Search PubMed⌕ Search

Biomedical subjects

S Minota

Publications and source records attributed to S Minota.

At least 109 records · Page 6Linked to original sources
PubMed1983

Prolonged action potential of frog skeletal muscle membrane in Ca-free EGTA solution.

The membrane of isolated frog skeletal muscle fibers with or without T-system is depolarized to about -30 mV in a Ca-free solution containing 2 mM EGTA. Under such a condition, the action potential can be produced by a cathodal pulse when the membrane is previously hyperpolarized to -70- -100 mV by a conditioning anodal current. The action potential consists of two different potential components, namely a spike potential and a following slow depolarizing response forming a plateau phase (plateau potential). The membrane conductance during the plateau potential is increased. Both spike and plateau potentials are abolished in the absence of NaCl. TTX blocks a spike potential without affecting a plateau potential, whereas Mn and D-600 act contrarily. The i-v relation shows an anomalous rectification in Na-free solution, suggesting that the K conductance during the plateau phase is decreased. It is suggested that spike and plateau potentials are produced by a movement of sodium ions through sodium and calcium channels of the membrane, respectively.

Action Potentials↗
PubMed1982

Post-tetanic depolarization in sympathetic neurones of the guinea-pig.

1. Repetitive intracellular stimulation at a frequency of 5-30 Hz for 1-10 s evoked in neurones of the isolated inferior mesenteric and superior cervical ganglia of the guinea-pig three types of post-spike membrane potential changes: (i) hyperpolarization, (ii) hyperpolarization followed by a slow depolarization, and (iii) a second hyperpolarization following the initial two responses.2. The initial post-spike hyperpolarization had a mean duration of 2.0 s and was often associated with a fall in membrane resistance; it could be elicited in every sympathetic neurone studied. This response was termed the post-tetanic hyperpolarization (PTH).3. The slow depolarization which could be induced only in a portion of neurones had a mean amplitude and duration of 2.2 mV and 27.5 s, respectively; it was termed the post-tetanic depolarization (PTD).4. PTD was associated with a fall in membrane resistance, augmented by membrane hyperpolarization, and reduced by depolarization; its mean extrapolated equilibrium potential was -38 mV.5. PTD was not blocked by nicotinic and muscarinic antagonists, or alpha-and beta-adrenergic receptor antagonists, whereas it was suppressed by adrenaline, noradrenaline, Co(2+) and a low Ca(2+) solution.6. The amplitude of the single spike after-hyperpolarization in normal Krebs solution as well as in high K(+) solution was increased during PTD; furthermore, conditioning hyperpolarization to the level of E(K) increased the amplitude of PTD in normal Krebs as well as in high K(+) solution.7. PTD with similar amplitude, time course and membrane characteristics could be evoked in a portion of neurones of the rabbit superior cervical ganglia; however, PTD was not detected in neurones of the rat superior cervical ganglia.8. Decentralization of the guinea-pig and rabbit superior cervical ganglia for 14 d did not alter the number of neurones in which PTD could be elicited, its amplitude, or its time course.9. Our results suggest that a chemical substance(s) is responsible for the generation of PTD; it may be released from the soma and/or dendrites and acts in an auto-receptive manner on the cells in question. The nature and origin of the second hyperpolarization remain to be clarified.

Action Potentials↗
PubMed1981

Antidromic inhibition of acetylcholine release from presynaptic nerve terminals in bullfrog's sympathetic ganglia.

In isolated bullfrog's sympathetic ganglia it was examined if the release of acetylcholine (ACh) from presynaptic nerve terminals was changed when postsynaptic ganglion cells were activated antidromically. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells was found to be depressed, whereas the nicotinic ACh potential of these cells was not depressed, immediately after these ganglion cells were activated by antidromic axonal or direct intracellular stimulations. This indicates that activation of ganglion cells results in inhibiton of the release of ACh from their presynaptic nerve terminals. Such an antidromic inhibition of ACh release could not be clearly observed when preparations were perfused with Ca2+-deficient solution or when adrenaline (10(-5) M) was added to the superfusion solution. Frequency of the spontaneous miniature EPSP was also found to be decreased after antidromic activation of ganglion cells. On the basis of these results it was concluded that some kind of transmitter was released from activated ganglion cells which inhibited ACh release by acting on preganglionic nerve terminals. This putative neurotransmitter was suggested to be adrenaline.

Acetylcholine↗
PubMed1981

Substance P-induced depolarization in sympathetic neurons: not simple K-inactivation.

Ionic mechanisms underlying substance P-induced depolarization of the inferior mesenteric ganglion cells of the guinea pig were analyzed by means of microelectrode methods. When the membrane potential was manually clamped at the resting level, substance P caused, in about equal number of neurons, increases and decreases of neuronal input resistance. In the majority of the cells tested the amplitude of substance P-induced depolarization was increased when the membrane was hyperpolarized to the level of EK; it was markedly reduced in a Na+-free media. These results suggest that substance P causes depolarization by simultaneously increasing Na+ and decreasing K+ permeability.

Animals↗
PubMed1981

Effects of substance P on neurones of the inferior mesenteric ganglia of the guinea-pig.

