[Prosthetic solutions with osseointegrated implants].
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Dental Implantation, Endosseous↗
Biomedical subjects
M Galvan
Publications and source records attributed to M Galvan.
Interaction of telenzepine with muscarinic receptors in mammalian sympathetic ganglia.
The interaction of the antimuscarinic drug telenzepine with muscarinic receptors was studied in rabbit and rat isolated superior cervical sympathetic ganglia. Radioligand binding demonstrated two muscarinic receptor sites in rabbit ganglia, with the characteristics of M1- and M2-receptors. Telenzepine bound to the M1 sites with a KI of 0.94 nmol/l and to the M2 sites with a KI of 17.8 nmol/l; the corresponding values for pirenzepine were 18.6 and 588 nmol/l; for AF-DX 116 the values were 891 and 33 nmol/l respectively. [3H]Telenzepine dissociated from the M1-receptors with a half time of 46 min at 37 degrees C. Electrophysiological experiments demonstrated that telenzepine reduced the amplitude of the extracellularly recorded slow excitatory postsynaptic potential and the slow inhibitory postsynaptic potential (ED50: 38 and 253 nmol/l respectively). In rat ganglia, application of muscarine or the M1-receptor agonist McN-A-343 increased the amplitude of submaximal population action potentials. This facilitation of synaptic transmission was potently blocked by telenzepine and pirenzepine but only weakly by AF-DX 116 (ED50: ca. 30, 150 and 20 mumol/l, respectively). It is concluded that telenzepine blocks the generation of the slow excitatory postsynaptic potential and the excitatory action of muscarine and McN-A-343 via an action on muscarinic M1-receptors.
Animals↗
Modulation of synaptic transmission in autonomic ganglia mediated via the activation of postganglionic muscarinic M1 receptors.
The facilitatory actions of muscarine on synaptic transmission were measured in rat superior cervical ganglia in vitro. Muscarine (300 nmol/l) induced increases in submaximal population action potentials, which were mimicked by the M1 receptor agonist McN-A-343 (1 mumol/l) and antagonized by the M1 receptor antagonist pirenzepine (100 nmol/l) and telenzepine (100 nmol/l), but not by the M2 receptor antagonist AF-DX 116 (1 mumol/l). Slow excitatory postsynaptic potentials recorded from curarized rabbit isolated superior cervical ganglia were also blocked by telenzepine (300 nmol/l) but not by AF-DX 116 (3 mumol/l). It is concluded that M1 receptors mediate the excitatory actions of muscarinic agonists in these sympathetic ganglia.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
Actions of MPTP and MPP+ on synaptic transmission in guinea-pig hippocampal slices.
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) causes a Parkinson's disease-like syndrome in man, monkeys, and mice. We studied the effects of MPTP and its metabolite, MPP+, on neuronal properties and synaptic transmission in isolated slices of guinea-pig hippocampus using intra- and extracellular recording methods. Addition of MPTP to the superfusate (50 to 100 microM) produced the following effects: Excitatory postsynaptic potentials and extracellularly recorded population spikes, evoked by stimulation of the Schaffer collaterals were increased in amplitude during the application period (30 min). Within 30 min of washing in normal solution, synaptic transmission was blocked, although axonal population action potentials could still be elicited. The block of synaptic transmission was prevented by prior incubation in pargyline, an inhibitor of monoamine oxidase. The membrane potential and resistance of single pyramidal neurons were virtually unaffected; action potentials elicited by depolarizing intracellular current pulses were also unchanged. MPP+ (50 microM) blocked synaptic transmission during the application period by a pargyline-in-sensitive mechanism. These results suggest that MPP+ blocks synaptic transmission in the hippocampus at a presynaptic site. This effect may be relevant for the acute action of MPTP and may provide some insight into its chronic action on nigrostriatal neurons.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Long-term potentiation in guinea pig hippocampal slices monitored by optical recording of neuronal activity.
