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E Puil

Publications and source records attributed to E Puil.

At least 73 records · Page 4Linked to original sources
PubMed1987

Voltage dependence of membrane properties of trigeminal root ganglion neurons.

1. Membrane potentials of trigeminal root ganglion neurons were varied systematically by intracellular injections of long-lasting step currents to determine the voltage dependence of their membrane electrical properties. The complex impedance and impedance magnitude functions were first determined using oscillatory input currents superimposed on these step currents. 2. Systematic step variations in the membrane potential led to qualitative changes in the impedance magnitude functions. Depolarization of neurons exhibiting resonance at their initial resting membrane potentials resulted in a reduction in the resonance behavior. Hyperpolarization of these neurons to membrane potentials of about -80 to -90 mV led to a disappearance of the resonant peak but increased the maximum of the impedance magnitude. 3. The complex impedance data were fitted with a neuronal model derived from linearized Hodgkin-Huxley-like equations, yielding estimates for the membrane properties. The four parameters of the model were 1) a time invariant, resting membrane conductance, Gr, 2) a voltage- and time-dependent conductance, GL, 3) a time constant, tau u, for the unknown ionic channels that are activated by the 2- to 5-mV oscillatory perturbation of the stepped membrane potential, and 4) Ci, the input capacitance. 4. The results of the curve-fitting procedures suggested that all parameters depended on membrane voltage. The most voltage-dependent parameters were GL and tau u throughout a 25- to 30-mV range that was subthreshold to the production of action potentials. Both Gr and GL increased with subthreshold depolarization. 5. These impedance data suggest the very important role of the membrane potential of the trigeminal root ganglion neurons on their abilities to synthesize and filter inputted electrical signals.

Animals↗
PubMed1987

Modifications in membrane properties of trigeminal sensory neurons during general anesthesia.

1. The effects of general anesthesia on passive and active membrane properties of trigeminal root ganglion neurons of decerebrate guinea pigs have been determined using frequency-domain analyses of small-amplitude perturbations of membrane voltage. Quantification of the effects was accomplished by fitting the complex impedance locus diagrams computed from the neuronal responses with a membrane model based on linearized Hodgkin-Huxley-like equations. 2. Endotracheal administrations of isoflurane (2-3% for periods of 30-180 s), the most extensively studied of five general anesthetics, did not elicit large changes in membrane potential or in electrical properties in 26 of the 38 neurons. In this relatively unresponsive group, application of isoflurane in higher concentrations (3-4%) tended to evoke small but significant changes (less than 20%) in membrane properties without altering membrane potential by greater than 5 mV. These changes consisted of increases in the effective input capacitance and input conductance. 3. The impedance magnitude functions were reduced in amplitude consistently in 12 of the 38 neurons during induction of general anesthesia with isoflurane (2-4%) or, in several cases, with halothane (2%). Such applications evoked depolarizations of 8-32 mV, which also were observed in several instances of anesthesia with enflurane and cyclopropane. Quantification of these effects on electrical properties by curve fitting with the linearized Hodgkin-Huxley model revealed increases in the effective input capacitance, in the time-invariant resting conductance, Gr, and in the voltage- and time-dependent conductance, GL. Sometimes, an initial decrease preceded the increase of Gr, and the relaxation time constant associated with GL usually was reduced by the anesthetic agent in the 12 neurons. 4. In 10 neurons, membrane resonance behavior (which was apparent as a large hump at low frequencies of the impedance magnitude functions) was reduced in amplitude, as well as broadened in bandwidth, when peak changes in membrane properties were evident, i.e., during surgical or deep anesthesia. These actions of isoflurane or halothane were correlated to a reduction in spike electrogenesis and they may account for the reduced tendency of neurons to fire repetitive action potentials during anesthesia with isoflurane or halothane.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, General↗
PubMed1986

Electrophysiological responses of human spinal neurons in culture.

Cell cultures were prepared from human fetal spinal cord and maintained in vitro for 30-100 days. Neurons were identified electrophysiologically by their ability to develop action potentials in response to intracellular depolarizing current pulses and in sister cultures by immunohistochemical and electron microscopic techniques. Extracellular applications of gamma-aminobutyric acid, glycine or histamine evoked hyperpolarizations which were associated with increases in membrane conductance. These data and the ultrastructural demonstrations of synapses suggest a functional differentiation of neurons in these cultures.

Action Potentials↗
PubMed1986

Quantification of membrane properties of trigeminal root ganglion neurons in guinea pigs.

