共查询到20条相似文献，搜索用时 31 毫秒
1.
Characterization of [
Coated vesicles prepared from bovine brain cerebral cortex exhibited [
]5-hydroxytryptamine (5-HT, serotonin) and [
]spiperone binding activities. The binding activities were localized in the inner core vesicles. Binding reached an equilibrium level by 30–45 min at 30°C, and was reversed by the addition of 100 μM 5-HT for [
]5-HT binding or 10 μM ketanserin for [
]spiperone binding. The saturation binding experiments indicated a single class of binding sites for [
]5-HT and [
]spiperone with apparent Kd values of 2.4 and 1.75 nM, respectively. The binding of [
]5-HT was displaced by 5-HT and 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), but not by ketanserin. The binding of [
]spiperone was displaced by spiperone and ketanserin but not by 5-HT or 8-OH-DPAT even at 1 mM. The coated vesicles were shown by immunoblotting assay to contain α-subunits of GTP-binding proteins, Gαs, Gαi2, Gαi3, Gαo and Gαq/11. Forskolin-stimulated adenylate cyclase activity in the coated vesicles was inhibited to 80% of the control level by 5-HT or 8-OH-DPAT. These results suggested that 5-HT1A and 5-HT2A receptors are present in bovine brain coated vesicles and that the 5-HT1A receptors are coupled to adenylate cyclase activity via GTP binding proteins. 相似文献
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2.
Takehiko Maeda Neng-neng Cheng Toshiaki Kume Satoshi Kaneko Hanae Kouchiyama Akinori Akaike Mutsuaki Ueda Masamichi Satoh Yoshio Goshima Yoshimi Misu 《Brain research》1997,771(1):259
The exposure of cultured rat striatal neurons to
-DOPA caused marked cell death. The
-DOPA cytotoxicity was inhibited by the addition of Mg2+ to and by the removal of Ca2+ from the culture medium, and also by the application of tetrodotoxin. Moreover, prolonged application of
-DOPA increased the glutamate content in the culture medium. These results indicate that
-DOPA produces neurotoxicity by facilitating glutamate release. 相似文献
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3.
Yasushi Ishida Hiroyuki Hashiguchi Kazunari Todaka Itsumi Kuwahara Yuta Ishizuka Hideyuki Nakane Daisuke Uchimura Toshikazu Nishimori Yoshio Mitsuyama 《Brain research》1998,788(1-2)
In vivo microdialysis was used to examine the effects of dopaminergic transplants on extracellular concentrations of dopamine (DA), serotonin (5-HT), and their precursors and major metabolites in the denervated rat striatum. Dialysis perfusates were collected from intact, 6-hydroxydopamine (6-OHDA) lesion plus sham grafted, and lesion plus fetal substantia nigra (SN) grafted striata. The SN transplants ameliorated the reduction of striatal DA and dihydroxyphenylacetic acid (DOPAC) levels in rats with unilateral 6-OHDA lesions of the mesostriatal pathway. The transplants also increased extracellular levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in the denervated striatum. In response to NSD-1015 (an inhibitor of aromatic
-amino acid decarboxylase), 5-hydroxytryptophan (5-HTP) levels were substantially elevated in the SN grafted striata as compared with those in the sham grafted controls, which continued even after subsequent administration of
-3,4-dihydroxyphenylalanine (
-DOPA, 100 mg/kg i.p.). Immunohistochemical analysis showed hyperinnervation of 5-HT fibers in the grafted striatum, which was consistent with the results of microdialysis experiments. These results indicated that implantation of SN grafts into the 6-OHDA-lesioned striatum of rats induces hyperactivity of 5-HT synthesis, release and metabolism. 相似文献
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4.
Since ATP has been reported to be a potent excitatory transmitter in the mammalian central nervous system (CNS), we studied the neurochemical characters of the binding sites of
,
-methylene ATP, an agonist of P2X receptors, in mouse crude synaptic membranes. ATP and its related compounds inhibited [3H]
,
-methylene ATP binding in a concentration-dependent manner. The potency order in the inhibition of the binding was as follows;
,
-methylene
>
> ATP ≥ ADP >
,
-methylene ATP UTP > 2-methylthio ATP. And adenosine did not affect the binding. The order was different from those reported in peripheral tissues. And Sr2+, Ca2+, Mg2+, and Cd2+ enhanced the binding. These results suggest that
,
-methylene ATP binding sites in CNS have different characters from those in peripheral tissues. 相似文献
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5.