Pre- and postsynaptic potential changes evoked by stimulation of the Schaffer collateral-commissural input to CA1 pyramidal neurons were optically recorded in guinea pig hippocampal slices after staining the preparation with a suitable voltage-sensitive fluorescent dye. Brief tetanic stimulation induced long-term potentiation of synaptic transmission as monitored both optically and electrically. The results demonstrate that non-invasive optical techniques can be used to study long-term changes in spatial neuronal interactions, possibly involved in learning and other higher functions of the nervous system.
Animals↗
[Proposal of a new cavity for amalgam].
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Dental Amalgam↗
Calcium-dependent action potentials and associated inward currents in guinea-pig neocortical neurons in vitro.
Calcium-dependent potential changes and inward currents were studied in guinea-pig neocortical neurons maintained in vitro. Under conditions of reduced outward potassium current, induced by external application of tetraethylammonium ions or internal application of caesium ions, regenerative Ca2+-dependent action potentials could be elicited. Strontium and barium ions could substitute for calcium as the charge carrier but not magnesium; cadmium blocked the calcium spikes. In caesium-loaded neurons, in the presence of tetrodotoxin and tetraethylammonium, inward currents were recorded when the membrane potential was step-depolarized to potentials more positive than -50 mV. These currents were blocked by cadmium. It is concluded that guinea-pig neocortical neurons are capable of generating a calcium action potential via the activation of a slow inward current.
Action Potentials↗
Voltage-dependent currents of vertebrate neurons and their role in membrane excitability.
This chapter reviews what is known of the voltage-dependent conductances of three classes of vertebrate nerve cell, as assessed by somatic voltage clamping. These classes are: (1) bullfrog paravertebral sympathetic ganglion cells; (2) rodent superior cervical sympathetic ganglion cells; and (3) rodent hippocampal pyramidal cells. Of these, bullfrog neurons are the most thoroughly characterized. They possess at least seven distinct voltage-activated conductances. Two of these, called GNa and GCa, carry inward, depolarizing current. They both activate rapidly, and can, under appropriate conditions, generate action potentials. The remaining five conductances are all potassium-mediated, and can thus in principle produce hyperpolarizations or repolarize the action potential. However, because each of these potassium conductances have different sizes, speeds, and voltage thresholds, they play a variety of hyperpolarizing, stabilizing, or braking roles. IC is large, fast, and voltage dependent. Action potentials trigger calcium influx, which rapidly turns on IC. This repolarizes the action potential and turns off IC. However another Ca-dependent current, IAHP, remains active even at negative potentials and leads to a prolonged hyperpolarization. If IC is blocked, spike repolarization slows somewhat, allowing the Hodgkin-Huxley delayed rectifier current IK to develop. This is also large enough to repolarize the spike rapidly, although it is normally preempted by IC. IA and IM are other small potassium currents that activate at more negative potentials than do IC, IK, and IAHP. IA is a transient outward current that mainly influences voltage trajectories following hyperpolarizing current pulses. IM activates progressively during prolonged depolarizing current pulses, and, together with IAHP, explains most of the adaptation seen in these cells. The harmonious counterpoint of this septet of currents explains most of the electrical excitability properties of these cells. However, several of the currents are also synaptically regulated, as a result of transmitters acting on muscarinic or peptide receptors. These slow synaptic actions can lead to dramatic changes in the electrical behavior of the cells. These currents all appear to be present in rat sympathetic ganglion cells also, although detailed analysis here has been hampered by the more complex geometry of these neurons. Furthermore, the roles of the various currents have not been completely defined. It seems possible that IA can contribute to spike repolarization, and clean separation of IC and IAHP has not yet been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Kindling-like stimulus patterns induce epileptiform discharges in the guinea pig in vitro hippocampus.
In the guinea pig in vitro hippocampal slice preparation, we have demonstrated that the repeated tetanic stimulation of the Schaffer collateral-commissural input to CA1 pyramidal neurones produces a progressive increase in the amplitude and duration of postsynaptic potentials, and stimulus-induced and spontaneous paroxysmal depolarization shifts (PDSs). Both the enhancement of synaptic transmission and the genesis of PDSs were reversibly blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist (+/-)-2-amino-5-phosphonovalerate (APV). These results provide evidence that progressive, stimulation-induced long-term potentiation may serve as the trigger for kindling-induced epileptogenesis, and this process is dependent on the repeated activation of an APV-sensitive receptor.