Passive and active (voltage- and time-dependent) membrane properties of trigeminal root ganglion neurons of decerebrate guinea pigs have been determined using frequency-domain analyses of small-amplitude perturbations of membrane voltage. The complex impedance functions of trigeminal ganglion neurons were computed from the ratios of the fast Fourier transforms of the intracellularly recorded voltage response from the neuron and of the input current, which had a defined oscillatory waveform. The impedance magnitude functions and corresponding impedance locus diagrams were fitted with various membrane models such that the passive and active properties were quantified. The complex impedances of less than one-quarter of the 105 neurons which were investigated extensively could be described by the complex impedance function for a simple RC-electrical circuit. In such neurons, the voltage responses to constant-current pulses, using conventional bridge-balance techniques, could be fitted with single exponential curves, also suggesting passive membrane behavior. A nonlinear least-squares fit of the complex impedance function for the simple model to the experimentally observed complex impedance yielded estimates of the resistance of the electrode, and of input capacitance (range, 56 to 490 pF) and input resistance (range, 0.8 to 30 M omega) of the neurons. The majority of trigeminal ganglion neurons were characterized by a resonance in the 50- to 250-Hz bandwidth of their impedance magnitude functions. Such neurons when injected with "large" hyperpolarizing current pulses using bridge-balance techniques showed membrane voltage responses that "sagged" (time-dependent rectification). Also, repetitive firing commonly occurred with depolarizing current pulses; this characteristic of neurons with resonance in their impedance magnitude functions was not observed in neurons with "purely" passive membrane behavior. A nonlinear least-squares fit of a five-parameter impedance fitting function based on a membrane model to the impedance locus diagram of a neuron with resonance yielded estimates of its membrane properties: input capacitance, the time-invariant part of the conductance, the conductance activated by the small oscillatory input current, and the relaxation time constant for this conductance. The ranges of the estimates for input capacitance and input resistance were comparable to the ranges of corresponding properties derived for neurons exhibiting "purely" passive behavior.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Attenuation of glutamate-action, excitatory postsynaptic potentials, and spikes by intracellular QX 222 in hippocampal neurons.

The effects of intracellular applications of QX 222, a quaternary analogue of lidocaine, were investigated in CA1 neurons of in vitro hippocampal slices of guinea-pig brain. QX 222 produced a strong depression of spontaneous, electrically-(by current injection) or orthodromically-evoked action potentials. These dose-dependent effects were characterized by a reduction in the rate of rise and amplitude of spikes, presumed to be mediated by a Na+-conductance. Although resting membrane conductance tended to diminish with prolonged applications of QX 222, marked changes in resting potential generally were not observed. The threshold for eliciting spikes by intracellular injection of depolarizing current was increased greatly by QX 222, reflecting the impairment of Na+-electrogenesis of spikes. The reduction of action potential amplitude by QX 222 may be partly attributable to enhanced inactivation of Na+-channels because brief depolarizing pulses preceded by strong tonic hyperpolarization, elicited spikes at a lower threshold and of considerably larger amplitude than in the absence of such tonic hyperpolarization. These observations on recovery are compatible with a removal of sodium inactivation. However, this experimental paradigm of current injection also might be expected to remove QX 222 molecules from their blocking sites at the inner end of Na+-channels. When spikes were abolished by QX 222, the depolarization evoked with application of S-glutamate by pressure ejection from an extracellular micropipette positioned close to the neuron was attenuated. This reversible blockade was reproducible in the 14 neurons where the interactions of QX 222 and glutamate were examined systematically. Excitatory postsynaptic potentials, evoked by stimulation of strata oriens or radiatum, were reduced in a similar manner by internal QX 222. These data confirm previous observations that voltage-dependent Na+-channels mediating spike genesis in CA1 neurons can be blocked by internal QX 222. However, QX 222 also apparently interferes with the functions of Na+-channels activated by glutamate-receptor interaction or by receptor interactions with neurotransmitter(s) associated with certain excitatory postsynaptic potentials in CA1 neurons.

Action Potentials↗
PubMed1984

Impedance profiles of peripheral and central neurons.

The electrical impedance of trigeminal ganglion cells (in vivo) and hippocampal CA1 neurons (in vitro) of guinea pigs was measured in the frequency range of 5-1250 Hz using intracellular recording techniques with single microelectrodes and computerized methodology. The transfer functions of the electrode and the electrode-neuron system were computed from the ratio of fast Fourier transforms of the output voltage response from the neuron and input current composed of sine waves with rapidly increasing frequency which displaced membrane potential by 2-5 mV. We believe these to be the first measurements of complex impedance and transfer functions in peripheral and central neurons of vertebrates and the first use of such input current functions. The majority of trigeminal ganglion cells did not exhibit electrical behaviour ascribable to a simple resistance-capacitance (RC) circuit but showed a hump at low frequencies (5-250 Hz) in the computed transfer function, probably attributable to resonance. The transfer function in less than 20% of the trigeminal neurons could be fitted approximately to a theoretical transfer function (resistance in series with a parallel RC circuit model) providing values for electrode resistance, effective input resistance, and effective input capacitance. The transfer functions measured in hippocampal CA1 neurons were characterized by a rapid fall-off in the low frequency range (less than 200 Hz). Impedance locus plots approximate the locus corresponding to a series RC circuit in parallel with a parallel RC circuit.