We studied the effects of
-DOPA on the firing patterns of pallidal neurons in experimental parkinsonism. After a unilateral injection of MPTP, we observed a decrease in the firing rate of GPe neurons, and a slight increase in their bursting activity. In the GPi, there was a considerable augmentation of both neuronal firing frequency and the number of bursting cells. During
-DOPA treatment (10 mg/kg), GPe neurons.pattern is almost unmodified. The firing frequency of GPi neurons, on the contrary, decreased even lower than the control level. A slight reduction was observed in bursting activity. These unexpected results would show that the normalizing effect of
-DOPA on GPi output is limited. 相似文献
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6.
The regulation of dopamine release by 6(R)-tetrahydrobiopterin (BH4) and
-arginine-derived nitric oxide was examined by using a method of superfusion of rat striatum slices in vitro.
-Arginine, which can produce nitric oxide (NO) through the action of NO synthase, induces a concentration-dependent increase of [
] dopamine release in the superfusate of striatum slices. Pretreatment with inhibitors of NO synthase or with inhibitors of BH4 synthesis diminishes the increase of [
] dopamine release mediated by arginine. This increase is almost completely restored following repletion of intracellular BH4 levels by incubation of the slices with 7,8-dihydrobiopterin. Adding exogenous BH4 directly to the superfusion fluid leads to a massive increase in [
] dopamine release which can be inhibited 75% by superoxide dismutase and catalase, but is not inhibited by NG-nitro-arginine, a NO synthase inhibitor, or alpha-methyl-p-tyrosine, a tyrosine hydroxylase inhibitor. The increase of intracellular BH4 concentration by dihydrobiopterin administration causes a small increase of dopamine release which can be partially diminished by NG-nitro-arginine or alpha-methyl-p-tyrosine. It is suggested that the increase of dopamine release stimulated by an enhancement of intracellular BH4 is dependent on its cofactor activity with NO synthase and tyrosine hydroxylase. This study has also demonstrated that BH4 is a regulator of NO-mediated dopamine release in the striatum. 相似文献
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7.
Effects of
Experiments involving single-unit recordings and microiontophoresis were carried out in the barrel cortex of awake, adult rats subjected to whisker pairing, an associative learning paradigm where deflections of the recorded neuron's principle vibrissa (S2) are repeatedly paired with those of a non-adjacent one (S1). Whisker pairing with a 300 ms interstimulus interval was applied to 61 cells. In 23 cases, there was no other manipulation whereas in the remaining 38, pairing occurred in the presence of one of three pharmacological agents previously shown to modulate learning, receptive field plasticity and long-term potentiation: N-methyl-
-aspartic acid (NMDA) (n=8), the NMDA receptor antagonist AP5 (n=17) or the nitric oxide synthase inhibitor
-nitro-arginine-N-methyl-ester (
-NAME) (n=13). Non-associative (unpaired) experiments (n=14) and delivery of pharmacological agents without pairing (n=14) served as controls. Changes in neuronal responsiveness to S1 following one of these procedures were calculated and adjusted relative to changes in the responses to S2. On average, whisker pairing alone yielded a 7% increase in the responses to S1. This enhancement differed significantly from the 17% decrease obtained in the non-associative control condition and could not be attributed to variations in the state of the animals because analysis of the cervical and facial muscle electromyograms revealed that periods of increased muscular activity, reflecting heightened arousal, were infrequent (less than 4% of a complete experiment on average) and occurred randomly. The enhancement of the responses to S1 was further increased when whisker pairing was performed in the presence of
-NAME (27%) or NMDA (35%) whereas AP5 reduced it to 1%. During the delivery period, NMDA enhanced both neuronal excitability and responsiveness to S1 whereas AP5 depressed them. However, the effects of both substances disappeared immediately after administration had ended.
