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1.
Calcium: is it required for transmitter secretion? 总被引：7，自引：0，他引：7
Ethanol multiplies miniature end-plate potential frequency independently of calcium ion concentrations and also multiplies calcium-dependent depolarization-evoked quantal release, to the same extent. This result implies a final common pathway, requiring little or no calcium, for both kinds of transmitter secretion. Chlorpromazine and hypertonicity act similarly to ethanol, but also depress depolarization-secretion coupling. 相似文献
2.
Wihtin 5 days after the leg nerves of a cockroach are injured, miniature end-plate potentials have disappeared. and the muscle is unresponsive to electrical stimulation. The soma of the injured neutron has a dense perinuclear ring of RNA. By 40 days after the injury, locomotor activity has returned, and the miniature end-plate potentials and evoked electrical responses have reappeared in the muscle. The RNA ring has disappeared, and the nucleus of the regenerating neuron has shifted to an eccentric position. 相似文献
3.
In a variety of vertebrates and invertebrates, long-lasting enhancement of synaptic transmission contributes to the storage of memory lasting one or more days. However, it has not been demonstrated directly whether this increase in synaptic transmission is caused by an enhancement of transmitter release or an increase in the sensitivity of the postsynaptic receptors. These possibilities can be distinguished by a quantal analysis in which the size of the miniature excitatory postsynaptic potential released spontaneously from the presynaptic terminal is used as a reference. By means of microcultures, in which single sensory and motor neurons of Aplysia were plated together, miniature excitatory postsynaptic potentials attributable to the spontaneous release of single transmitter quanta from individual presynaptic neurons were recorded and used to analyze long-term facilitation induced by repeated applications of 5-hydroxytryptamine. The results indicate that the facilitation is caused by an increase in the number of transmitter quanta released by the presynaptic neuron. 相似文献
4.
Coggan JS Bartol TM Esquenazi E Stiles JR Lamont S Martone ME Berg DK Ellisman MH Sejnowski TJ 《Science (New York, N.Y.)》2005,309(5733):446-451
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
5.
Voltage-dependent potassium ion (K+) channels (Kv channels) conduct K+ ions across the cell membrane in response to changes in the membrane voltage, thereby regulating neuronal excitability by modulating the shape and frequency of action potentials. Here we report the crystal structure, at a resolution of 2.9 angstroms, of a mammalian Kv channel, Kv1.2, which is a member of the Shaker K+ channel family. This structure is in complex with an oxido-reductase beta subunit of the kind that can regulate mammalian Kv channels in their native cell environment. The activation gate of the pore is open. Large side portals communicate between the pore and the cytoplasm. Electrostatic properties of the side portals and positions of the T1 domain and beta subunit are consistent with electrophysiological studies of inactivation gating and with the possibility of K+ channel regulation by the beta subunit. 相似文献
6.
The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials. 相似文献
7.
Berkefeld H Sailer CA Bildl W Rohde V Thumfart JO Eble S Klugbauer N Reisinger E Bischofberger J Oliver D Knaus HG Schulte U Fakler B 《Science (New York, N.Y.)》2006,314(5799):615-620
Large-conductance calcium- and voltage-activated potassium channels (BKCa) are dually activated by membrane depolarization and elevation of cytosolic calcium ions (Ca2+). Under normal cellular conditions, BKCa channel activation requires Ca2+ concentrations that typically occur in close proximity to Ca2+ sources. We show that BKCa channels affinity-purified from rat brain are assembled into macromolecular complexes with the voltage-gated calcium channels Cav1.2 (L-type), Cav2.1 (P/Q-type), and Cav2.2 (N-type). Heterologously expressed BKCa-Cav complexes reconstitute a functional "Ca2+ nanodomain" where Ca2+ influx through the Cav channel activates BKCa in the physiological voltage range with submillisecond kinetics. Complex formation with distinct Cav channels enables BKCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system. 相似文献
8.
Improved liquid ion-exchanger microelectrodes made possible the observation of large, rapid decreases in the concentration of extracellular calcium ions during single epileptic spikes. Moreover, in definite cortical layers the decreases regularly started shortly before the onset of each epileptic spike. In view of the prominent role played by extracellular calcium ions in neuronal processes, including transmitter release and membrane excitability, these alterations probably exert a profound influence on the cellular events underlying epileptiform activity. 相似文献
9.
