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941.
Neuroprotective effect of riluzole in MPTP-treated mice 总被引:7,自引:0,他引:7
Tsutomu Araki Toshihiko Kumagai Katsuyuki Tanaka Mitsunobu Matsubara Hiroyuki Kato Yasuto Itoyama Yutaka Imai 《Brain research》2001,918(1-2):176-181
The neuroprotective effects of riluzole, a Na(+) channel blocker with antiglutamatergic activity, and MK-801, a blocker of N-methyl-D-aspartate (NMDA) receptors, were compared in the model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced depletion of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels in mice. The mice were injected intraperitoneally (i.p.) with four administrations of MPTP (10 mg/kg) at 1 h intervals and then the brains were analyzed 1, 3 and 7 days after the treatment. Dopamine and DOPAC levels were significantly decreased in the striatum from 1 day after MPTP treatment. A severe depletion in dopamine and DOPAC levels was found in the striatum 3 and 7 days after MPTP treatment. Riluzole antagonized the MPTP-induced decrease in dopamine, DOPAC and HVA levels in the striatum. On the other hand, MK-801 prevented the MPTP-induced decrease in DOPAC levels, but not in dopamine levels in the striatum. An immunohistochemical study indicated that riluzole can protect against MPTP-induced neuronal damage in the substantia nigra. These results suggest that riluzole is effective against MPTP-induced neurodegeneration of the nigrostriatal dopaminergic neuronal pathway. 相似文献
942.
目的 研究大鼠脑内 (第 2 9层面 )N 甲基 D 门冬氨酸 (NMDA)受体的分布特征。方法采用3 H MK 80 1为配基的受体放射自显影体外结合实验。结果 3 H MK 80 1结合位点在大鼠脑内的分布广泛而不均匀 ,海马区密度最高 (CA1>DGmb >DGlb >CA3) ,其他依次为杏仁核、大脑皮层、纹状体尾状核、丘脑核团和下丘脑腹内侧区。结论 3 H MK 80 1结合位点的分布密度可反映NMDA受体的分布情况。 相似文献
943.
The present study examined the regional differences in dopamine transporter binding sites and NMDA receptor complex binding based on autoradiographic images obtained in postmortem sections of human normal brain tissues. In middle-aged control tissues, high and comparable levels of [3H]CFT binding were observed in the caudate nucleus, putamen, and accumbens nucleus without significant alteration along the rostrocaudal axis and ventral and dorsal parts of these nuclei. In aging normal brain tissues, dopamine binding sites for [3H]CFT were significantly reduced in the caudate nucleus, putamen, and accumbens nucleus.
-[3H]Glutamate, [3H]MK-801, and [3H]glycine binding to the NMDA receptor complex was lower in aging brain tissues than in middle-aged controls. Significant correlation did occur between age and [3H]CFT binding and between age and
-[3H]glutamate, [3H]MK-801, and [3H]glycine binding sites. These results demonstrate that the basal ganglia have age-associated reductions in dopamine transporter uptake and NMDA receptors. These data support hypoactive activity of the NMDA receptor complex system with advancing age. The dopamine transporter uptake and NMDA receptors appear to be vulnerable to the aging process in the basal ganglia. 相似文献
944.
We examined the cytotoxicity of MK-801 on cultured microglia and demonstrated its cytotoxicity. Cytotoxicity of MK-801 was reduced by the addition of L-glutamate, kainate and NMDA. The action of MK-801 was due to the direct action of microglia. It suggested the existence of glutamate receptor in microglia. Cytotoxicity of MK-801 was reduced by the addition of atropine sulfate which suggested the presence of muscarinic receptor in microglia. 相似文献
945.
The effect of treatment with the competitive (CGP 43487) and non-competitive (MK-801) NMDA antagonists on behaviors induced by the stimulation of D1 (SKF 38393 induced grooming), D2 (LY 171555 elicited hypermotility) or D1/D2 (apomorphine induced locomotion and stereotypies) was observed in intact rats. The administration of low doses of MK-801 (0.03 and 0.06 mg/kg) or CGP 43487 (0.375 and 0.75 mg/kg), which were without effect by themselves on animal locomotion, reduced the hyperactivity induced by LY 171555 (0.15 mg/kg) and did not change the stimulating motor effect of a low dose of apomorphine (0.15 mg/kg). Spontaneous grooming behavior was inhibited by both NMDA antagonists, whereas the administration of CGP 43487 but not of MK-801 potentiated grooming response to SKF 38393 (10 mg/kg). Both antagonists increased stereotyped behavior induced by 0.25 mg/kg apomorphine. The results, according to those obtained by other authors in DA depleted/lesioned animals, support the view of interaction between NMDA/D1,D2 receptors in intact rats. 相似文献
946.
