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1.
Tetrodotoxin-resistant and tetrodotoxin-sensitive Na+ channels contribute to the abnormal spontaneous firing in dorsal root ganglion neurons associated with neuropathic pain. Effects of the anti-nociceptive agent ralfinamide on tetrodotoxin-resistant and tetrodotoxin-sensitive currents in rat dorsal root ganglion neurons were therefore investigated by patch clamp experiments. Ralfinamide inhibition was voltage-dependent showing highest potency towards inactivated channels. IC50 values for tonic block of half-maximal inactivated tetrodotoxin-resistant and tetrodotoxin-sensitive currents were 10 μM and 22 μM. Carbamazepine, an anticonvulsant used in the treatment of pain, showed significantly lower potency. Ralfinamide produced a hyperpolarising shift in the steady-state inactivation curves of both currents confirming the preferential interaction with inactivated channels. Additionally, ralfinamide use and frequency dependently inhibited both currents and significantly delayed repriming from inactivation. All effects were more pronounced for tetrodotoxin-resistant than tetrodotoxin-sensitive currents. The potency and mechanisms of actions of ralfinamide provide a hypothesis for the anti-nociceptive properties found in animal models.  相似文献   

2.
The inhibitor cystine-knot motif identified in the structure of CSTX-1 from Cupiennius salei venom suggests that this toxin may act as a blocker of ion channels. Whole-cell patch-clamp experiments performed on cockroach neurons revealed that CSTX-1 produced a slow voltage-independent block of both mid/low- (M-LVA) and high-voltage-activated (HVA) insect Cav channels. Since C. salei venom affects both insect as well as rodent species, we investigated whether Cav channel currents of rat neurons are also inhibited by CSTX-1. CSTX-1 blocked rat neuronal L-type, but no other types of HVA Cav channels, and failed to modulate LVA Cav channel currents. Using neuroendocrine GH3 and GH4 cells, CSTX-1 produced a rapid voltage-independent block of L-type Cav channel currents. The concentration–response curve was biphasic in GH4 neurons and the subnanomolar IC50 values were at least 1000-fold lower than in GH3 cells. L-type Cav channel currents of skeletal muscle myoballs and other voltage-gated ion currents of rat neurons, such as INa(v) or IK(v) were not affected by CSTX-1. The high potency and selectivity of CSTX-1 for a subset of L-type channels in mammalian neurons may enable the toxin to be used as a molecular tool for the investigation of this family of Cav channels.  相似文献   

3.
大鼠背根神经节酸感受离子通道(ASICs)的药理学特性研究   总被引:1,自引:1,他引:1  
目的研究大鼠背根神经节(DRG)细胞酸感受离子通道(ASICs)的电生理学和药理学特性。方法应用全细胞膜片钳技术,在急性分散的成年大鼠DRG细胞上记录并分析由不同浓度H+(降低pH值)诱发的ASICs电流。结果在266个大鼠DRG神经元上记录到由H+诱发的3种不同类型的ASICs电流,分别为ASIC1样电流(n=66,24·8%)、ASIC2样电流(n=81,30·4%)和ASIC3样电流(n=119,44·7%)。ASIC1样电流具有快速失活成份,衰减快;ASIC2样电流具有稳态失活成份,衰减十分缓慢;而ASIC3样电流具有快速失活与稳态失活双相成份。三者均不具有整流现象。此3种电流对细胞外H+表现出不同的敏感性,H+诱发电流的pH50分别是:ASIC1-like,pH5·82;ASIC2-like,pH5·18;ASIC3-like,pH6·24。氨氯吡咪以浓度依赖性方式可逆性阻断大鼠DRG神经元的ASICs,对3种ASICs电流的抑制效应差异有显著性。其IC50分别为:ASIC1-like,19·86μmol·L-1;ASIC2-like,42·73μmol·L-1;ASIC3-like,27·91μmol·L-1。结论成年大鼠DRG神经元细胞上表达了3种不同类型的ASICs,且其在表达率、H+敏感性、失敏以及氨氯吡咪敏感性等方面差异均有显著性。  相似文献   

