共查询到20条相似文献,搜索用时 15 毫秒
1.
V Saano 《Medical biology》1987,65(2-3):167-173
This short review describes the benzodiazepine receptors, their interplay with GABAergic transmission and chloride ionophore, the search for endogenous ligands, and the drug responses that can be evoked through these receptors. Benzodiazepine receptors offer a unique pathway through which opposite drug actions e.g., anxiogenic and anxiolytic effects can be exerted, and these actions can be inhibited with competitive receptor antagonists. The most plausible endogenous ligand for benzodiazepine receptors discovered so far, a polypeptide DBI, exerts actions opposite to those of the benzodiazepines used in clinical therapy. This has been the stimulus for a new look at the physiological role for these receptors. 相似文献
2.
Shymans'kyĭ IO Kuchmerov'ska TM Donchenko HV Velykyĭ MM Klymenko AP Palyvoda OM Kuchmerovs'kyĭ MO 《Ukrainski? biokhimicheski? zhurnal》2002,74(5):89-95
Concentration of lipid peroxidation products and antioxidant enzyme activities in rat brain and erythrocytes and the effects of nicotinamide and nicotinoyl-GABA administration on these parameters were estimated on 21st day of streptozotocin-induced diabetes. It was demonstrated more then two-fold diabetes-induced accumulation of conjugated dienes and malondialdehyde in tissues studied. Superoxide dismutase and glutathione reductase activities of both brain homogenate and erythrocytes as well as catalase and glutathione peroxidase activities of brain homogenate were shown to decrease significantly in diabetic rats, meanwhile, catalase activity of erythrocytes was increased and glutathione peroxidase unchanged. So the correlation between changes in enzymatic antioxidant system in brain and erythocytes failed to be found. Alterations observed were virtually prevented by the course of nicotinamide and nicotinoyl-GABA treatment. The results suggested that the suppression of antioxidant system could be primary biochemical disturbance in diabetic neuropathy progression. It was shown that the antioxidant efficacy of nicotinoyl-GABA is lower than that of nicotinamide. It was suggested that the mechanism of antioxidant action of nicotinamide and its structural analogue consists of both scavenging of lipid peroxides and NAD biosynthesis that leads to activation and normalization of altered energy and lipid metabolism. 相似文献
3.
T A Voronina L D Smirnov U M Tilekeeva K M Diumaev 《Biulleten' eksperimental'no? biologii i meditsiny》1986,101(5):571-573
The experiments on rats, using conflict situation method, have established that anxiolytic effect of 3-hydroxypyridine derivative is removed by bicucullin and picrotoxin, but not by Ro 5-3663, specific antagonist of benzodiazepine receptors Ro 15-1788 and inversive antagonist ethyl beta-carboline-3-carboxylate. The data obtained suggest that GABA-chloriontophor complex is involved into the realization of 3-hydroxypyridine anxiolytic effect. 相似文献
4.
T M Kuchmerovs'ka 《Ukrainski? biokhimicheski? zhurnal》1998,70(6):126-131
It was established, that the content of nicotinamide adenine dinucleotides and the binding of NAD by isolated brain cortex synaptic membranes under experimental parkinsonism are impaired. Treatment of the experimental results in the Scatchard plots for binding of [U-14C]NAD to the brain cortex synaptic membranes demonstrated that binding capacities lowered, without changes of affinities. NAD-glycohydrolase involved in development of this pathology. The modulative effect of in vivo administered NAm and nicotinoyl-GABA supposes that NAm acts via NAD which binds specifically with synaptic membranes. Thus, NAm and nicotinoyl-GABA are involved in the regulation of the processes in the brain under experimental parkinsonism. 相似文献
5.
Modulation of the GABA-benzodiazepine receptor complex by taurine in rat brain membranes 总被引:1,自引:0,他引:1
The interactions of taurine and its precursor hypotaurine with the GABA-benzodiazepine receptor complex were studied by investigating their effects on GABA and flunitrazepam binding in rat brain membranes. Taurine, and to a lesser degree also hypotaurine, displaced the high- and low-affinity GABA binding. The maximal binding capacities of both sites were decreased in the presence of taurine, while the binding constants remained the same, suggesting noncompetitive interactions. Taurine and hypotaurine affected flunitrazepam binding only at a very high concentration (50 mmol/l), whereas GABA (within the concentration range of 0.1–100 mol/l) significantly enhanced the binding. Taurine inhibited the GABA-stimulated binding dose-dependently. These modulatory effects of taurine on the GABA-benzodiazepine receptor complex could result from interactions with the GABA recognition site but not from direct actions on the benzodiazepine site. 相似文献
6.
