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F Eusebi

Publications and source records attributed to F Eusebi.

At least 109 records · Page 6Linked to original sources
PubMed1985

Post-synaptic calcium influx at the giant synapse of the squid during activation by glutamate.

Changes in free calcium were monitored in the post-synaptic axon of the giant synapse of the squid, using the calcium indicators aequorin and Arsenazo III. The peak size of the calcium-dependent optical signals recorded from aequorin and Arsenazo III both showed a linear relation with the amount of calcium injected ionophoretically into the axon, but the Arsenazo signal had a slower time course than the aequorin. Ionophoretic application of glutamate to the post-synaptic axon depolarized the axon and caused a rise in intracellular free calcium. Aequorin signals were detected in natural sea water, and their size increased when the calcium concentration in the sea water was raised. Arsenazo signals could be detected only in high-calcium (55 mM) sea water. Intracellular calcium signals were detected also during bath application of several glutamate analogues, including kainate, ibotenate, and aspartate. The peak amplitude of the intracellular calcium signal, monitored with both indicators, increased with increasing ionophoretic glutamate dose, and varied linearly with the integral of the glutamate-induced membrane depolarization. No calcium signals were detected when depolarizations, similar to those produced by glutamate, were induced by current injection in the absence of glutamate. We conclude that glutamate increases the calcium permeability of the post-synaptic membrane, independently of the glutamate-induced depolarization. The glutamate-induced depolarization and the rise in intracellular free calcium increased roughly linearly as the membrane potential was made more negative. Extrapolation of these data indicated that the glutamate depolarization would reduce to zero at about -30 mV, while the calcium signals would be suppressed at about +50 mV.

Aequorin↗
PubMed1984

Acetylcholine receptors in monkey and rabbit oocytes.

Membrane potential responses to acetylcholine (ACh, 10(-7)-10(-3 M) were investigated in monkey and rabbit ovarian oocytes. In monkey oocytes ACh most commonly elicited a short-latency hyperpolarization concomitant with a decreased membrane input resistance (Rin). Under voltage-clamp short-latency ACh currents had an equilibrium potential of approximately -40 mV. In rabbit oocytes responses to ACh consisted of an increase in Rin or of a depolarization with an equilibrium potential of approximately -15 mV. Curare, hexamethonium, and atropine (10(-5)-10(-3) M) did not block these ACh responses. Thus, the oocyte membrane in the rabbit contains ACh receptors that cannot be classified as either muscarinic or nicotinic.

Acetylcholine↗
PubMed1984

Reduced acetylcholine sensitivity in dystrophic mouse myotubes in vitro.

Acetylcholine (ACh) sensitivity in cultured myotubes from normal or dystrophic mice was investigated using conventional techniques. Dystrophic multinucleate myotubes were found to be less responsive to the ACh with respect to the control preparation. Such a reduced sensitivity to ACh in dystrophic myotubes was accompanied by a reduced binding to 125I-alpha-bungarotoxin. The possible biological significance of these results on the muscle disease is discussed.

Acetylcholine↗
PubMed1984

Acetylcholine receptors in human oocytes.

Neurotransmitter receptors have been studied by conventional electrophysiological techniques in the membrane of human ovarian oocytes isolated from ovarian fragments obtained from pre-menopausal women undergoing abdominal surgery for gynaecological conditions. Ovarian oocytes respond to acetylcholine (ACh) concentrations as low as 10(-10) M by hyperpolarizing the membrane and by concomitantly increasing input resistance, in a dose-dependent manner. The response lasts as long as the transmitter is present in the extracellular fluid. No response is elicited by ionophoretically applied ACh. The ACh response has an apparent latency of less than 1 s and a reversal potential of about -12 mV. The response to ACh (10(-8) - 10(-3) M) is unaffected by curare (10(-5) - 10(-4) g/ml) and is blocked by atropine (10(-6) - 10(-4) g/ml). This indicates that ACh receptors in the human oocyte membrane are probably muscarinic in nature. No response is elicited by the amino acids glutamate, aspartate and glycine (up to 10(-3) M), or by noradrenaline, adrenaline and 5-hydroxytryptamine (up to 10(-3) M). On the basis of analogies to the response elicited by agents which activate parthenogenetic development in the oocytes of other mammals, it is suggested that the sperm-carried ACh might be involved in activation processes triggered by sperm-egg interaction.

Acetylcholine↗
PubMed1983

Voltage oscillations in mammalian metaphase II oocytes.

The membrane potential has been measured in ovulated mouse oocytes using conventional electrophysiological techniques. Temporal oscillations in membrane voltage have been observed in the oocytes, with periods of about 6 h. This oscillatory pattern, peculiar to oocytes in metaphase II, might explain the differences in membrane potential values reported in several studies on mammalian oocytes.

Animals↗
PubMed1983

Divalent cations and temperature dependent block of impulse propagation at the frog neuromuscular junction.

End-plate potentials were recorded from superficial muscle fibers of the frog sartorius nerve-muscle preparation. Exposure of the preparation to a medium containing a high divalent cation concentration, produced a temperature dependent failure of neuromuscular transmission. Failure of transmission developed in an "all-or-none" mode and was reversed by decreasing the bath temperature or divalent cation concentration. This blockage of the neurotransmission is attributed to a presynaptic block of impulse propagation.

Animals↗
PubMed1983

An electrophysiological study of parthenogenetic activation in mammalian oocytes.

