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1.
Recent evidence implicates the endogenous excitotoxin, glutamate (Glu), in several neurologic disorders, including seizure-related brain damage. Ketamine, phencyclidine, and MK-801, which are noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) subtype of Glu receptor (but do not antagonize kainic acid receptors) were tested in the present study for their effects on behavioral and/or electrographic seizures and seizure-related brain damage induced by kainic acid. Behavioral seizure activity was reduced by these agents, as was spread of electrographic seizures to neocortex, but seizures recorded from deep brain regions such as hippocampus, piriform cortex, and amygdala were not significantly diminished. All three agents prevented seizure-related brain damage in the amygdala, piriform cortex, thalamus, and CA1 region of the hippocampus but conferred little or no protection in the lateral septum and CA3 region of the hippocampus. The regional selectivity of the neuroprotective effect suggests that NMDA receptors may play a more dominant role in seizure-related brain damage in some brain regions than in others. The ability of NMDA antagonists to prevent seizure-related damage in several brain regions without suppressing seizure activity suggests that in these brain regions persistent seizure activity can be maintained by other transmitter systems, with or without NMDA receptor participation, but that seizure-related brain damage is critically dependent on NMDA receptor participation.  相似文献
2.
Summary We investigated the neuroprotective effect of the noncompetitive N -methyl- d -asparatate (NMDA) antagonist ketamine when administered after onset of lithium-pilocarpine-induced status epilepticus (SE). Seizures were induced in Wistar rats with lithium chloride (3 mEq/kg) and pilocarpine (PC) (30–60 mg/kg intraperitoneally, i.p.). Fifteen minutes after SE onset, either ketamine 100 mg/kg or normal saline was injected i.p., and 3 h after SE onset atropine, diazepam (DZP), and phenobarbital (PB) were administered i.p. to terminate the seizures. Twentyfour hours later, rats underwent brain perfusion-fixation, with subsequent brain processing for light-microscopic examination. Rats administered saline (n = 5) had neuronal damage in 24 of 25 brain regions examined. Rats administered ketamine (n = 7) had significant neuroprotection in 22 of 24 damaged regions. Ketamine reduced the amplitude of seizure discharges, and in 3 rats EEG seizur activity ceased in 30 min; none of these rats had neuronal damage. In the other 4 rats, EEG seizure discharges persisted >90 min; in these animals, 21 of 24 damaged regions were protected. In contrast, rats with 1-h high-dose PC-induced SE (400 mg/kg i.p. without lithium chloride preadministration) had 14 damaged regions, of which 7 were significantly different from the undamaged regions of the ketamine subgroup with persistent electrographic seizures. Thus, ketamine is remarkably neuroprotective when administered after onset of SE, whether or not seizure discharges are eliminated.  相似文献
3.
Ketamine is a non-competitive antagonist to the phencyclidine site of N-methyl-d-aspartate (NMDA) receptor. Clinical findings point to a rapid onset of action for ketamine on the treatment of major depression. Considering that classic antidepressants may take long-lasting time to exhibit their main therapeutic effects, the present study aims to compare the behavioral effects and the BDNF hippocampus levels of acute administration of ketamine and imipramine in rats. To this aim, rats were acutely treated with ketamine (5, 10 and 15 mg/kg) and imipramine (10, 20 and 30 mg/kg) and animal behavioral was assessed in the forced swimming and open-field tests. Afterwards, BDNF protein hippocampal levels were assessed in imipramine- and ketamine-treated rats by ELISA-sandwich assay. We observed that ketamine at the doses of 10 and 15 mg/kg, and imipramine at 20 and 30 mg/kg reduced immobility time compared to saline group, without affecting locomotor activity. Interesting enough, acute administration of ketamine at the higher dose, but not imipramine, increased BDNF protein levels in the rat hippocampus. In conclusion, our findings suggest that the increase of hippocampal BDNF protein levels induced by ketamine might be necessary to produce a rapid onset of antidepressant action.  相似文献
4.