-NAME did not affect the level of ongoing activity and responses to S1 significantly. From these data, we concluded that, since the changes in the responses to S1 lasted longer than the periods of both whisker pairing and drug delivery, they were not residual excitatory or inhibitory drug effects on neuronal excitability. Thus, our results indicate that, relative to the unpaired controls, whisker pairing led to a 24% increase in the responsiveness of barrel cortex neurons to peripheral stimulation and that these changes were modulated by the local application of pharmacological agents that act upon NMDA receptors and pathways involving nitric oxide. We can infer that somatosensory cerebral cortex is one site where plasticity emerges following whisker pairing. 相似文献
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8.
Modulatory effect of
We investigated whether NG-nitro-
-arginine methyl ester (
-NAME), a specific inhibitor of nitric oxide synthase (NOS), can modify the stress-induced adrenocorticotropic hormone (ACTH) and corticosterone responses, because we found that immobilization-induced stress increases NOS mRNA and protein levels and enzyme activity in the adrenal cortex. The physiological significance of these phenomena, however, remains unknown. Plasma ACTH and corticosterone levels were determined by radioimmunoassay (RIA) of systemic blood samples and NOS enzyme activity was measured as the rate of [3H]arginine conversion to [3H]citrulline in the presence of tissue homogenate of adrenal cortex separated from the adrenal gland. The NOS enzyme activity in the adrenal cortex of rats pre-injected with saline at 2 h after the 2-h immobilization was significantly higher (P<0.01) than that in the non-stressed controls. Pre-injection of
-NAME (100 mg/kg, s.c.) almost completely abolished the activity. This dose of
-NAME maintained a significantly elevated plasma corticosterone level (P<0.05, compared with basal level) even 2 h after the 2-h stress, whereas the plasma corticosterone level in rats pre-injected with saline returned to the basal level at the same time point. Plasma ACTH level in
-NAME-pre-treated rats was higher than that in those pre-treated with saline 2 h after the stress, but the difference was not significant. This dose of
-NAME did not influence plasma ACTH or corticosterone levels under resting conditions without stress. These findings suggest that the stress-induced increase in NO synthesis in the adrenal cortex can modify the stress-induced corticosterone response to facilitate the recovery from the elevated corticosterone secretion by stress in the adrenal cortex to the resting basal level. 相似文献
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9.
Unique properties of [
In order to investigate possible differences between NMDA receptor-coupled ion channels in the spinal cord and in the cerebral cortex, we have characterized [
]MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine] binding and its regulation by glutamate and glycine in membrane preparations of the rat spinal cord and cerebral cortex. The KD value of [
]MK-801 binding was higher in the spinal cord than in the cerebral cortex, mainly due to a lower association rate constant. When corrected for the concentrations of residual endogenous amino acids, the EC50 values for glycine were lower at spinal NMDA receptors compared to those in the cerebral cortex, whereas the EC50 values for glutamate were similar in both regions. The IC50 values of
-((3)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (
-CPP) were significantly lower in the spinal cord in the presence of saturating concentrations of glutamate. The IC50 values of 7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-2(H)-quinoline (L-701,324) were significantly lower in the spinal cord under all conditions. These results suggest that NMDA receptors in the spinal cord display low affinity for MK-801, which may correspond to a lower affinity of the voltage-dependent Mg2+ block. Furthermore, NMDA receptors in the spinal cord appear to display high sensitivity to glycine and to glutamate and glycine antagonists. 相似文献
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10.
The activity and regional distribution of
-amino acid oxidase (DAO), an enzyme that inactivates
-serine, were examined in the medulla and spinal cord of the rat by biochemical and histochemical procedures. DAO activity was noticeably low or absent in the nucleus of the solitary tract, ventrolateral medulla and intramediolateral cell column of the spinal cord. This may be indicative of a neuromodulatory role for endogenous
-serine (at the NMDA-glycine site) in the central control of blood pressure. 相似文献
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11.