Using conventional electrophysiological techniques, we have investigated the electrical responses of mouse and hamster oocytes in metaphase of the second meiotic division to agents which induce parthenogenetic activation. Oocytes from MF1 mice responded to 8.7% ethanol and to 0.3% benzyl alcohol by a depolarization (sometimes preceded by a brief hyperpolarization). The response to ethanol did not "desensitize," and the membrane potential recovered completely when the exposure to ethanol was interrupted. The response was accompanied by a decrease in membrane input resistance (Rin) and had an equilibrium potential of about +5 mV in standard medium and of -10mV in Na-free medium. The oocytes responded to A23187 and to La3+ by an increased Rin, and usually lysed during or after treatment. Multiphasic responses were elicited by ethanol and by Ca-ionophore in metaphase II hamster oocytes; an early hyperpolarization accompanied by a decreased Rin was a common feature of the response to both activating agents. The early hyperpolarization was no longer elicited when the cells were exposed for a second time to ethanol or A23187. K+ and Cl- were the ions mainly involved in the hyperpolarizing potential elicited by A23187, and K+ (but not Cl-) was the ionic species mainly involved in ethanol response. The above responses were peculiar to metaphase II oocytes since mouse and hamster ovarian oocytes (in prophase I) and fertilized eggs either failed to respond to the activating agents, or responded by increasing Rin. The variety of electrical responses to parthenogenetic agents indicates that in mammalian oocytes parthenogenetic activation is not triggered by a "classical" activation potential.

Animals↗
PubMed1983

Intercellular communication in rat seminiferous tubules.

Intercellular electrical coupling in seminiferous tubules from prepubescent and adult Wistar rats has been studied by using conventional techniques. It is found that cells in the seminiferous epithelium are electrically coupled. Experiments performed using "Sertoli cell-enriched" seminiferous tubules indicate the existence of intercellular ionic communication between Sertoli cells. Junctional conductance is independent of the direction of electrical field and it is affected by A23187 Ca ionophore (5 microM) but not by exposure to the neurotransmitter norepinephrine (1-5 X 10(-5) M). Intracellular resistivity (including junctional resistance) is higher in mature as compared to immature germinal epithelium. These findings suggest that cell metabolites or second messenger molecules could be transferred via the low-resistance pathways between epithelium cells to coordinate cellular activity.

Aging↗
PubMed1983

Aequorin-calcium transients in frog twitch muscle fibres.

Intracellular Ca2+ transients, evoked either by action potentials or depolarizing clamp pulses, were studied in frog sartorius muscle fibres injected with aequorin. The time course of the Ca2+ transients became shorter as the temperature was increased. The half rise time and decay time constants showed straight lines between 3 and 30 degrees C in Arrhenius plots, with a Q10 of 2.5 and 2.3 respectively. The potential dependence of the Ca2+ transient was examined under voltage clamp. The peak light amplitude reached a plateau at around +50 mV, suggesting that Ca2+ release continues beyond the potential level at which contraction was saturated. During a prolonged depolarization, the Ca2+ transient gradually declined. The time course of decline became faster when long depolarizing pulses were repeated, or when the temperature was increased. The Q10 for half duration of the Ca2+ transient evoked by prolonged depolarization was 2.2. A Ca2+ transient could be evoked in Ca2+-free Ringer solution containing EGTA. Formamide, which is known to abolish excitation-contraction coupling, also abolished the Ca2+ transient. During maintained depolarization, the time integral of the Ca2+ transient was larger for larger depolarizations, suggesting that the total amount of Ca2+ released was greater for the more intense depolarization. The decline of the Ca2+ transient during maintained depolarization is probably due to inactivation of excitation-contraction coupling rather than the depletion of intracellular Ca2+ stores. These findings support the view that in frog skeletal muscle fibres the increase in intracellular Ca2+, caused by membrane depolarization, is produced by the release of Ca2+ from intracellular stores and that any influx of Ca2+ from the external medium does not contribute appreciably to the aequorin-Ca2+ transient.

Action Potentials↗
PubMed1980

Calcium transients in mammalian muscles.

Contraction of vertebrate skeletal muscle is caused by calcium ions released from the sarcoplasmic reticulum (see refs 1, 2 for reviews). The ensuing transient change in the intracellular level of ionised calcium has been monitored using various Ca2+ indicators, sich as murexide, aequorin, and arsenazo III. So far, most of what is known about these calcium transient derives from experiments on barnacle or frog muscles fibres, and it is desirable to extend such studies to mammalian muscle. We report here that the photoprotein aequorin can be used to monitor calcium transients in rat and human muscles, and that the transients decay more quickly in fast contracting muscle fibres.

Aequorin↗
PubMed1978

Kainic acid and synaptic transmission in the stellate ganglion of the squid.

Kainate, a conformational analogue of glutamate, blocks synaptic transmission across the giant synapse of the squid. In the presence of blocking doses of kainate, impulses continue to propagate into the nerve terminal, but action potentials are slightly reduced in size and the subsequent hyperpolarization is greatly diminished. Kainate depolarizes the postsynaptic axon. Since the depolarizing action of kainate is confined to the postsynaptic membrane, it appears that kainate can combine with the receptors which are normally activated by the transmitter. This results in a diminished effect of the transmitter released by a presynaptic nerve impulse.

Animals↗
PubMed1978

Action of glutamic acid and of some glutamate analogues on the molluscan central neurones.

The effects of L-glutamic acid and of some glutamate analogues have been studied on the central nervous system of the snail Heobania vermiculata, using conventional electrophysiological techniques. The glutamate H-response had the mean equilibrium value of -(57 +/- 4) mV and was associated with a Cl- conductance change. The D-response to glutamate application showed an involvement of sodium ions. Aspartate was agonist of glutamate action and displayed similar equilibrium value of the H-response, whereas quisqualate H-response was 'non-invertible'.

Animals↗