Animals↗
PubMed1981

Ibotenic acid: its excitatory and possibly sedative actions in cerebral cortex.

A slowly developing excitation with after discharge is produced by microiontophoretic application of the racemate of ibotenic acid to pericruciate cortical neurons of cats which had been "decerebrated" by forebrain isolation during brief anesthesia. The extracellular observed excitation tended to accumulate with repeated applications. In many instances the ibotenate excitation was blocked with local administration of H2-receptor antagonists which also "'antagonized" glutamate excitation. With intracellular recording, similar iontophoretic applications of ibotenate were observed to produce longlasting depolarizations and repetitive firing which was not maintained despite suprathreshold depolarization. These actions were not accompanied by consistent changes in membrane resistance. A most striking feature of ibotenate action was to increase spontaneous synaptic activity and the amplitude of EPSP's evoked by electrical stimulation of the cortical surface or n. ventralis lateralis of the thalamus. These new data are strongly suggestive of presynaptic actions of ibotenate in the cerebral cortex although postsynaptic actions of this isoxazole presumably are also important to an understanding of how ibotenate produces its inebriating and hypnotic effects in animals and man.

Animals↗
PubMed1981

Internal cesium ions block various K conductances in spinal motoneurons.

Conventional intracellular recording with low resistance electrodes was used to examine the effects of iontophoretic injections of Cs+ ions (30-200 nA for 30-500 s) into spinal motoneurons of cats anesthetized with pentobarbital and paralyzed with gallamine. The most striking effects of internal Cs+ were a great prolongation of the falling phase of action potentials, a large reduction in the amplitude of their afterhyperpolarizations, and a considerable increase in the size of delayed depolarizations. A reduction of resting membrane conductance (up to half of control values) and a small increase in membrane potential usually were evident. Although the rate of rise and amplitude of spikes sometimes were increased, the above effects on membrane properties usually were accompanied by block of antidromic invasion or synaptic spike generation, and inactivation of directly evoked spikes. Recovery of spike genesis was very rapid but the prolongation of spikes and other effects of Cs+ lasted 4-35 min, depending on the amount of Cs+ application. Larger injections of Cs+ resulted in greater depolarizations of up to 13 mV. It is concluded that internal Cs+ ions block voltage-dependent K+ conductance of spike repolarization, the Ca2+-activated K+ conductance responsible for the afterhyperpolarization, and some of the K+ conductance responsible for the resting potential. It is suggested that the enhanced delayed depolarization may result from a Cs+-blockade of an early outward K+ current which would unmask an inward current of Ca2+ ions.

Action Potentials↗
PubMed1980

Steroid anaesthetics: inhibition of depolarization-secretion coupling at the mouse motor nerve terminal.

The coupling between nerve terminal depolarization and quantal secretion of acetylcholine at the mouse neuromuscular junction was estimated by measuring the multiplication of the frequency of miniature end-plate potentials (m.e.p.p.s) produced by increasing the concentration of calcium in the medium from 0.1 to 1.0 mM in the presence of 15 mM potassium. Depolarization-secretion coupling was inhibited by the anaesthetic steroids progesterone, pregnanedione, and alphaxalone. The nonanaesthetic steroid delta 16-alphaxalone also inhibited depolarization-secretion coupling with the same potency as alphaxalone. This results indicates that inhibition of depolarization-secretion coupling in nerve terminals is unlikely to play a major role in the production of anaesthesia.

Anesthetics↗
PubMed1979

Intracellular divalent cations and neuronal excitability.

Itracellular injections of Mg into cat spinal motoneurones have a depolarizing action, associated with a fall in input conductance, and depression of the postspike hyperpolarizing after-potential (a.h.p.) as well as its underlying conductance increase. There is also an increase in excitability, sometimes leading to outright discharge, and a change in the current-firing relation: the normal primary range is largely abolished and the firing appears to have the characteristics of the normal secondary range. Intracellular effects of Mg are thus mainly opposite to those of Ca, possibly owing to competition at sites where Ca activates K channels. Intracellular injections of Mn also tend to depress the a.h.p. but have relatively little effect on resting potential and conductance, or action potentials. Co also depresses the a.h.p. but has a more pronounced depolarizing action, and produces particularly strong depression of action potentials. By contrast intracellular Sr tends to raise the membrane conductance and has a mild hyperpolarizing effect. During the injection of Sr, a.h.p's are depressed but this is followed by a rebound of increased a.h.p. amplitude and conductance. Unlike the other divalent cations tested, Sr strongly depressed excitatory postsynaptic potentials. In most respects Sr appears to behave like Ca.