Correction by nicotinamide and nicotinoyl-GABA of dopamine metabolism in rat brain in experimental Parkinson's disease 总被引:2,自引:0,他引:2
Kuchmerovs'ka TM Donchenko HV Fomenko HI Chichkovs'ka HV Pakirbaieva LV Klymenko AN 《Ukrainski? biokhimicheski? zhurnal》2001,73(6):108-112
It was established, that serotonin and dopamine content and dopamine uptake by brain nerve endings under experimental parkinsonism are decreased. Nicotinamide nicotinoyl-GABA administration leads to normalization these parameters. It was shown that NAm was more effective on serotonin content while nicotinoyl-GABA on dopamine one. Dopamine uptake was impaired at experimental parkinsonism and partially was normalized by incubation with NAD (10(-6) M). Thus, NAm, nicotinoyl-GABA and NAD are involved in the regulation of brain neurotransmission under experimental parkinsonism and can be useful in treatment of Parkinson's disease. 相似文献
7.
Iu A Blednov M L Gorde? S B Seredenin 《Biulleten' eksperimental'no? biologii i meditsiny》1990,109(4):385-387
The displacement curves of the effect of GABA on the S35-tert-butyl bicyclophosphorothionate binding to the brain membranes of inbred mice were analysed. It was revealed the lack of marked interstrain differences in dependent on the ionic force of incubation medium modification of IC50. After incomplete stimulation of Cl(-)-ionophore subunit (50 mM NaCl) reliable interstrain differences in the value of nHill were shown. Bicuculline in the same conditions prevented the inhibitory effect of GABA (10(-5) M). But submaximal concentrations of bicuculline (5 X 10(-6) M, 10(-6) M) stimulated the radioligand binding in the presence of GABA (10(-6) M). It was marked more expressed bicuculline stimulation effect on the membranes of C57Bl/6 mice, as compared to BALB/c mice. 相似文献
8.
Jae-Seung Hong Jing-Hui Feng Jung-Seok Park Hee-Jung Lee Jae-Yong Lee Soon-Sung Lim 《Animal cells and systems.》2020,24(3):143-150
ABSTRACT Chrysin, a natural flavonoid, is the main ingredient of many medicinal plants, which shows potent pharmacological properties. In the present study, the antinociceptive effects of chrysin were examined in ICR mice. Chrysin orally administered at the doses of from 10 to 100?mg/kg exerted the reductions of formalin-induced pain behaviors observed during the second phase in the formalin test in a dose-dependent manner. In addition, the antinociceptive effect of chrysin was further characterized in streptozotocin-induced diabetic neuropathy model. Oral administration chrysin caused reversals of decreased pain threshold observed in diabetic-induced peripheral neuropathy model. Intraperitoneally (i.p.) pretreatment with naloxone (a classic opioid receptor antagonist), but not yohimbine (an antagonist of α2-adrenergic receptors) or methysergide (an antagonist of serotonergic receptors), effectively reversed chrysin-induced antinociceptive effect in the formalin test. Moreover, chrysin caused a reduction of formalin-induced up-regulated spinal p-CREB level, which was also reversed by i.t. pretreated naloxone. Finally, chrysin also suppressed the increase of the spinal p-CREB level induced by diabetic neuropathy. Our results suggest that chrysin shows an antinociceptive property in formalin-induced pain and diabetic neuropathy models. In addition, spinal opioid receptors and CREB protein appear to mediate chrysin-induced antinociception in the formalin-induced pain model. 相似文献
9.
P V Sergeev P I Sizov A S Dukhanin E N Mineeva 《Biulleten' eksperimental'no? biologii i meditsiny》1990,110(10):382-384
A specific [3H] GABA and [14C] flunitrazepam binding sites have been identified in a membrane fraction of human myometrium. The specific binding of [14C] GABA was displaced by unlabelled GABA and bicuculline. It was shown that the binding of [3H] flunitrazepam to membrane preparations is enhanced in the presence of GABA. A similar reciprocal effect of benzodiazepines to enhance [14C] GABA binding has been demonstrated. The present results indicate that GABAA-BD receptors complexes may have a functional significance in human ovary. 相似文献
10.
11.
L.S. Lopes S.S. Pereira L.L. Silva K.A. Figueiredo B.A. Moura F.R.C. Almeida F.C.F. Sousa 《Life sciences》2009,84(3-4):105-110
This study assesses the antinociceptive effect induced by different dosages of topiramate (TP), an anticonvulsant drug that is orally administered in models of neuropathic pain and acute pain in rats and mice, respectively. Orally administered TP (80 mg/Kg) in mice causes antinociception in the first and second phases of a formalin test, while in doses of 20 and 40 mg/Kg it was only effective in the second phase. TP (80 mg/Kg, p.o) also exhibited antinociceptive action in the hot plate test, however, it did not have an effect in the capsaicin test in mice, nor in the model of neuropathic pain in diabetic rats. The antinociceptive effect caused by TP (80 mg/Kg, p.o) in the formalin test was reversed by prior treatment with naloxone (opioid antagonist), but not with glibenclamide (antagonist of the potassium channel), ondansetron (antagonist of the serotonin 5HT3 receptor) or cyproheptadine (antagonist of the serotonin 5HT2A receptor).The data show that TP has an important antinociceptive effect in the models of nociception induced by chemical (formalin) or thermal (hot plate) stimuli, and that the opioid system plays a part in the antinociceptive effect, as shown by formalin. 相似文献
12.
13.
14.
