
• In primary cultures of rat cortex the activity of NQO1 was measured after treatment with ethylcholine aziridinium (AF64A; 40 micro m), inducing mainly apoptotic cell death, or oxygen-glucose deprivation (OGD; 120 min), which combines features of apoptotic and necrotic cell death [12].

Biological context of Ethylcholine aziridinium

• Changes of cholinergic, noradrenergic and serotonergic synaptic transmission indices elicited by ethylcholine aziridinium ion (AF64A) infused intraventricularly [13].
• Previous studies revealed that cholinergic neurons possessing long axons are extremely sensitive to ethylcholine aziridinium ion (AF64A) administration [Neuropharmacology 31 (1992) 397] [14].
• Oxidative stress in the brain following intraventricular administration of ethylcholine aziridinium (AF64A) [15].
• Influences of cholinergic neurotoxin ethylcholine aziridinium ion on circadian rhythms in rats [16].

Anatomical context of Ethylcholine aziridinium

• The effect of ethylcholine aziridinium ion (AF64A) on choline transport in hippocampal, striatal, and cerebrocortical synaptosomes was studied [17].
• A cholinergically disrupted laboratory animal has been produced by administration of the cholinotoxin ethylcholine aziridinium mustard (AF64A), which produced a dysfunction in the cholinergic forebrain system [18].
• In vivo, following injection of ethylcholine aziridinium (2 nmol) into the lateral ventricle of rat brain a high incidence of apoptotic cells as verified by in situ tailing was visible in the periventricular tissue [19].
• The putative cholinergic neurotoxin, ethylcholine aziridinium ion (AF64A), was injected bilaterally into the cerebral ventricles of male rats [20].
• Regional differences in ethylcholine mustard aziridinium ion (AF64A)-induced deficits in presynaptic cholinergic markers for the rat central nervous system [21].

Associations of Ethylcholine aziridinium with other chemical compounds

• In this study the role of nitric oxide was investigated in a model of NMDA-independent, delayed apoptotic cell death, induced by the neurotoxin ethylcholine aziridinium ethylcholine aziridinium both in vivo and in vitro [22].
• These findings are consistent with the neurochemical data obtained in parallel experiments with the morphological study in which it was found that acetylcholine content of the hippocampus was reduced by 73.4% 7 days after ethylcholine mustard aziridinium ion treatment, while dopamine, noradrenaline and serotonin levels were unaffected [23].
• The effects of a sustained-release formulation of thyrotropin-releasing hormone (TRH-SR) on learning impairments induced by scopolamine and a cholinergic neurotoxin, ethylcholine aziridinium ion (AF64A), were examined in rodents [24].
• The effect of early postnatal (day 8) intracerebroventricular injections of the putative cholinotoxin ethylcholine aziridinium mustard (AF64A) on development of cholinergic innervation and postsynaptic muscarinic acetylcholine receptors in the rat hippocampus was examined [25].
• The shortened latency was prolonged when indeloxazine was administered before training in rats subjected to scopolamine-injection, ethylcholine aziridinium ion (AF64A)-treatment and nucleus basalis magnocellularis (NBM) lesion [26].

Gene context of Ethylcholine aziridinium

• After bilateral intracerebroventricular injection of the cholinotoxin ethylcholine aziridinium (AF64A; 1 or 2 nmol/ventricle) in rats, the activity of choline acetyltransferase (ChAT) started to decline in the hippocampus within 24 h [27].
• Cholinergic deficit induced by ethylcholine aziridinium (AF64A) transiently affects somatostatin and neuropeptide Y levels in rat brain [27].
• A cholinotoxin, ethylcholine mustard aziridinium ion, (AF64A) specifically and irreversibly blocks the intraaxonal transport of acetylcholinesterase in the rat [28].
• Selective lesion of neurons in primary cell cultures by MPTP and ethylcholine aziridinium ion (AF64A) [29].

Analytical, diagnostic and therapeutic context of Ethylcholine aziridinium

• Rats received a single intrathecal injection of saline or one of three different doses of the cholinergic neurotoxin, ethylcholine mustard aziridinium ion (AF64-A; 2, 5, and 15 nmol) [30].
• Self-administration was examined before and after the pedunculopontine tegmental nucleus was lesioned with the ethylcholine mustard aziridinium ion, a selective cholinergic toxin [31].
• Ethylcholine aziridinium (AF64A) induces cholinergic lesion in animal models of AD [32].
• Non-specific effects of the putative cholinergic neurotoxin ethylcholine mustard aziridinium ion in the rat brain examined by autoradiography, immunocytochemistry and gel electrophoresis [33].
• Ethylcholine mustard aziridinium ion (AF64A), a synthesized cholinergic neurotoxin, was administered via intraperitoneal injection to the rat to study its effect on the central cholinergic nervous system [34].

References