Action Potentials↗
PubMed1978

EGTA and motoneuronal after-potentials.

1. Intracellular iontophoretic injections of EGTA (5--20 nA) into cat spinal motoneurones consistently greatly reduce the amplitude of the delayed after hyperpolarization (a.h.p.) that follows the spike. 2. This effect is accompanied by a large reduction (on average by 3/4) in the marked increase in input conductance normally associated with the a.h.p. 3. There is also a consistent, though less regular, tendency for the resting input conductance to decrease (on average by 1/5), as well as some depolarization. 4. Recovery of the a.h.p., the associated conductance increase and the resting conductance is ver slow. It is sometimes accelerated by injections of citrate and Cl-, or CA2+. 5. Other hyperpolarizing phenomena, such as recurrent or othodromically-evoked i.p.s.p.s, are not depressed by injections of EGTA. 6. When depolarization is minimal EGTA injections that markedly depress the a.h.p. do not affect the rate of rise or fall of the spike. If, as a result of depolarization, an early a.h.p. is visible, it is patently insensitive to EGTA. 7. The post-spike depolarizing after-potential (delayed depolarization) is not obviously affected by EGTA, apart from the usual diminution seen during depolarization. 8. Since the main action of EGTA is to bind free Ca2+, the marked depression of the a.h.p. indicates that the sharp increase in K conductance which generates the a.h.p. is probably caused by a influx of Ca2+ accompanying the action potential. It is suggested that this inward Ca2+ current may be manifested in the depolarizing after-potential.

Action Potentials↗
PubMed1978

Significance of 2,4-dinitrophenol action on spinal motoneurones.

1. Extracellular iontophoretic applications of DNP lead to an increase in the membrane conductance of cat spinal motoneurones, manifested by a rise in input conductance, a slower rate of rise and fall of action potentials, and occlusion of the afterhyperpolarization. 2. There is also some hyperpolarization, but the reversal potential for the action of DNP is only about 12 mV more negative than the resting potential. 3. These effect of DNP can be abolished or significantly reduced by intracellular injections of EGTA. On the other hand, DNP can partly reverse the decreased conductance and the depression of the slow afterhyperpolarization caused by EGTA. 4. Intracellular injections of DNP also induce a rise in input conductance; when repeated, they tend to have a depolarizing effect, mainly irreversible. 5. It is concluded that DNP acts principally inside the motoneurone, by liberating bound internal Ca, the free Ca ions then raising membrane conductance, especially GK.

Action Potentials↗
PubMed1978

Excitation and inhibition of neurons in the trigeminal nucleus caudalis following periaqueductal gray stimulation.

Electrical stimulation (3-4 shocks, 300 Hz, 30-150 microamperemeter) of the periaqueductal gray matter (CG) or dorsal raphé nucleus (DR) of decerebrate cats reduced or abolished the jaw-opening reflex response evoked by stimulation of either the tooth pulp or infraorbital nerve. In addition, CG or DR stimulation inhibited the response of 12 out of 16 trigeminal nucleus caudalis neurons to activation of their sensory afferent inputs. Ten other neurons recorded in the same sites, and often at the same time, but which did not respond to the sensory inputs utilized, were excited by identical stimuli to CG or DR. This excitatory response was blocked by intravenously administered naloxone (0.1-0.2 mg/kg). It is suggested that those neurons which are excited by CG and DR stimulation may be interneurons involved in pre- and post-synaptic inhibition of sensory transmission during stimulus-produced or narcotic analgesia.

Animals↗
PubMed1978

Enkephalin and substance P effects related to trigeminal pain.

Iontophoretic applications of enkephalin (20-150 nA) reduced the spontaneous firing frequency of nociceptive neurons in the trigeminal nucleus caudalis of decerebrated cats. The response evoked by noxious stimulation (tooth pulp) was gradually inhibited during the 1st minute of application of the opioid and generally remained depressed for 5 min after the current was turned off. These effects of enkephalin were blocked by intravenously or iontophoretically administered naloxone. Nonnociceptive neurons or nociceptive neurons responding to nonnoxious inputs were less frequently inhibited by enkephalin. When tested on nonnociceptive cells, similar applications of substance P usually had little effect. Nociceptive neurons, however, were strongly excited by substance P. This action was not constant and was interrupted by periods of inactivation. Both types of peptide action were similar in temporal aspects. The results suggest a functional interrelationship between enkephalin and substance P in a trigeminal system mediating nociception.

Analgesics↗