Inhibition of NMDA-induced increase in brain temperature by N-ω-nitro-
Shuichi Hara Toshiji Mukai Fumi Kuriiwa Nobuhisa Iwata Takeshi Yanase Sadao Kano Takahiko Endo 《Brain research》1997,756(1-2)
Intracerebroventricular administration of N-methyl-
-aspartate (NMDA) caused an increase in brain temperature, which appeared rapidly and preceded that in rectal temperature, in urethane-anesthetized rats. The increase in brain temperature was divided into two phases, an early increase and a late increase. Intracerebroventricular indomethacin, a cyclooxygenase inhibitor, completely abolished the NMDA-induced late increase, but not the early increase, in brain temperature. On the other hand, intracerebroventricular N-ω-nitro-
-arginine, a potent inhibitor of nitric oxide synthase, strongly suppressed both the early and the late increases. These findings suggest that both nitric oxide and prostaglandins may be involved in the increase in brain temperature after NMDA receptor activation. 相似文献
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12.
Ana Alonso-Llamazares Emilio Casanova Daniel Zamanillo Sergio Ovalle Pedro Calvo Miguel A Chinchetru 《Brain research bulletin》1997,42(6):427-430
The third intracellular loop of adrenergic receptors has been implicated in their interaction with guanine nucleotide-binding proteins (G proteins). One of the mechanisms involved in the modulation of receptor function is the phosphorylation of specific residues by intracellular kinases.
-Adrenergic receptor is phosphorylated in vitro by cAMP-dependent protein kinase (PKA), although its physiological effect remains to be determined. We have produced fusion proteins formed by glutathione S-transferase and sequences of the third intracellular loop of mouse
-,
-, and
-adrenergic receptor subtypes, and used them as substrates for PKA. Only the fusion protein containing the
sequence was phosphorylated in vitro by this kinase. Site-directed mutagenesis of a serine (homologue to serine 278 of the rat sequence, RSS) to an alanine residue precluded phosphorylation by PKA. 相似文献
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13.
It has been reported that glutamate-induced neurotoxicity is related to an increase in nitric oxide (NO) concentration. An NO-sensitive electrode has been developed to measure NO concentration directly. Using this electrode, we examined NO concentration and neuronal survival after glutamate application in rat cultured cortical neurons. We also examined the effects of NMDA receptor antagonists, MK-801 and ketamine, and the NO synthetase inhibitor,
-NMMA on NO production and neuronal death. After 7 days in culture, application of glutamate (1 mM) or
-arginine (0.3 mM) to the cultured medium increased NO concentration, and decreased the number of anti-microtubule-associated protein 2 positive neurons. Both pretreatment with MK-801 (300 μm) and ketamine (300 μm) prevented glutamate-, but not
-arginine-induced increase in NO concentration and neuronal death.
-NMMA prevented both glutamate- and
-arginine-induced NO production and neuronal death. The nitric oxide donor, S-nitroso-N-acetyl-
,
-penicillamine (SNAP) also caused neuronal death, and MK-801, ketamine and
-NMMA did not prevent SNAP-induced toxicity. We have demonstrated excitatory amino acid-induced changes of NO concentration and the parallel relationship between changes of NO concentration and neuronal death. In conclusion, an increase in NO concentration does induce neuronal death, and the inhibition of the production of NO prevents glutamate-induced neuronal death. 相似文献
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14.
The effects of
The present study examined the effects of GM1 ganglioside and the monoamine oxidase B (MAO-B) inhibitor
-deprenyl, alone and in combination, on striatal dopamine (DA) and DOPAC levels, and the density of tyrosine hydroxylase (TH) positive neurons in the substantia nigra pars compacta (SNc) of C57bl/6J mice following MPTP administration (20 mg/kg, s.c., twice daily for 5 days). GM1 treatment (30 mg/kg, i.p., daily for 3 weeks, beginning 24 h after the last MPTP injection) partially restored striatal DA levels and rescued SNc neurons. A high dose of
-deprenyl, inhibiting MAO-B activity, (10 mg/kg, i.p. every other day for 3 weeks beginning 3 days after the last MPTP injection) increased striatal DA content, but did not rescue TH-positive SNc neurons. A low dose of
-deprenyl (0.01 mg/kg, i.p. every other day for 3 weeks beginning 3 days after the last MPTP injection) had no effect on either striatal neurochemistry or the rescue of SNc TH-positive neurons. Co-administration of GM1 and high dose
-deprenyl caused a synergistic increase in striatal DA levels, above that obtained with either GM1 or high dose
-deprenyl alone. Co-administration of GM1 and low dose
-deprenyl was not only not synergistic, but caused GM1s effects to be antagonized. The results do not confirm previous findings that low dose
-deprenyl administration in vivo after MPTP can rescue SNc neurons. Given GM1's potential as an adjunct to present anti-parkinsonian medications which include
-deprenyl, it will be important to further investigate the interactions between these two potential therapies. 相似文献
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15.