4.
Lacosamide (LCM) is anticonvulsant in animal models and is in phase 3 assessment for epilepsy and neuropathic pain. Here we seek to identify cellular actions for the new drug and effects on recognised target sites for anticonvulsant drugs. Radioligand binding and electrophysiology were used to study the effects of LCM at well-established mammalian targets for clinical anticonvulsants. 10 μM LCM did not bind with high affinity to a plethora of rodent, guinea pig or human receptor sites including: AMPA; Kainate; NMDA (glycine/PCP/MK801); GABAA (muscimol/benzodiazepine); GABAB; adenosine A1,2,3; 1, 2; β1, β2; M1,2,3,4,5; H1,2,3; CB1,2; D1,2,3,4,5; 5HT1A,1B,2A,2C,3,5A,6,7 and KATP. Weak displacement (25%) was evident at batrachotoxin site 2 on voltage gated Na+ channels. LCM did not inhibit neurotransmitter transport mechanisms for norepinephrine, dopamine, 5-HT or GABA, nor did it inhibit GABA transaminase. LCM at 100 μM produced a significant reduction in the incidence of excitatory postsynaptic currents (EPSC's) and inhibitory postsynaptic currents (IPSC's) in cultured cortical cells and blocked spontaneous action potentials (EC50 61 μM). LCM did not alter resting membrane potential or passive membrane properties following application of voltage ramps between −70 to +20 mV. The voltage-gated sodium channel (VGSC) blocker phenytoin potently blocked sustained repetitive firing (SRF) but, in contrast, 100 μM LCM failed to block SRF. No effect was observed on voltage-clamped Ca2+ channels (T-, L-, N- or P-type). Delayed-rectifier or A-type potassium currents were not modulated by LCM (100 μM). LCM did not mimic the effects of diazepam as an allosteric modulator of GABAA receptor currents, nor did it significantly modulate evoked excitatory neurotransmission mediated by NMDA or AMPA receptors (n ≥ 5). Evidently LCM perturbs excitability in primary cortical cultures but does not appear to do so via a high-affinity interaction with an acknowledged recognition site on a target for existing antiepileptic drugs.  相似文献   

5.
Electrophysiological investigations have previously suggested that phospholipase A2 (PLA2) neurotoxins from snake venoms increase the release of acetylcholine (Ach) at the neuromuscular junction by blocking voltage-gated K+ channels in motor nerve terminals.

We have tested some of the most potent presynaptically-acting neurotoxins from snake venoms, namely β-bungarotoxin (BuTx), taipoxin, notexin, crotoxin, ammodytoxin C and A (Amotx C & A), for effects on several types of cloned voltage-gated K+ channels (mKv1.1, rKv1.2, mKv1.3, hKv1.5 and mKv3.1) stably expressed in mammalian cell lines. By use of the whole-cell configuration of the patch clamp recording technique and concentrations of toxins greater than those required to affect acetylcholine release, these neurotoxins have been shown not to block any of these voltage-gated K+ channels. In addition, internal perfusion of the neurotoxins (100 μg/ml) into mouse B82 fibroblast cells that expressed rKv1.2 channels also did not substantially depress K+ currents. The results of this study suggest that the mechanism by which these neurotoxins increase the release of acetylcholine at the neuromuscular junction is not related to the direct blockage of voltage-activated Kv1.1, Kv1.2, Kv1.3, Kv1.5 and Kv3.1 K+ channels.  相似文献   


6.
Our previous studies revealed that interleukin-2 (IL-2) exerted peripheral antinociception that was partially mediated by μ opioid receptors. No ionic explanations of this effect have yet been reported. The present study was designed to investigate effects of IL-2 on the physiological properties of capsaicin-sensitive small dorsal root ganglion (DRG) neurons, which are predominantly responsible for nociceptive transmission from the periphery to the spinal cord. Intracellualr recordings of DRG neurons were made in DRG/peripheral nerve preparation in vitro. IL-2 (103 U/ml) produced membrane hyperpolarization of –9.4 ± 3.0 mV and this effect was blocked by β-FNA (5 μM), a μ opioid receptor antagonist. Under whole-cell patch clamp recordings, transient high-threshold Ca2+ currents were inhibited by –56.6 ± 11.3% by IL-2. Simultaneous calcium imaging showed that this cytokine also inhibited depolarization-evoked increase in intracellular calcium concentration. All the effects of IL-2 were blocked by naloxone (1 μM). Consistent with previous studies, DAMGO, a selective μ opioid agonist, exerted similar inhibitory effects on membrane potentials and Ca2+ currents.