2-Amino-5-phosphonovalerate↗
Spontaneous inhibitory postsynaptic potentials in guinea pig neocortex and olfactory cortex neurones.
The membrane potential of olfactory cortex and neocortex neurones in vitro was recorded using conventional microelectrode techniques. During recordings with KCl- or CsCl-filled microelectrodes, spontaneous, subthreshold, transient membrane depolarizations were observed. These were abolished by the GABAA-receptor antagonist, bicuculline methiodide, and were prolonged by the barbiturate pentobarbitone. In most cells they were abolished by tetrodotoxin. It is concluded that these spontaneous depolarizations are inhibitory postsynaptic potentials arising from spontaneous activity in inhibitory interneurones.
Animals↗
Calcium-dependent action potentials in guinea-pig olfactory cortex neurones.
Ca2+-dependent action potentials were recorded in guinea pig olfactory neurones in vitro (23 degrees--25 degrees C). In most cells (in the presence of tetrodotoxin: TTX) the current-voltage relationship displayed 'anomalous' rectification (apparent high slope resistance) at potentials approximately 20 mV depolarized to the resting membrane potential (approximately -80 mV) and strong outward rectification at more positive potentials. Intracellular Cs+-loading blocked outward rectification and increased action potential duration. Such spikes were TTX-insensitive and were further prolonged by external addition of tetraethylammonium (TEA) or Ba2+. Spikes recorded from Cs+-loaded, TTX/TEA-treated neurones displayed a prolonged plateau and an after-depolarization. They persisted when Ba2+ or Sr2+ were substituted for external Ca2+, but not when Mg2+ was the sole extracellular divalent cation. The spikes were blocked in the presence of Cd2+ but persisted when 82% of the extracellular Na+ was substituted by choline. A TTX-insensitive, slowly inactivating inward current at depolarized potentials is believed to account for the subthreshold 'anomalous' rectification and prolonged spike plateau.
Acetates↗
Calcium-dependent inward currents in voltage-clamped guinea-pig olfactory cortex neurones.
Guinea-pig olfactory cortex neurones in vitro (23 degrees C--25 degrees C) were voltage clamped by means of a single microelectrode sample-and-hold technique. In most Cs+-loaded neurones (in the presence of tetrodotoxin), membrane depolarization beyond -60 mV elicited inward currents, which had rapid activation kinetics. The steady-state current-voltage relationship was N-shaped with a region of negative slope conductance between - 50 mV and - 20 mV. The rate of inactivation varied according to the holding potential and the command potential. The inward currents were maintained when external Ca2+ was replaced by Ba2+, and were blocked by Cd2+, suggesting that Ca2+ was the principal charge carrier. The results demonstrate the existence of calcium current in olfactory cortex neurones.
Animals↗
Actions of potassium channel blockers on guinea-pig lateral olfactory tract axons.
Population action potentials were recorded from the guinea-pig isolated lateral olfactory tract. At 30 degrees C, the conduction velocity of the fibres was about 4 m/s and the absolute refractory period was less than or equal to 1.5 ms. The population spike was unaffected by removal of calcium ions from the superfusate but was abolished in tetrodotoxin. Tetraethylammonium ions (10 mmol/l) had no effect on the population spike, however the following potassium channel blocking drugs increased the duration in a concentration-dependent manner (in order of decreasing potency): 3,4-diaminopyridine, 4-aminopyridine, 3-aminopyridine, sparteine, cesium ions and barium ions. In addition to a prolongation, these substances also reduced the amplitude of the conducted spike. It is concluded that the rising phase of the spike is generated by a voltage-dependent increase in sodium conductance and that an increase in potassium conductance contributes to the falling phase. The potassium channels are potently blocked by aminopyridine like drugs.
4-Aminopyridine↗
Intracellular electrolyte concentrations in rat sympathetic neurones measured with an electron microprobe.
