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1.
Functional nicotinic cholinergic receptors are found on mammalian retinal ganglion cell neurons in culture. The neurotransmitter acetylcholine (ACh) can be detected in the medium of many of these retinal cultures, after release presumably from the choline acetyltransferase-positive amacrine cells. The postsynaptic effect of endogenous or applied ACh on the ganglion cells can be blocked with specific nicotinic antagonists. Here it is shown that within 24 hours of producing such a pharmacologic blockade, the retinal ganglion cells begin to sprout or regenerate neuronal processes. Thus, the growth-enhancing effect of nicotinic antagonists may be due to the removal of inhibition to growth by tonic levels of ACh present in the culture medium. Since there is a spontaneous leak of ACh in the intact retina, the effects of nicotinic cholinergic drugs on process outgrowth in culture may reflect a normal control mechanism for growth or regeneration of retinal ganglion cell processes that is exerted by ACh in vivo.  相似文献   

2.
Many limb movements are composed of alternating flexions and extensions. However, the underlying spinal network mechanisms remain poorly defined. Here, we show that the intensity of synaptic excitation and inhibition in limb motoneurons varies in phase rather than out of phase during rhythmic scratchlike network activity in the turtle. Inhibition and excitation peak with the total neuron conductance during the depolarizing waves of scratch episodes. Furthermore, spike activity is driven by depolarizing synaptic transients rather than pacemaker properties. These findings show that balanced excitation and inhibition and irregular firing are fundamental motifs in certain spinal network functions.  相似文献   

3.
The temporal resolution of neuronal integration depends on the time window within which excitatory inputs summate to reach the threshold for spike generation. Here, we show that in rat hippocampal pyramidal cells this window is very narrow (less than 2 milliseconds). This narrowness results from the short delay with which disynaptic feed-forward inhibition follows monosynaptic excitation. Simultaneous somatic and dendritic recordings indicate that feed-forward inhibition is much stronger in the soma than in the dendrites, resulting in a broader integration window in the latter compartment. Thus, the subcellular partitioning of feed-forward inhibition enforces precise coincidence detection in the soma, while allowing dendrites to sum incoming activity over broader time windows.  相似文献   

4.
在室温条件下,通过固相反应合成了铜(Ⅱ)的烟酸、L-α-丙氨酸三元配合物,采用元素分析、红外光谱、紫外光谱以及X-射线粉末衍射光谱对配合物进行了表征。结果表明,烟酸脱掉羧酸上的质子以酸根的形式与铜离子配位,而吡啶环上的氮原子未参与配位,L-α-丙氨酸的氨基氮与羧基氧同时与铜离子配位。抑菌活性试验表明,该配合物对金黄色葡萄球菌、枯草芽孢杆菌、大肠杆菌、铜绿假单胞菌、嗜水气单胞菌和耶尔森氏菌都具有抑菌活性,对枯草芽孢杆菌的抑菌效果最好,配合物浓度为0.5 mmol/L时,抑菌圈直径达13.4 mm,最低抑菌浓度为0.031 25 mmol/L。  相似文献   

5.
Neurohistological and neurophysiological studies have shown that the bilaterally represented Mauthner's cells in teleosts are related both structurally and functionally. The VIIIth nerve afferents, as well as the axoaxonal collaterals, display a distribution pattern which supports the concept of polar function of the neuron. Inasmuch as it is possible to alter the staining reaction of both the Mauthner's cells by unilateral stimulation of the entering VIIIth nerve roots, it is proposed that the synaptic endings serve principally as activators and that neuronal excitation or inhibition is determined by the chemical state of the dendrites, the cell body, and the axon hillock region.  相似文献   

6.
Axons in the cerebral cortex receive synaptic input at the axon initial segment almost exclusively from gamma-aminobutyric acid-releasing (GABAergic) axo-axonic cells (AACs). The axon has the lowest threshold for action potential generation in neurons; thus, AACs are considered to be strategically placed inhibitory neurons controlling neuronal output. However, we found that AACs can depolarize pyramidal cells and can initiate stereotyped series of synaptic events in rat and human cortical networks because of a depolarized reversal potential for axonal relative to perisomatic GABAergic inputs. Excitation and signal propagation initiated by AACs is supported by the absence of the potassium chloride cotransporter 2 in the axon.  相似文献   