The present results indicated that μ opioid receptors were involved in the regulatory effects of IL-2 on membrane potentials and calcium channels in DRG neurons, which may contribute to IL-2-induced peripheral analgesia.  相似文献   


7.
The diuretic amiloride has been suggested as a specific inhibitor of T-type neuronal Ca2+ channels. The effects of amiloride on glutamate receptor-gated cationic channels and glutamate-induced, Ca2+-dependent neuronal death were investigated in primary neuronal cultures from neonatal rats. In primary cultures of cerebellar granule neurons of the rat, receiving 50 μM glutamate for 15 min, at 22°C, in the absence of Mg2+, about 80% of neurons were killed in about 24 hr. Exposure of neurons to such a pulse of glutamate, in the presence of various concentrations of amiloride, resulted in a dose-dependent protection from neurotoxicity (EC50 300 μM, complete protection 1 mM). In voltage-clamped cortical and cerebellar neurons of neonatal rats in primary culture, 100 μM amiloride diminished (by about 25%) glutamate- and/or NMDA-evoked cationic currents, recorded in the whole-cell mode. About 80% of the NMDA- (20 μM) stimulated current was inhibited by 700 μM amiloride. The inhibitory effect of amiloride was not voltage-dependent. In outside-out membrane patches, excised from granule cells and held at −50 mV, 100 μM amiloride changed the NMDA-elicited single channel activity into a fast flickering between the open and closed states. The noise analysis of the data revealed that, although resembling the Mg2+-induced flickering, the amiloride-induced channel block was more similar to the effects described for the action of local anaesthetics on the nicotinic cholinergic channel. The pharmacological relevance of this action of amiloride requires further characterization; the data point out the necessity of a cautious use of amiloride in studying neuronal function.  相似文献   

8.
9.
In this study, we pharmacologically characterized gambierol, a marine polycyclic ether toxin which is produced by the dinoflagellate Gambierdiscus toxicus. Besides several other polycyclic ether toxins like ciguatoxins, this scarcely studied toxin is one of the compounds that may be responsible for ciguatera fish poisoning (CFP). Unfortunately, the biological target(s) that underlies CFP is still partly unknown. Today, ciguatoxins are described to specifically activate voltage-gated sodium channels by interacting with their receptor site 5. But some dispute about the role of gambierol in the CFP story shows up: some describe voltage-gated sodium channels as the target, while others pinpoint voltage-gated potassium channels as targets. Since gambierol was never tested on isolated ion channels before, it was subjected in this work to extensive screening on a panel of 17 ion channels: nine cloned voltage-gated ion channels (mammalian Nav1.1–Nav1.8 and insect Para) and eight cloned voltage-gated potassium channels (mammalian Kv1.1–Kv1.6, hERG and insect ShakerIR) expressed in Xenopus laevis oocytes using two-electrode voltage-clamp technique. All tested sodium channel subtypes are insensitive to gambierol concentrations up to 10 μM. In contrast, Kv1.2 is the most sensitive voltage-gated potassium channel subtype with almost full block (>97%) and an half maximal inhibitory concentration (IC50) of 34.5 nM. To the best of our knowledge, this is the first study where the selectivity of gambierol is tested on isolated voltage-gated ion channels. Therefore, these results lead to a better understanding of gambierol and its possible role in CFP and they may also be useful in the development of more effective treatments.  相似文献   

10.
The whole cell variant of the patch clamp technique was used to investigate the actions of the polyamine amide spider toxin, argiotoxin-636, on the excitability of cultured dorsal root ganglion neurones. Synthesized argiotoxin-636 (0.1–100 μM) reduced neuronal excitability when applied to the extracellular environment by low pressure ejection or to the intracellular environment via the patch pipette solution. The toxin prolonged the duration of evoked action potentials and reduced the peak amplitude of action potentials. Intracellular and extracellular application of argiotoxin-636 also decreased the number of action potentials evoked in response to 800-ms depolarizing current commands. This action of the toxin was mimicked by 100 μM tetraethylammonium. Extracellular application of argiotoxin-636 inhibited voltage-activated K+ currents in a dose-dependent manner over the complete voltage range. This inhibition occurred without any significant changes in the voltage dependence of activation or inactivation. Intracellular application of argiotoxin-636, during 5–10 min of whole cell recording, also inhibited voltage-activated K+ currents without changing the voltage dependence of activation or steady-state inactivation. Extracellular or intracellular spermidine (250 μM) reversibly attenuated the inhibitory actions of extracellular argiotoxin-636. Argiotoxin-636 also inhibited voltage-activated Na+ currents; this effect was dependent on repeated activation of the currents and the period during which the neurones were in culture. We conclude that application of argiotoxin-636 to either the extracellular or intracellular environment reduced excitability of cultured sensory neurones from neonatal rats and that this involved inhibition of both voltage-activated K+ and Na+ currents. The data suggest that the toxin was more effective at attenuating action potentials when neurones were repeatedly excited, and that access to inhibitory sites of action on the voltage-activated ion channels can be achieved from the inside of the neurone.  相似文献   