1. The membrane effects of substance P on neurones of isolated inferior mesenteric ganglia and the underlying ionic mechanisms were investigated by means of intracellular recording techniques.2. When applied to the neurones by superfusion, substance P (0.5 mum) caused a membrane depolarization; in a few neurones, the depolarization was preceded by a small hyperpolarization. Substance P effects were not altered in a low Ca(2+)/high Mg(2+) solution or in a solution containing d-tubocurarine and atropine.3. When the membrane potential was clamped manually at the resting level between -50 and -60 mV, substance P caused, in about an equal number of neurones, a slight to moderate decrease and also increase of membrane resistance; a brief increase occurred prior to the decrease of membrane resistance.4. In neurones with high resting membrane potential (> -70 mV), substance P elicited a large depolarization accompanied by a marked increase in membrane resistance; the latter was probably due to anomalous rectification.5. Conditioning hyperpolarization of the membrane close to the level of E(K) increased and decreased substance P-induced depolarization in eleven and two neurones, respectively.6. Substitution of external Na(+) with an equimolar amount of either sucrose or Tris buffer markedly attenuated the depolarizing effect of substance P.7. The substance P-induced depolarization was diminished in a high K(+) (10 mm) solution, and it could be augmented when membrane was hyperpolarized to E(K). On the other hand, the effect of substance P was not appreciably affected in a low Cl(-) solution.8. It is concluded that substance P depolarizes the sympathetic neurones by increasing and decreasing membrane permeability to Na(+) and K(+), respectively, and that the concomitant membrane resistance change depends on interaction of G(Na) activation and G(K) inactivation.9. The possibility that substance P is the transmitter mediating the non-cholinergic slow excitatory potential elicited by repetitive preganglionic stimulation in the neurones of the inferior mesenteric ganglia is suggested.

Animals↗
PubMed1978

Recurrent synaptic activation of the bullfrog sympathetic ganglion cells by direct intracellular stimulation.

In a certain group (type 2 cells) of bullfrog sympathetic ganglion cells, an action potential exhibiting a triphasic after-potential was produced when the cells were activated by direct intracellular stimulation. This triphasic after-potential consisted of two different potential components, namely, a depolarizing response (DR) and an after-hyperpolarization. The amplitude of DR was increased by increasing the interval between stimuli. Large DRs exceeded the threshold of the cell membrane and produced repetitive firings of spike potentials. The DR was selectively depressed and eventually eliminated in a low-Ca solution. Eserine (10(-5) M) reversibly increased both the amplitude and duration of the DR, and d-tubocurarine reversibly depressed it. These results indicate that the DR of type 2 cells is the EPSP mediated by the nicotinic action of acetylcholine released from preganglionic nerve terminals. Preganglionic nerve fibers innervating type 2 cells are activated through some kind of recurrent pathway formed between them. Recurrent activation of type 2 cells seems to be thus induced when the cells are activated by direct intracellular stimulation.

Action Potentials↗
PubMed1977

Effects of adrenaline on the action potential of sympathetic ganglion cells in bullfrogs.

The effects of catecholamines (adrenaline, noradrenaline and isoproterenol) on ionic conductance changes during the generation of action potentials of bullfrog sympathetic and spinal ganglion cells were studied with intracellular microelectrodes. In sympathetic ganglion cells, adrenaline (3X10(-5)-1X10(-3)M) reversibly decreased the peak amplitude and positive after-potential of action potentials, and prolonged the duration of spike potentials without changes in the resting membrane potential and conductance in the Ringer solution. The maximum rates of rise and fall of spike potentials were also decreased. The action of noradrenaline was similar to that of adrenaline, but isoproterenol did not show any effects. Adrenaline (3X10(-5)-3X10(-4)M) markedly depressed the peak amplitude and maximum rate of rise of both TEA-potential and Ca-potential produced either in TEA solution containing TTX or in the isotonic CaCl2 solution. Similar actions were observed with noradrenaline but not isoproterenol. In spinal ganglion cells, catecholamines did not show any effects of the action potentials in Ringer and TEA solutions. It was concluded that adrenaline inhibited the increases in Ca2+, K+ and Na+ conductances during the generation of action potentials of sympathetic ganglion cells.

Action Potentials↗
PubMed1976

The actions of trimetazidine on nerve and muscle cells in frogs.

The effect of trimetazidine (TMZ) on cardiac, skeletal muscle fibres and sympathetic ganglion cells in frogs were studied. In cardiac muscles, the contraction was depressed and the duration of action potentials were shortened by 1.5 mM TMZ. In skeletal muscles, the contraction induced by motor nerve stimulations was depressed by 0.3 mM TMZ, and the amplitude of end-plate potentials was decreased under this condition. The nicotinic transmission in sympathetic ganglia was inhibited by 0.003 mM TMZ, but the muscarinic transmission was not affected by 1.5 mM TMZ. In a Na-free TEA solution, prolonged action potentials (TEA potentials) of sympathetic ganglion cell, which appeared to be produced by an inward Ca movement across the membrane, were shortened by 1.5 mM TMZ. These results suggest that TMZ has a dual action, namely 1) a blocking action of nicotinic transmissions and 2) a blocking action of Ca movement during the generation of action potentials.

Action Potentials↗