Neuropeptide Y antibody attenuates 2-deoxy-
2-Deoxy-
-glucose (2-DG) has been shown to induce increased feeding responses in animals. Recent studies suggest the possible involvement of neuropeptide Y (NPY) in 2-DG-induced feeding. The present study examined the effect of immunoneutralization of endogenous NPY on 2-DG-induced feeding. NPY antibody injected into the paraventricular nucleus of the rats significantly attenuated 2-DG-induced feeding, suggesting that hypothalamic NPY may mediate, at least partly, the effect of 2-DG on food intake. 相似文献
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16.
To investigate the cardiovascular role of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM), NOC 18, an NO donor, was microinjected into the RVLM of rats. NOC 18 significantly decreased mean arterial pressure (MAP). Pre-treatment with an NO trapper, carboxy-PTIO, abolished the NOC 18-induced decrease in MAP. Microinjection of
-NAME, an NO synthase inhibitor, increased MAP.
-Arginine reduced MAP and inhibited the pressor response induced by
-NAME. Results suggest that NO acts on the RVLM neurons and plays an important role in cardiovascular regulation. 相似文献
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17.
Sukrut Shah Alokesh Duttaroy Billy T. Chen Joanne Carroll Byron C. Yoburn 《Brain research bulletin》1997,42(6):479-484
The present study examined the effect of in vivo antisense oligodeoxynucleotide treatment on naltrexone (NTX)-induced functional supersensitivity and
-opioid receptor upregulation in mice. On day 1 mice were implanted SC with a NTX or placebo pellet and injected IT and ICV with dH2O or oligodeoxynucleotides. The oligodeoxynucleotides were designed so that they were either perfectly complementary to the first 18 bases of the coding region of mouse
-opioid receptor mRNA, or had one (Mismatch-1) or four (Mismatch-4) mismatches. On days 3, 5, 7, and 9, mice were again injected IT and ICV with dH2O or one of the oligodeoxynucleotides. After the final injections on day 9, placebo and NTX pellets were removed, and 24 h later mice were tested for morphine analgesia or sacrificed for saturation binding studies ([3H]DAMGO). Naltrexone increased the analgesic potency of morphine in dH2O treated mice by ≈ 70%. In binding studies, NTX significantly increased density of brain (≈ 60%) and spinal cord (≈ 140%)
-opioid receptors without affecting affinity. The
-opioid antisense and the oligodeoxynucleotide with one mismatch (Mismatch-1) significantly reduced the potency of morphine by ≈ twofold in placebo-treated mice. The oligodeoxynucleotide with four mismatches (Mismatch-4) did not significantly alter morphine potency. When placebo-treated mice were treated with either the antisense to the mouse
-opioid receptor, Mismatch-4 or Mismatch-1 there were no significant changes in the density of
-opioid receptors. Thus,
-opioid antisense significantly reduced morphine potency without changing
-opioid receptor density. When NTX and oligodeoxynucleotide treatments were combined, there was no change in NTX-induced supersensitivity and
-opioid receptor upregulation. These data suggest that opioid antagonist-induced supersensitivity and upregulation of
-opioid receptors does not involve changes in gene expression. 相似文献
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18.