11.
The molecular basis of mechanosensation in sensory neurons has yet to be defined. We found that ND-C cells, a hybrid cell line derived from neonatal rat DRG neurons, express mechanosensitive ion channels, and provide a useful expression system for testing candidate mechanosensitive ion channels. ND-C cells retain some important features of DRG neurons such as the expression of TTX-sensitive Na+ and acid-activated currents as well as the ability to respond to mechanical stimulation with cationic currents sensitive to the analgesic peptide NMB1. ND-C cells do not respond to agonists of the ‘thermoTRP’ channels, suggesting that these channels are not responsible for MA currents in these cells and DRG neurons. Furthermore, transfecting ND-C cells with the candidate mechanotransducer channel TRPA1 does not increase MA current amplitudes, despite TRPA1 being functionally expressed at the plasma membrane. This correlates well with the fact that all types of MA currents can be recorded from TRPA1-negative DRG neurons.  相似文献   

12.

BACKGROUND AND PURPOSE

Sinomenine (SN), a bioactive alkaloid, has been utilized clinically to treat rheumatoid arthritis in China. Our preliminary experiments indicated that it could protect PC12 cells from oxygen-glucose deprivation-reperfusion (OGD-R), we thus investigated the possible effects of SN on cerebral ischaemia and the related mechanism.

EXPERIMENTAL APPROACH

Middle cerebral artery occlusion in rats was used as an animal model of ischaemic stroke in vivo. The mechanisms of the effects of SN were investigated in vitro using whole-cell patch-clamp recording, calcium imaging in PC12 cells and rat cortical neurons subjected to OGD-R.

KEY RESULTS

Pretreatment with SN (10 and 30 mg·kg−1, i.p.) significantly decreased brain infarction and the overactivation of calcium-mediated events in rats subjected to 2 h ischaemia followed by 24 h reperfusion. Extracellular application of SN inhibited the currents mediated by acid-sensing ion channel 1a and L-type voltage-gated calcium channels, in the rat cultured neurons, in a concentration-dependent manner. These inhibitory effects contribute to the neuroprotection of SN against OGD-R and extracellular acidosis-induced cytotoxicity. More importantly, administration of SN (30 mg·kg−1, i.p.) at 1 and 2 h after cerebral ischaemia also decreased brain infarction and improved functional recovery.

CONCLUSION AND IMPLICATIONS

SN exerts potent protective effects against ischaemic brain injury when administered before ischaemia or even after the injury. The inhibitory effects of SN on acid-sensing ion channel 1a and L-type calcium channels are involved in this neuroprotection.  相似文献   

13.

BACKGROUND AND PURPOSE

Celecoxib is a selective cyclooxygenase-2 (COX-2) inhibitor used for the treatment of pain and inflammation. Emerging and accumulating evidence suggests that celecoxib can affect cellular targets other than COX, such as ion channels. In this study, we characterized the effects of celecoxib on Kv7 K+ channels and compared its effects with the well-established Kv7 channel opener retigabine.

EXPERIMENTAL APPROACH

A perforated whole-cell patch technique was used to record Kv7currents expressed in HEK 293 cells and M-type currents from rat superior cervical ganglion neurons.

