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picrotoxin/atrofia
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 23 risultati
Strychnine and L-allylglycine but not bicuculline and picrotoxin induce transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats.
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The effects of the convulsants strychnine, bicuculline, picrotoxin and L-allylglycine on the transsynaptic destruction of medullary dorsal horn neurons were examined following transection of the inferior alveolar nerve in adult rats. Strychnine and L-allylglycine enhanced the transsynaptic effect of
Delayed impairment of response extinction after single seizures induced by picrotoxin.
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Male Wistar rats were trained with a food rewarded task and treated with single convulsive dose of picrotoxin. Behavioural test for response extinction by non-reinforcement procedure, which was considered as inhibitory learning, was performed 1, 2, 5, or 7 days after the treatment. The results
Changes in cortical acetylcholine output induced by modulation of the nucleus basalis.
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The modulatory inputs of the cholinergic neurons of the nucleus basalis have been investigated in midpontine transected and freely moving rats by measuring acetylcholine release from the cerebral cortex using the cortical cup technique. Acetylcholine release was found to be the same in both groups
Quantification of zinc toxicity using neuronal networks on microelectrode arrays.
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Murine neuronal networks, derived from embryonic frontal cortex (FC) tissue grown on microelectrode arrays, were used to investigate zinc toxicity at concentrations ranging from 20 to 2000 microM total zinc acetate added to the culture medium. Continual multi-channel recording of spontaneous action
Excitotoxic mechanisms of epileptic brain damage.
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It is well established that the putative excitatory neurotransmitters, glutamate (Glu) and aspartate (Asp), are neurotoxins that have the potential of destroying central neurons by an excitatory mechanism. Kainic acid (KA), a rigid structural analog of Glu, powerfully reproduces the excitatory
[Effects of L-dopa and transcranial magnetic stimulation on behavioral reactions in kindled rats].
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In acute experiment in rats, the chronic epileptogenesis was reproduced in the form of pharmacological kindling induced via repeated picrotoxin administrations (1.0-1.2 mg/kg, intraperitoneally). A reduction of exploratory behavior was shown in the early period of kindling (24 h as of the moment of
Neonatal triethyltin exposure alters adult electrophysiology in rats.
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In adults, triethyltin (TET) produces degeneration of white matter, edema, vacuolization on myelin and histotoxic hypoxia. To determine the functional consequences of perinatal exposure to TET, albino rats were administered either 0, 3, 6, or 9 mg/kg TET on postnatal day 5. Upon reaching adulthood,
Neuroprotection by propofol in acute mechanical injury: role of GABAergic inhibition.
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1. Whole cell patch-clamp and extracellular field recordings were obtained from granule cells of the dentate gyrus in 400-microns-thick brain slices of the adult rat to determine the actions of the intravenous general anesthetic 2,6-diisopropylphenol (propofol) on acute neuronal survival and
Spine loss in experimental epilepsy: quantitative light and electron microscopic analysis of intracellularly stained CA3 pyramidal cells in hippocampal slice cultures.
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The sequence of neuronal alterations resulting from epileptic activity is poorly understood. In the hippocampus of some epileptic patients, there is a loss of certain neuronal types in the hilar region and in CA3. The neuronal alterations preceding this degeneration probably affect synaptic
Involvement of AMPA/kainate-excitotoxicity in MK801-induced neuronal death in the retrosplenial cortex.
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MK801 is a prototypical non-competitive NMDA receptor-antagonist that induces behavioural changes and reversible toxicity at low doses, while at higher doses triggers neuronal death that mainly affects the retrosplenial cortex (RSC) and to a lesser extent other structures such as the posterolateral
Improved spatial learning is associated with increased hippocampal but not prefrontal long-term potentiation in mGluR4 knockout mice.
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Although much information about metabotropic glutamate receptors (mGluRs) and their role in normal and pathologic brain function has been accumulated during the last decades, the role of group III mGluRs is still scarcely documented. Here, we examined mGluR4 knockout mice for types of behavior and
Quinolinic acid toxicity on orexin neurons blocked by gamma aminobutyric acid type A receptor stimulation.
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Selective degeneration of hypothalamic orexin neurons, a hallmark of pathology in narcolepsy patients, is in part reproduced in hypothalamic slice cultures by application of an endogenous excitotoxin quinolinic acid. Depolarized membrane potential may be responsible for the vulnerability of orexin
Reversible loss of dendritic spines and altered excitability after chronic epilepsy in hippocampal slice cultures.
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The morphological and functional consequences of epileptic activity were investigated by applying the convulsants bicuculline and/or picrotoxin to mature rat hippocampal slice cultures. After 3 days, some cells in all hippocampal subfields showed signs of degeneration, including swollen somata,
Epileptiform activity in vitro can produce long-term synaptic failure and persistent neuronal depolarization.
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A large, extracellular negative DC shift, termed epileptic depolarization, could be elicited during zero magnesium-induced epileptic activity in the rat hippocampal slice. In 10 mM glucose medium, epileptic depolarization was elicited by high-frequency synaptic stimulation. During epileptic
Pharmacological analysis of cerebellar contributions to the timing and expression of conditioned eyelid responses.
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Contradictory results have been reported regarding the effects of cerebellar cortex lesions on the expression of conditioned eyelid responses--either no effect, partial to complete abolition of responses, or disruption of response timing. This uncertainty is increased by debates regarding the
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