Miriam Melis Giampaolo Mereu Vanessa Lilliu Marina Quartu Marco Diana Gian Luigi Gessa 《Brain research》1998,783(1):507
A widely accepted theory postulates that chronic treatment with neuroleptics causes, in rats, the depolarization block of the majority of midbrain dopamine (DA) neurons. However, we reported that such treatment fails to reduce the number of spontaneously active DA neurons when the neuronal sampling is performed in the
-tubocurarine-paralyzed instead of chloral-hydrate anesthetized preparation. The present experiments were aimed at verifying whether the negative results might be due to the use of
-tubocurarine as paralyzing agent. Rats were chronically treated with haloperidol (0.5 mg kg−1 i.p., daily) for 3 to 4 weeks. Two to three hours after the last injection, the number of spontaneously active DA neurons in the ventral tegmental area (VTA) were sampled, and their discharging characteristics analyzed, both in animals under chloral hydrate anesthesia and in rats immobilized either with
-tubocurarine, gallamine or succinylcholine. The results indicate that chronic treatment with haloperidol reduced the number of spontaneously active VTA–DA neurons by about 65% in animals under chloral hydrate anesthesia, but failed to modify the number of spontaneously firing DA neurons in rats immobilized with
-tubocurarine, gallamine or succinylcholine. The results indicate that the depolarization block of DA neurons does not occur in the paralyzed preparation and raise doubts about the presence of this phenomenon in the intact non- anesthetized unrestrained animal. 相似文献
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19.
Claudia M. Testa Zane R. Hollingsworth Haruhiko Shinozaki John B. Penney Jr. Anne B. Young 《Brain research》1997,773(1-2)
Metabotropic glutamate receptors (mGluRs) are thought to mediate diverse processes in brain including synaptic plasticity and excitotoxicity. These receptors are often divided into three groups by their pharmacological profiles. [3H]Glutamate binding in the presence of compounds selective for ionotropic glutamate receptors can be used as a general assay for these receptors; subtypes of this non-ionotropic [3H]glutamate binding differ in both pharmacology and anatomical distribution, and are differentially sensitive to quisqualate. The characteristics of these binding sites are consistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGluRs. Under our assay conditions, no [3H]glutamate binding to group 3-like (
-AP4 sensitive) sites could be demonstrated. We have attempted to characterize particular agents which may selectively measure [3H]glutamate binding to mGluR subtypes. We used two isomers of 2-(carboxycyclopropyl)glycine,
-CCG-I and
-CCG-II, and the (2S,1′R,2′R,3′R) isomer of 2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV) as competitors of non-ionotropic [3H]glutamate binding sites. DCG-IV clearly distinguishes two binding sites. Quantitative levels of DCG-IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding correlates with high-affinity quisqualate binding.
-CCG-II displaces only one type of non-ionotropic [3H]glutamate binding, corresponding to high-affinity quisqualate binding. Therefore DCG-IV and
-CCG-II at appropriate concentrations appear to distinguish binding to putative group 2 vs. group 1 mGluRs.
-CCG-I displaces both high- and low-affinity quisqualate binding sites, but unlike the other two compounds, does not clearly distinguish between them. 相似文献
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20.
p-Chlorophenylalanine and fluoxetine inhibit
-Fenfluramine, a putative serotonin releaser and reuptake inhibitor, is commonly prescribed for the treatment of obesity. Brain sites activated by
-fenfluramine have been mapped via the expression of the immediate early gene Fos. However, it is not clear that serotonin release in the brain mediates the effects of
-fenfluramine on Fos expression. The present study determined whether
-fenfluramine induces the expression of Fos in the brain through the release of serotonin. Rats were pretreated either with the serotonin depleting drug p-chlorophenylalanine (PCPA) or with the serotonin reuptake inhibitor fluoxetine. Both drugs inhibited
-fenfluramine-induced Fos expression in the cingulate cortex, frontal cortex, and the parvocellular subdivision of the paraventricular nucleus of the hypothalamus. Neither drug reduced
-fenfluramine-induced Fos responses in several other brain areas, including the caudate–putamen, amygdala, and brainstem regions such as the lateral parabrachial nucleus and nucleus of the solitary tract. These results indicate regional specificity of mechanisms mediating
-fenfluramine-induced Fos expression. It is likely that
-fenfluramine-induced Fos expression at various sites in the brain is mediated via a combination of serotonin release and other, as yet unidentified, neurotransmitters. 相似文献
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