7.
远辉  丁春瑞  郝明明 《安徽农业科学》2012,40(34):16801-16802
[目的]研究测定新疆开心果中烟酸的含量。[方法]采用高效液相色谱法测定新疆开心果中水溶性维生素烟酸的含量,试验采用Symmetry Shield RP18(4.6 mm×250 mm×5μm)为分离柱,以10 mmol/L磷酸二氢钾为流动相,采用紫外检测器在波长266 nm下进行检测。[结果]试验得出,新疆开心果中烟酸的含量为113.1 mg/kg,表明新疆开心果中含有比较丰富的烟酸,具有较高的营养价值,适量食用开心果可有效补充人体所需的烟酸。[结论]该方法操作简单,结果准确,为新疆开心果的进一步开发应用研究提供了一定的科学依据。  相似文献   

8.
An endogenous polypeptide of rat brain has been identified that is capable of displacing 1,4-benzodiazepines and the esters of the 3-carboxylic acid derivatives of beta-carbolines from their specific synaptic binding sites. This polypeptide was termed diazepam-binding inhibitor (DBI). Previous studies have shown that DBI injected intraventricularly in rodents elicits "proconflict" responses and antagonizes the "anticonflict" action of benzodiazepines. An antiserum to this peptide, directed toward an immunodeterminant near its amino terminus, makes it possible to detect, measure, and study the neuronal location of this peptide in rat brain. In the rat cerebral cortex, DBI immunoreactivity is located in neurons that are not GABAergic (GABA, gamma-aminobutyric acid); in the cerebellum and hippocampus, however, it might be present also in GABAergic neurons.  相似文献   

9.
In rats ischemia of the forebrain induced by a 30-minute occlusion of the carotid artery, followed by 120 minutes of arterial reperfusion, produced ischemic lesions of selectively vulnerable pyramidal cells in both hippocampi. Focal microinfusion into the dorsal hippocampus of 2-amino-7-phosphonoheptanoic acid, an antagonist of excitation at the N-methyl-D-aspartate-preferring receptor, before ischemia was induced protected against the development of ischemic damage. It is proposed that excitatory neurotransmission plays an important role in selective neuronal loss due to cerebral ischemia.  相似文献   

10.
Some implications of a mathematical theory relating neuronal geometry to the parameters of excitation in unconditioned response of planarians to electric shock are experimentally verified. The regions and patterns of primary neural excitation depend on the relation between the distribution of neural sizes and the wave form of the electric stimulus.  相似文献   

11.
以烟酸与锌盐为原料,用室温固相合成方法合成烟酸锌配合物,考察了锌源、反应时间、原料配比对合成产物的影响.结果表明,最佳的合成工艺条件为:以醋酸锌为锌源,反应时间为6h,醋酸锌∶烟酸(摩尔比)=1∶2.通过摩尔电导、元素分析、红外光谱、紫外光谱以及X-射线粉末衍射光谱对所合成的配合物进行了表征.  相似文献   

12.
假定资产价格变化过程服从跳跃-扩散过程,那么基于它的欧式期权就满足一个偏积分-微分方程(PIDE),本文利用差分法来离散这个PIDE方程,用两种迭代方法得到方程的数值解:基于雅可比正则分裂法和预条件共轭梯度法.  相似文献   

13.
[目的]探讨中华蟾蜍(Bufo bufo gargarizans)胚后嗅球神经元自发电活的电生理学特性的发育变化。[方法]应用微电极电生理技术,对中华蟾蜍胚后嗅球神经元的自发放电活动进行在体胞外记录。[结果]随着嗅球的发育,其神经元的放电形式逐渐增多,单个放电振幅逐渐增大,且在变态期达最大;连续放电振幅在胚后发育的中期变化不大,但高于发育的早期和成体期;连续簇状放电频率随着发育时期而降低,但在成体期再次升高,而连续单个放电频率只在成体期增大。[结论]随着嗅球的发育,神经元的兴奋性逐步提高,神经元电活动形式逐渐呈现多样化。  相似文献   

14.
Supraoptic neurosecretory cells: adrenergic and cholinergic sensitivity   总被引:3,自引:0,他引:3  
Adrenergic and cholinergic agonists and antagonists were applied microelectrophoretically to over 700 neurons in the cat supraoptic nucleus, 20 percent of which were antidromically identified as neurosecretory cells. Norepinephrine uniformly depressed all sensitive cells. Acetylcholine caused both muscarinic depression and nicotinic excitation which were antagonized by atropine and dihydro-beta-erythroidine, respectively. These results support the hypothesis that norepinephrine and acetylcholine are directly involved in controlling the release of antidiuretic hormone.  相似文献   