The effects of anesthetic and nonanesthetic doses of ketamine hydrochloride were studied in male adult rats in which a primary and a projected epileptic focus were induced with implantation of cobalt in the right or left frontal cortex. Electrical activity was recorded from the frontal, parietal, and occipital cortices. Nonanesthetic doses of ketamine were associated with activation or enhancement of primary and projected focal electrical activity, as well as turning behavior toward the side of the cobalt focus. Anesthetic doses of ketamine also enhanced or activated the primary and projected foci. These animals demonstrated turning behavior toward the side of the cobalt focus prior to and following the cataleptoid state. During catalepsy, forelimb twitching and oscillating movements of the vibrissae occurred. The activation of primary and projected foci by ketamine at anesthetic and nonanesthetic doses supports the clinical findings that ketamine is epileptogenic in certain patients with a seizure disorder.  相似文献
5.
The effect of ketamine has been tested on the phase of the vertical vestibulo-ocular reflex of rabbits sinusoidally oscillated at various frequencies. A significant phase lag, predominantly affecting the macular component of the reflex, was observed. This action resembles that induced by Nembutal in the same preparation. A specific action of ketamine on synaptic transmission is suggested. Erroneous phase relationship between natural stimuli and responses can be obtained in experiments employing ketamine.  相似文献
6.
A neurophysiological investigation of the effects of phencyclidine (PCP) and ketamine on synaptic transmission was carried out at the level of two excitatory connections of the hippocampal formation: the interhippocampal projections from contralateral CA3 (cCA3) to CA1 and the entorhino-dentate pathway.In urethane-anesthetized rats PCP i.v. produced a moderate depression of the population EPSP elicited in the stratum radiatum of CA1 by cCA3 stimulations (16–40%) and a large decrease (up to 97%) of the amplitude of the corresponding population spike recorded at the level of the CA1 pyramidal cell bodies (ED50:1.83 mg/kg).Single-unit analysis of CA1 pyramidal cell activation triggered by cCA3 stimulations indicated that i.v. PCP did not decrease the amplitude of individual action potentials suggesting that the decrease in the size of the population spike was due to a decrease in the number of CA1 pyramidal cells activated by the stimulus. Moreover, PCP administered i.v. in the same dose range (0.6-4.0 mg/kg) reduced the maintained activity of CA1 pyramidal cells and their excitation by iontophoretically applied glutamate or ACh.Similar effects on both field potentials and single-unit activity in the CA1 area were also observed following the administration of larger i.v. doses of ketamine (ED50: 7.2 mg/kg), but the effects of the latter drug were of considerably shorter duration than those of PCP.  相似文献
7.
8.
The relative potencies of the stereoisomers of ketamine, N-allylnormetazocine and cyclazocine were determined at μ opiate and σ opiate/phenycyclidine (PCP) receptors in vitro in rat brain homogenates, as well as in a discriminative stimulus behavioral paradigm in rats trained to discriminate PCP from saline. In all cases the in vivo and in vitro data were in agreement. The (+)-isomers of N-allylnormetazocine and cyclazocine are highly specific sigma opiate/PCP ligands.  相似文献
9.
Intracellular recordings were made from dentate and CA1 pyramidal cells of the mouse hippocampal slice preparation. N-methyl-dl-aspartate (NMDLA), quisqualate and kainate and the anaesthetic agent, ketamine, were applied by microelectrophoresis. Excitation by NMDLA but not by the other amino acids, was associated with increased outward rectification. Ketamine had no effect on the resting potential or current/voltage relation of the cells, but selectively antagonised the responses to NMDLA. Action potentials evoked by NMDLA were characteristically broader than those evoked by the other amino acids or by the passage of depolarising current through the electrode.  相似文献
10.
Ketamine hydrochloride, 10 mg/kg by intramuscular injection, inhibited aggregation of platelets from three out of three baboons. Aggregation to ADP, arachidonic acid, epinephrine, and collagen was inhibited but aggregation to ristocetin was normal. Two baboons anaesthetised with the related drug phencyclidine, 1.0 mg/kg intramuscularly, had delayed aggregation. Ketamine inhibition of human platelets was irreversible in that aggregation could not be restored by either gel filtration of inhibited platelets and the re-addition of normal plasma, or by increasing the concentrations of agonists. Mixtures of human ketamine inhibited and aspirinised platelets failed to aggregated. Thromboxane B2 production was reduced to 3% of the amount produced by non inhibited platelets but the oxygen burst was not inhibited.  相似文献
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