KEY RESULTS

Celecoxib enhanced Kv7.2–7.4, Kv7.2/7.3 and Kv7.3/7.5 currents but inhibited Kv7.1 and Kv7.1/KCNE1 currents and these effects were concentration dependent. The IC50 value for inhibition of Kv7.1 channels was approximately 4 µM and the EC50 values for activation of Kv7.2–7.4, Kv7.2/Kv7.3 and Kv7.3/Kv7.5 channels were approximately 2–5 µM. The effects of celecoxib were manifested by increasing current amplitudes, shifting the voltage-dependent activation curve in a more negative direction and slowing the deactivation of Kv7 currents. 2,5-Dimethyl-celecoxib, a celecoxib analogue devoid of COX inhibition activity, has similar but greater effects on Kv7currents. Kv7.2(A235T) and Kv7.2(W236L) mutant channels, which have greatly attenuated responses to retigabine, showed a reversed response to celecoxib, from activation to inhibition.

CONCLUSIONS AND IMPLICATIONS

These results suggest that Kv7 channels are targets of celecoxib action and provide new mechanistic evidence for understanding the effects of celecoxib. They also provide a new approach to developing Kv7 modulators and for studying the structure–function relationship of Kv7 channels.  相似文献   

14.
Cibacron blue allosterically modulates the rat P2X4 receptor   总被引:1,自引:0,他引:1  
We have used whole-cell patch clamp electrophysiology to characterise the actions of the P2 antagonist, cibacron blue, on the rat recombinant P2X4 receptor, stably expressed in human embryonic kidney 293 (HEK293) cells. In single cells, adenosine triphosphate (ATP) evoked inward currents, but the response was subject to considerable run down which precluded obtaining quantitative data. However, when recordings were made from cells that were part of a group of 20–40 electrically coupled cells (cell rafts), run-down of current was not observed and reproducible responses could be obtained. When studied using cell rafts, cibacron blue was a weak antagonist of the rat P2X4 receptor (IC50>300 μM) when co-applied with ATP. However, when cell rafts were preincubated with low concentrations of cibacron blue (3–30 μM) for 5 min prior to ATP addition, cibacron blue increased responses to ATP by increasing its potency (up to 4-fold) without affecting the maximum current. Potentiation of ATP-evoked currents was also observed following washout of high, inhibitory concentrations of cibacron blue (300 μM). In contrast to these effects on P2X4 receptors, cibacron blue inhibited the ATP-induced response in both single cells and rafts of HEK293 cells expressing the P2X2 receptor (IC50600–800 nM). The effects of cibacron blue on the P2X4 receptor were quantitatively similar to those of Zn2+ which also increased ATP-evoked currents by decreasing the EC50 of ATP (up to 3.5-fold). These data are consistent with the concept that cibacron blue, like zinc, allosterically regulates the function of the P2X4 receptor.  相似文献   

15.
在非洲爪蟾培养的胚胎神经元和骨骼肌细胞上, 本文采用细胞膜片钳技术, 研究新型抗胆碱能药物盐酸戊乙奎醚(PHC)及其4种光学异构体对骨骼肌细胞N受体离子通道的作用. 结果表明PHC可阻断神经肌肉接头乙酰胆碱传递; 其4种光学异构体与之相比在对抗强度上无明显差别. PHC优先阻断开放时间长、电流强度大的N受体通道. 此外, PHC及其4种光学异构体对钠和钾离子通道也具有一定强度的阻断作用.  相似文献   

16.
在非洲爪蟾培养的胚胎神经元和骨骼肌细胞上,本文采用细胞膜片钳技术,研究新型抗胆碱能药物盐酸戊乙奎醚(PHC)及其4种光学异构体对骨骼肌细胞N受体离子通道的作用.结果表明PHC可阻断神经肌肉接头乙酰胆碱传递;其4种光学异构体与之相比在对抗强度上无明显差别.PHC优先阻断开放时间长、电流强度大的N受体通道.此外,PHC及其4种光学异构体对钠和钾离子通道也具有一定强度的阻断作用  相似文献   

17.

BACKGROUND AND PURPOSE

In spite of its widespread clinical application, there is little information on the cellular cardiac effects of the antidiabetic drug rosiglitazone in larger experimental animals. In the present study therefore concentration-dependent effects of rosiglitazone on action potential morphology and the underlying ion currents were studied in dog hearts.

EXPERIMENTAL APPROACH

Standard microelectrode techniques, conventional whole cell patch clamp and action potential voltage clamp techniques were applied in enzymatically dispersed ventricular cells from dog hearts.