Intracellular element concentrations were measured in rat sympathetic neurones using energy dispersive electron microprobe analysis. The resting intracellular concentrations of sodium potassium and chloride measured in ganglia maintained for about 90 min in vitro at 25 degrees C were 3, 155 and 25 mmol/kg total tissue wet weight respectively. Recalculated in mmol/l cell water, these values are 5, 196 and 32 respectively. There were no significant differences between the nuclear and cytoplasmic values of these ions. Incubation in either carbachol (180 mumol/l, 4 min) or ouabain (1 mmol/1, 60 min) significantly increased the intracellular sodium and decreased the intracellular potassium concentrations. Neither substance materially altered the intracellular chloride concentration. The data obtained are compared and contrasted to those obtained in mammalian sympathetic neurones using chemical analysis and ion-sensitive microelectrodes.
Animals↗
Outward currents in voltage-clamped rat sympathetic neurones.
Outward membrane currents were studied in neurones of the isolated rat superior cervical ganglion by using a two-micro-electrode or single-micro-electrode voltage-clamp technique. Under current clamp, depolarization elicited electrotonic potentials that displayed marked outward rectification. From negative resting potentials (-70 mV) a short latency, short duration outward rectification was observed. From more positive potentials (-40 mV) a longer latency persistent outward rectification could be demonstrated. Under voltage clamp, four distinct outward currents were observed: a delayed rectifier (IK); a transient outward current (IA); a Ca2+-activated current (IC) and the M-current (IM). The maximum amplitude of IK, IA and IC was 1-2 orders of magnitude greater than IM. Depolarizing from -40 mV to potentials more positive than -20 mV co-activated IK and IC, producing a characteristic N-shaped current voltage curve with a minimum at about +80 mV. Superfusion with Mn2+-containing solutions reduced outward current at all voltages and abolished the N-characteristic; the remaining current (IK) slowly inactivated (tau greater than 1 s). Raising [K+]o from 6 to 36 mmol/l reversed outward tail currents observed in normal solution. Addition of tetraethylammonium ions (1-3 mmol/l) strongly reduced the amplitude of IK and IC. IA was characterized by very rapid activation at potentials more positive than -60 mV and by fast and complete inactivation at potentials in the activation range. The amplitude of IA was dependent on [K+]o and was reduced by external 4-aminopyridine (1-3 mmol/l). The activation appeared to depend on the nature and concentration of divalent cations present in the superfusate. It is concluded that the soma membrane of rat sympathetic neurones, like many other vertebrate and invertebrate neurones, contains multiple populations of K+ channels. The possible functions of these in the control of ganglion cell excitability are discussed.
4-Aminopyridine↗
M-current in voltage-clamped olfactory cortex neurones.
The soma of olfactory cortex neurones in vitro was voltage-clamped by means of a single microelectrode sample-and-hold technique. In most neurones, hyperpolarizing voltage commands from relatively positive holding potentials (-40 to -50 mV) elicited a slow inward current relaxation with voltage-dependent and kinetic properties similar to the non-inactivating K+-current (M-current; IM), first described in amphibian sympathetic neurons. Deactivation of IM at negative potentials probably accounts for the slow sag of the hyperpolarizing electrotonic potential measured during current-clamp experiments. IM was inhibited by the cholinergic agonist muscarine or barium ions.
Animals↗
[Effects of 4-aminopyridine on nerve cells].
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4-Aminopyridine↗
An N-shaped current-voltage relationship in rat sympathetic neurones.
Neurones in the rat isolated superior cervical ganglion were voltage clamped using 2 independent microelectrodes. From a holding potential of -40mV, depolarizing voltage commands to potentials more positive than -20mV elicited outward currents. The current-voltage relationship displayed an N-characteristic with a minimum at +80 to +100mV. Replacement of the external Ca++ ions with Mn++ reversibly abolished a part of the total outward current. The results indicate that rat sympathetic neurones exhibit two potassium currents, a delayed rectifier current and a Ca++-dependent potassium current.
Animals↗