The inhibitory effects of microiontophoretically-applied serotonin (5-HT) and 6-chloro-2[1-piperazinyl]pyrazine (MK-212) were examined on spontaneously firing somatosensory cerebral cortical neurons and dorsal raphe neurons in rats anesthetized with chloral hydrate. On cortical neurons, MK-212 caused only weak and variable inhibition of extracellularly recorded neuronal activity, compared to the effects of 5-HT. However, on raphe cells, MK-212 exerted potent inhibitory effects, equivalent to those observed with 5-HT. In contrast to the inhibitory actions of D-lysergic acid diethylamide (LSD) and 5-HT at presumed 5-HT autoreceptors, MK-212 did not affect the in vitro release of [3H]5-HT from slices of rat hypothalamus stimulated by methiothepin. These findings, coupled with previously reported behavioral, biochemical and electrophysiological effects of MK-212 may indicate that this novel serotonergic agonist uniquely discriminates between subsets of serotonergic receptors in the CNS. 相似文献
947.
Robert C. Osburne E.Ann Myers David Rodbard Kenneth D. Burman Leon P. Georges John T. OBrian 《Metabolism: clinical and experimental》1983,32(1):9-13
We have investigated the physiologic significance of the decline in serum triiodothyronine (T3) occurring during hypocaloric feeding by measurement of changes in cardiovascular function. The QKd interval, the interval between the Q wave of the electrocardiogram and the onset of Korotkoff sounds at diastolic pressure at the brachial artery, is the sum of the preejection period and pulsetransmission time, and has proven to be a sensitive and effective measure of the effect of thyroid hormones on the cardiovascular system. Fifteen euthyroid obese volunteers underwent successive 2 wk periods of hypocaloric feeding (200–400 calories per day) interspersed with periods of at least 2 wk of re-feeding on a weight-maintaining diet (1500 calories). In a later phase subjects received oral supplementation of triiodothyronine (T3) in addition to the diet to prevent the fall in serum T3. In the last study phase, subjects on the diet received supplementation with oral thyroxine (T4), which prevented the fall in serum T3 and resulted in a slight increase in serum T4. During the first 2 wk period of hypocaloric feeding, there was a statistically significant increase in QKd, and a decrease in pulse rate, compatible with a hypothyroid state relative to initial measurements. When oral T3 supplementation was given, the rise in QKd and fall in pulse rate were prevented. Likewise, with oral T4 supplementation, the changes in QKd and pulse were prevented. Thus, the fall in serum T3 occurring during hypocaloric feeding is associated with changes in the cardiovascular system which are qualitatively similar to those observed during hypothyroidism. The present data, taken with other data in the literature, suggest that the decline in serum T3 during hypocaloric feeding may be an adaptive mechanism to conserve energy during caloric deprivation. 相似文献
948.
Opiate tolerance involves both associative and non-associative changes. However, procedures designed to distinguish between
these two processes have rarely been employed when investigating the physiological basis of such plasticity. The present experiments
assessed some of the mechanisms contributing to both associative and non-associative decreases in morphine analgesic potency
following repeated IV morphine administration (4 days, 5 mg/kg per day). For one group of rats, testing for morphine analgesia
(tailflick) occurred in a context that had been repeatedly paired with morphine administration. Another group of rats, exposed
equally to the testing context, handling procedures and morphine, was tested for morphine analgesia in a context that was
specifically unpaired with prior drug. Although both of these groups showed a decrease in the drug effect following repeated
administrations, those rats tested in the morphine-associated context were significantly more tolerant than the unpaired group.
We evaluated the spinal cord involvement of NMDA receptors, as well as the peptide neurotensin in these two types of tolerance.
NMDA receptors appeared to mediate non-associative changes in drug potency, as rats tested in either context were less tolerant
when morphine administration was preceded with the non-competitive NMDA antagonist, MK-801 (2.5 and 5 nmol). Spinal neurotensin
antagonism with [d-Trp11]neurotensin (3 pmol) selectively abolished associative tolerance. These findings provide information about the mechanisms
of opiate tolerance and support the distinction between associative and non-associative processes underlying these changes.
Received: 20 December 1995 / Final version: 11 June 1996 相似文献
949.
O. Ghribi J. Callebert C. Verrecchia M. Plotkine and RG Boulu 《Fundamental & clinical pharmacology》1995,9(2):141-146
Summary— Brain microdialysis was used to study changes in the glutamate and aspartate extracellular concentrations in the striatum of conscious rats submitted to 30 minutes cerebral ischaemia, using the four-vessel occlusion model. Perfusion of the N-methyl-D-aspartate (NMDA) receptor channel blockers, dizocilpine (MK-801; 75 μM) and Mg2+ (2.5 mM), inhibited the ischaemia-induced accumulation of glutamate and aspartate. The AMPA/kainate receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulfamylbenzo (F) quinoxaline (NBQX; 15 μM and 450 μM) had no effect on glutamate and aspartate levels during ischaemia. On the other hand, omission of Ca2+ from the perfusing solution did not alter the increases in glutamate and aspartate induced by ischaemia. These results suggest that the glutamate and aspartate accumulation in four-vessel occlusion ischaemia is mediated by activation of NMDA receptors in a Ca2+ independent manner. 相似文献
950.
In the present immunocytochemical study, we investigated the mechanism of Fos protein induction and the regional distribution of the Fos protein in brains of spontaneously hypertensive rats subjected to 2 h of permanent middle cerebral artery occlusion (MCAO). Rats were administered either saline or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions mediated by NMDA receptors in the infarct borderzone, and that Fos protein due to its persistence in the tissue can be used as a histochemical marker of borderzone tissue at risk for eventually becoming recruited in the infarct. 相似文献