KEY RESULTS

At concentrations ≥10 µM rosiglitazone decreased the amplitude of phase-1 repolarization, reduced the maximum velocity of depolarization and caused depression of the plateau potential. These effects developed rapidly and were readily reversible upon washout. Rosiglitazone suppressed several transmembrane ion currents, concentration-dependently, under conventional voltage clamp conditions and altered their kinetic properties. The EC50 value for this inhibition was 25.2 ± 2.7 µM for the transient outward K+ current (Ito), 72.3 ± 9.3 µM for the rapid delayed rectifier K+ current (IKr) and 82.5 ± 9.4 µM for the L-type Ca2+ current (ICa) with Hill coefficients close to unity. The inward rectifier K+ current (IK1) was not affected by rosiglitazone up to concentrations of 100 µM. Suppression of Ito, IKr, and ICa was confirmed also under action potential voltage clamp conditions.

CONCLUSIONS AND IMPLICATIONS

Alterations in the densities and kinetic properties of ion currents may carry serious pro-arrhythmic risk in case of overdose with rosiglitazone, especially in patients having multiple cardiovascular risk factors, like elderly diabetic patients.

LINKED ARTICLE

This article is commented on by Hancox, pp. 496–498 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476-5381.2011.01281.x  相似文献   

18.
P. Fan  F. F. Weight 《Neuropharmacology》1994,33(12):1573-1579
Previous studies have shown that local anesthetics block voltage-dependent Na+ channels and nicotinic acetylcholine receptors. The present study investigated the effect of the local anesthetic, procaine on another ligand-gated ion channel, the 5-HT3 receptor, in rat nodose ganglion neurons. Procaine (0.01–100 μM) inhibited the 5-HT3 receptor-mediated inward current in the whole-cell patch clamp recording. The inhibition was fully reversible, concentration-dependent but not sensitive to changes in membrane potential. Concentration-response curves indicated that procaine appears to produce a competitive inhibition on 5-HT3 receptors with a KD of 1.7 μM. These observations suggest that one of the actions of procaine in nervous system is on 5-HT3 receptors.  相似文献   

19.
目的 研究 2, 3 二甲基 2 丁胺衍生物对大脑皮层神经细胞钾通道的影响。方法 在原代培养的新生大鼠大脑皮层神经元细胞上,用细胞膜片钳全细胞记录技术,评价新衍生物对神经元IA及IK电流的影响。结果 在评价的 9个新化合物中,化合物(5) (6) (7) (9)不影响皮层神经元细胞上钾通道的活性, 化合物 ( 4 ) ( 8 )能降低皮层神经元IK电流, 这 6个化合物均可激活血管平滑肌钾通道; 另一方面,其余 3个化合物对血管平滑肌钾通道功能无明显影响,但其中的化合物 (3)可降低神经元上的IK电流。结论 2, 3 二甲基 2 丁胺衍生物对脑神经细胞上钾通道的作用不同于其在血管平滑肌上钾通道的作用特点。  相似文献   

20.
Aim: Metergoline is an ergot-derived psychoactive drug that acts as a ligand for serotonin and dopamine receptors. The aim of this study was to investigate the regulatory effects of metergoline on the neuronal Nav1.2 voltage-dependent Na^+ channels in vitro. Methods: Xenopus oocytes were injected with cRNAs encoding rat brain Nav1.2 α and β1 subunits. Voltage-activated Na^+ currents were recorded using two-electrode voltage clamp technique. Drugs were applied though perfusion. Results: Both metergoline and lidocaine reversibly and concentration-dependently inhibited the peak of Na^+ currents with IC50 values of 3.6±4.2 and 916.9±98.8 μmol/L, respectively. Metergoline (3 pmol/L) caused a 6.8±1.2 mV depolarizing shift of the steady-state activation curve of the Na^+ currents, and did not alter the inactivation curve. In contrast, lidocaine (3 μmol/L) caused a 12.7±1.2 mV hyperpolarizing shift of the inactivation curve of the Na^+ currents without changing the steady-state activation curve. Both metergoline and lidocaine produced tonic and use-dependent inhibition on the peak of Na^+ currents. Conclusion: Metergoline exerts potent inhibition on the activity of neuronal Nav1.2 channels, which may contribute to its actions on the central nervous system.  相似文献   

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