Neuronal death induced by activating N-methyl-D-aspartate (NMDA) receptors has been linked to Ca2+ and Na+ influx through associated channels. Whole-cell recording from cultured mouse cortical neurons revealed a NMDA-evoked outward current, INMDA-K, carried by K+ efflux at membrane potentials positive to -86 millivolts. Cortical neurons exposed to NMDA in medium containing reduced Na+ and Ca2+ (as found in ischemic brain tissue) lost substantial intracellular K+ and underwent apoptosis. Both K+ loss and apoptosis were attenuated by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked. Thus NMDA receptor-mediated K+ efflux may contribute to neuronal apoptosis after brain ischemia. 相似文献
10.
The earliest known response of eggs to sperm in many species is a change in egg membrane potential. However, for no species is it known what components of the sperm cause the opening of the egg plasma membrane channels. Protein isolated from sperm acrosomal granules of the marine worm Urechis caused electrical responses in oocytes with the same form, amplitude, and ion dependence as the fertilization potentials induced by living sperm. Sperm initiated fertilization potentials in oocytes when sperm-oocyte fusion, but not binding, was inhibited by clamping oocyte membrane potentials to positive values. Acrosomal protein also initiated electrical responses in clamped oocytes. These results support the hypothesis that it is the sperm acrosomal protein that opens ion channels in the oocyte membrane. 相似文献
11.
Modulation of calcium channels in cardiac and neuronal cells by an endogenous peptide 总被引：8，自引：0，他引：8
Calcium channels mediate the generation of action potentials, pacemaking, excitation-contraction coupling, and secretion and signal integration in muscle, secretory, and neuronal cells. The physiological regulation of the L-type calcium channel is thought to be mediated primarily by guanine nucleotide-binding proteins (G proteins). A low molecular weight endogenous peptide has been isolated and purified from rat brain. This peptide regulates up and down the cardiac and neuronal calcium channels, respectively. In cardiac myocytes, the peptide-induced enhancement of the L-type calcium current had a slow onset (half-time approximately 75 seconds), occurred via a G protein-independent mechanism, and could not be inhibited by alpha 1-adrenergic, beta-adrenergic, or angiotensin II blockers. In neuronal cells, on the other hand, the negative effect had a rapid onset (half-time less than 500 milliseconds) and was observed on both T-type and L-type calcium channels. 相似文献
12.
Transmission between pairs of hippocampal slice neurons: quantal levels, oscillations, and LTP 总被引：3，自引：0，他引：3
R Malinow 《Science (New York, N.Y.)》1991,252(5006):722-724
Long-term potentiation (LTP) of synaptic transmission after coincident pre- and postsynaptic activity is considered a cellular model of changes underlying learning and memory. In intact tissue, LTP has been observed only between populations of neurons, making analysis of mechanisms difficult. Transmission between individual pre- and postsynaptic hippocampal cells was studied, suggesting quantal amplitude distributions with little variability in quantal size. LTP between such pairs is manifested by large, persistent, and synapse-specific potentiation with a shift in amplitude distribution that suggests presynaptic changes. Oscillations in amplitude of transmission, apparently of presynaptic origin, are common and can be triggered by LTP. 相似文献
13.
Bacterial endotoxin increases the frequency of miniature excitatory postsynaptic potentials, decreases facilitation, and increases the evoked excitatory postsynaptic potential without changing membrane resistance. These data indicate that endotoxin acts on the presynaptic nerve terminal by increasing the amount of transmitter substance released in response to an applied stimulus. 相似文献
14.
Quisqualate activates a rapidly inactivating high conductance ionic channel in hippocampal neurons 总被引：12，自引：0，他引：12
Glutamate activates a number of different receptor-channel complexes, each of which may contribute to generation of excitatory postsynaptic potentials in the mammalian central nervous system. The rapid application of the selective glutamate agonist, quisqualate, activates a large rapidly inactivating current (3 to 8 milliseconds), which is mediated by a neuronal ionic channel with high unitary conductance (35 picosiemens). The current through this channel shows pharmacologic characteristics similar to those observed for the fast excitatory postsynaptic current (EPSC); it reverses near 0 millivolts and shows no significant voltage dependence. The amplitude of the current through this channel is many times larger than that through the other non-NMDA (N-methyl-D-aspartate) channels. These results suggest that this high-conductance quisqualate-activated channel may mediate the fast EPSC in the mammalian central nervous system. 相似文献
15.