15.
There are two types of inhibitory postsynaptic potentials in the cerebral cortex. Fast inhibition is mediated by ionotropic gamma-aminobutyric acid type A (GABA(A)) receptors, and slow inhibition is due to metabotropic GABA(B) receptors. Several neuron classes elicit inhibitory postsynaptic potentials through GABA(A) receptors, but possible distinct sources of slow inhibition remain unknown. We identified a class of GABAergic interneurons, the neurogliaform cells, that, in contrast to other GABA-releasing cells, elicited combined GABA(A) and GABA(B) receptor-mediated responses with single action potentials and that predominantly targeted the dendritic spines of pyramidal neurons. Slow inhibition evoked by a distinct interneuron in spatially restricted postsynaptic compartments could locally and selectively modulate cortical excitability.  相似文献   

16.
Although it is generally agreed that general anesthetics ultimately act on neuronal ion channels, there is considerable controversy over whether this occurs by direct binding to protein or secondarily by nonspecific perturbation of lipids. Very pure optical isomers of the inhalational general anesthetic isoflurane exhibited clear stereoselectivity in their effects on particularly sensitive ion channels in identified molluscan central nervous system neurons. At the human median effect dose (ED50) for general anesthesia, the (+)-isomer was about twofold more effective than the (-)-isomer both in eliciting the anesthetic-activated potassium current IK(An) and in inhibiting a current mediated by neuronal nicotinic acetylcholine receptors. For inhibiting the much less sensitive transient potassium current IA, the (-)-isomer was marginally more potent than the (+)-isomer. Both isomers were equally effective at disrupting lipid bilayers.  相似文献   

17.
Puromycin: action on neuronal mitochondria   总被引:6,自引:0,他引:6  
Puromycin, in dosages that inhibit cerebral protein synthesis and expression of memory in mice, produces swelling of neuronal mitochondria. Acetoxycycloheximide, which inhibits cerebral protein synthesis to the same extent as puromycin, fails to produce swelling of neuronal mitochondria. Puromycin and heximide mixtures produce severe inhibition of protein synthesis, but result in a minimal swelling of neuronal mitochondria and in a decrease of peptidylpuromycin complexes to a level of 30 percent of that following the injection of puromycin alone. It is concluded that swelling of neuronal mitochondria in the presence of puromycin is not due to inhibition of cerebral protein synthesis per se, but is related to a specific action of puromycin on ribosomal protein synthesis. The findings are consistent with the hypothesis that peptidyl-puromycin complexes are responsible for mitochondrial swelling.  相似文献   

18.
Thalidomide inhibits growth of some protozoa. This inhibition was counteracted by nicotinic acid, nicotinamide, nicotinamide adenine dinucleotide, and vitamin K(1). The mechanism of toxicity may be an interference of cellular oxidation. A protozoan test system is useful for studying the potential "side actions" of drugs in higher animals and man.  相似文献   

19.
Neurotransmitter release is well known to occur at specialized synaptic regions that include presynaptic active zones and postsynaptic densities. At cholinergic synapses in the chick ciliary ganglion, however, membrane formations and physiological measurements suggest that release distant from postsynaptic densities can activate the predominantly extrasynaptic alpha7 nicotinic receptor subtype. We explored such ectopic neurotransmission with a novel model synapse that combines Monte Carlo simulations with high-resolution serial electron microscopic tomography. Simulated synaptic activity is consistent with experimental recordings of miniature excitatory postsynaptic currents only when ectopic transmission is included in the model, broadening the possibilities for mechanisms of neuronal communication.  相似文献   

20.
In an investigation of the mechanism by which brain lesions result in delayed degeneration of neurons remote from the site of injury, neurons within the caudate nucleus of rats were destroyed by local injection of the excitotoxin ibotenic acid. Treatment resulted in the rapid degeneration of the striatonigral pathway including projections containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and delayed transneuronal death of neurons in the substantia nigra pars reticulata. The distribution of nigral cell loss corresponded to the loss of GABAergic terminals. Neuronal death was prevented by long-term intraventricular infusion of the GABA agonist muscimol. Delayed transneuronal degeneration may be produced by neuronal disinhibition consequent to loss of inhibitory inputs. Replacement of inhibitory transmitters by suitable drugs may prevent some forms of delayed neuronal death.  相似文献   

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