N. Voitenko 《Neurophysiology》2004,36(4):310-314
Diabetic neuropathy is a frequent complication of diabetes mellitus, for which no adequate clinical treatment is currently available. One of the main reasons for the absence of effective treatment of this disease is that information on how metabolic, vascular, and other abnormalities involved in the pathogenesis of diabetic neuropathy lead to dysfunction of nerve cells and pathways remains insufficient. Recent studies demonstrated that substantial abnormalities of calcium homeostasis in input neurons of the somatosensory nociceptive system are associated with many symptoms of diabetic neuropathy. Although proof of the causal linkage between calcium abnormalities and neuropathic complications is not conclusive, current research in neuroscience mostly indicates that such a linkage exists. Practically all known modifications of synaptic transmission in both central and peripheral nervous systems result from calcium-dependent modifications of the molecular players involved in this transmission. This is why the main goal of our review is to analyze in detail the fundamental cellular and molecular calcium-regulating mechanisms that are deteriorated in diabetes. As an important end-point of the proposed review, the capability of a widely used calcium channel blocker, nimodipine, to correct cytosolic and endoplasmic reticulum calcium abnormalities in neurons of the dorsal root ganglia and spinal dorsal horn and possible curative value of this agent in diabetic neuropathy are discussed.Neirofiziologiya/Neurophysiology, Vol. 36, No. 4, pp. 348–353, July–August, 2004.This revised version was published online in April 2005 with a corrected cover date. 相似文献
15.
16.
Guo Jingjing Sheng Xuan Dan Yu Xu Yurong Zhang Yuanruohan Ji Huihong Wang Jiayue Xu Zixi Che Hongyu Li Guodong Liang Shangdong Li Guilin 《Purinergic signalling》2021,17(1):163-163
Purinergic Signalling - Due to the authors’ carelessness, we mistakenly used similar images between the Fig. 6b on the expression of IL-1β protein (upper) and Fig. 7c on the expression... 相似文献
17.
Pancreatic regeneration after pancreatectomy has been well documented in the animal models. We have recently reported that STZ diabetic animals operated for partial pancreatectomy showed normoglycemic status after the operation as compared to uncontrolled hyperglycemia and even death in the diabetic sham operated animals. In drug and virus-induced experimental diabetic models there is a high mortality of animals due to uncontrolled destruction of the beta-cells. In order to destroy sufficient beta-cell mass so as to induce diabetes but prevent mortality, we designed present studies to investigate the combined effect of pancreatectomy, nicotinamide, and streptozotocin (STZ) on diabetic status of BALB/c mice. BALB/c mice of either sex were subjected to 50% pancreatectomy. These were then treated with nicotinamide (350 mg/kg body weight) before and after streptozotocin (200 mg/kg body weight) administration. The changes in body weight, blood glucose levels, serum and pancreatic insulin contents of these animals were monitored in experimental and control group for 12 weeks, and follow up studies were made of these animals for further 12 weeks. It was found that there was a drastic loss of body weight, decreased serum and pancreatic insulin levels coupled with sustained and low levels of hyperglycemia in the experimental group as opposed to the control group. The results indicate that partial pancreatectomy followed by nicotinamide and streptozotocin treatment leads to a long-lasting hyperglycemic state, depicting the clinical symptom of NIDDM without mortality. The study probably reveals a new model for experimental diabetes. 相似文献
18.
19.
20.
Blankenburg M Kraemer N Hirschfeld G Krumova EK Maier C Hechler T Aksu F Magerl W Reinehr T Wiesel T Zernikow B 《Diabetic medicine : a journal of the British Diabetic Association》2012,29(11):1425-1432
Aim Sensory diabetic neuropathy, determined by nerve conduction studies, is common in children with Type?1 diabetes. Diabetic neuropathy diagnoses are rarely made in paediatric daily care because they are asymptomatic, vibration detection is mostly normal and nerve-conduction testing is impractical. The present study aims to: (1) describe somatosensory dysfunction in children with diabetes, (2) test whether diabetes duration and HbA(1c) are related to somatosensory dysfunction and (3) identify the best screening test for large-fibre dysfunction, as indicated by nerve conduction studies. Methods Forty-five children (age 13.2?±?2.5?years) with Type?1 diabetes for 6.7?±?2.5?years and matched control subjects were assessed by neurological examinations, nerve conduction tests and quantitative sensory testing on the feet using the protocol of the German Research Network on Neuropathic Pain. Abnormal nerve conduction was used as gold standard to define neuropathies. Results We found a high prevalence of mechanical (38%) and thermal (24%) hypoesthesia often associated with hyperalgesia (47%). Tactile hypoesthesia (33%) was more frequent than pallhypaesthesia (11%). Only cold detection and mechanical pain thresholds were related to HbA(1c) . Tactile hypoesthesia had the highest sensitivity (75%), specificity (89%) and positive (75%) and negative (89%) predictive values for neuropathies defined by nerve conduction tests (31% abnormal). Conclusions Almost half of the children with diabetes have subclinical large- and small-fibre neuropathies. Tactile detection was better than vibration for neuropathy assessment. Quantitative sensory testing is a valuable tool for assessment of neuropathy as well as a target of interventional studies in children with diabetes. 相似文献