Identification of an intracellular peptide segment involved in sodium channel inactivation 总被引：25，自引：0，他引：25
Antibodies directed against a conserved intracellular segment of the sodium channel alpha subunit slow the inactivation of sodium channels in rat muscle cells. Of four site-directed antibodies tested, only antibodies against the short intracellular segment between homologous transmembrane domains III and IV slowed inactivation, and their effects were blocked by the corresponding peptide antigen. No effects on the voltage dependence of sodium channel activation or of steady-state inactivation were observed, but the rate of onset of the antibody effect and the extent of slowing of inactivation were voltage-dependent. Antibody binding was more rapid at negative potentials, at which sodium channels are not inactivated; antibody-induced slowing of inactivation was greater during depolarizations to more positive membrane potentials. The peptide segment recognized by this antibody appears to participate directly in rapid sodium channel inactivation during large depolarizations and to undergo a conformational change that reduces its accessibility to antibodies as the channel inactivates. 相似文献
16.
Although ion channels have been detected in mitochondria, scientists have not been able to record ion transport in mitochondria of intact cells. A variation of the patch clamp technique was used to record ion channel activity from intracellular organelles in the presynaptic terminal of the squid. Electron microscopy indicated that mitochondria are numerous in this terminal and are the only organelles compatible with the tips of the pipettes. Before synaptic stimulation, channel activity was infrequent and its conductance was small, although large conductances ( approximately 0.5 to 2.5 nanosiemens) could be detected occasionally. During a train of action potentials, the conductance of the mitochondrial membrane increased up to 60-fold. The conductance increased after a delay of several hundred milliseconds and continued to increase after stimulation had stopped. Recovery occurred over tens of seconds. 相似文献
17.
The molecular basis of neuronal excitability 总被引：25，自引：0，他引：25
W A Catterall 《Science (New York, N.Y.)》1984,223(4637):653-661
Neurons process and transmit information in the form of electrical signals. Their electrical excitability is due to the presence of voltage-sensitive ion channels in the neuronal plasma membrane. In recent years, the voltage-sensitive sodium channel of mammalian brain has become the first of these important neuronal components to be studied at the molecular level. This article describes the distribution of sodium channels among the functional compartments of the neuron and reviews work leading to the identification, purification, and characterization of this membrane glycoprotein. 相似文献
18.
1990: annus mirabilis of potassium channels 总被引：17，自引：0，他引：17
C Miller 《Science (New York, N.Y.)》1991,252(5010):1092-1096
Voltage-gated potassium channels make up a large molecular family of integral membrane proteins that are fundamentally involved in the generation of bioelectric signals such as nerve impulses. These proteins span the cell membrane, forming potassium-selective pores that are rapidly switched open or closed by changes in membrane voltage. After the cloning of the first potassium channel over 3 years ago, recombinant DNA manipulation of potassium channel genes is now leading to a molecular understanding of potassium channel behavior. During the past year, functional domains responsible for channel gating and potassium selectivity have been identified, and detailed structural pictures underlying these functions are beginning to emerge. 相似文献
19.
Voltage-dependent calcium channels in glial cells 总被引：16，自引：0，他引：16
B A MacVicar 《Science (New York, N.Y.)》1984,226(4680):1345-1347
The electrophysiological properties of glial cells were examined in primary culture in the presence of tetraethylammonium and Ba2+, a treatment that reduces K+ permeability of the membrane and enhances currents through voltage-dependent Ca2+ channels. Under these conditions, glial cells showed both spontaneous action potentials and action potentials evoked by the injections of current. These responses appear to represent entry of Ba2+ through Ca2+ channels because they were resistant to tetrodotoxin but were blocked by Mn2+ or Cd2+. 相似文献
20.
Development of two types of calcium channels in cultured mammalian hippocampal neurons 总被引：16，自引：0，他引：16
Calcium influx through voltage-gated membrane channels plays a crucial role in a variety of neuronal processes, including long-term potentiation and epileptogenesis in the mammalian cortex. Recent studies indicate that calcium channels in some cell types are heterogeneous. This heterogeneity has now been shown for calcium channels in mammalian cortical neurons. When dissociated embryonic hippocampal neurons from rat were grown in culture they first had only low voltage-activated, fully inactivating somatic calcium channels. These channels were metabolically stable and conducted calcium better than barium. Appearing later in conjunction with neurite outgrowth and eventually predominating in the dendrites, were high voltage-activated, slowly inactivating calcium channels. These were metabolically labile and more selective to barium than to calcium. Both types of calcium currents were reduced by classical calcium channel antagonists, but the low voltage-activated channels were more strongly blocked by the anticonvulsant drug phenytoin. These findings demonstrate the development and coexistence of two distinct types of calcium channels in mammalian cortical neurons. 相似文献