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A Stefani

Publications and source records attributed to A Stefani.

85 records · Page 5Linked to original sources
PubMed1991

Developmental regulation of a slowly-inactivating potassium conductance in rat neostriatal neurons.

In late embryonic and early post-natal rat neostriatal neurons, the voltage-dependent potassium currents activated by depolarization are largely attributable to a rapidly inactivating A-current and a delayed rectifier current. Over the first 4 weeks of post-natal life, a third potassium current emerges in most cells. This slowly inactivating conductance is distinct from the A-current and delayed rectifier in voltage-dependence, kinetics and pharmacology. The properties of this conductance suggest that it may be of central importance to the integrative behavior of neostriatal neurons by controlling such features as first spike latency and interspike interval.

Animals↗
PubMed1991

GABA depolarizes neurons in the rat striatum: an in vivo study.

GABA, applied by iontophoresis to striatal neurons of the rat in an in vivo preparation, depolarized the membrane potential and decreased the input resistance in a dose-dependent manner. The null potential of the GABA depolarization was about -50 mV. In addition, a fading of the GABA-induced response was observed for prolonged and relatively high amino acid application. We conclude that GABA has a depolarizing effect on striatal cells. This is in line with recent in vitro works describing a depolarizing effect of GABA in the rat neostriatum.

Animals↗
PubMed1991

Ascorbate system in Dasypyrum villosum from different environments.

Ascorbic acid content and redox-enzymes activities of AA system are determined in four population of Dasypyrum villosum adapted to live in different environments. In D. villosum from the driest and warmest environment (Pachino), AFR reductase and AA peroxidase have activities lower than in the other populations. The results point out the role of AA peroxidase as the main "scavenger" of the H2O2 produced by cell metabolism.

Ascorbate Peroxidases↗
PubMed1990

Serotonin enhances excitability in neostriatal neurons by reducing voltage-dependent potassium currents.

The physiological effects of serotonin (5-HT) on rat neostriatal neurons were investigated using current-clamp techniques in neostriatal slices and voltage-clamp techniques in acutely dissociated adult neostriatal neurons. In most neurons (35/51), bath-applied 5-HT (10-60 microM) decreased the first spike latency and increased the evoked firing frequency. Membrane input resistance was also increased in most neurons (33/35) but could not explain the enhanced responsiveness. Tetrodotoxin, at concentrations sufficient to block spike production, did not block the ability of 5-HT to enhance the slow ramp-like voltage trajectory produced by depolarizing current injection. The role of potassium currents in the 5-HT effect was examined using whole cell voltage-clamp; in 6 of 9 neurons, 5-HT reversibly decreased inactivating potassium currents activated by depolarization. These experiments suggest that 5-HT's effect on the ramp trajectory may be mediated by a reduction of potassium currents activated by sub-threshold depolarization.

Animals↗
PubMed1990

Synaptic and intrinsic control of membrane excitability of neostriatal neurons. I. An in vivo analysis.

1. The relationship between membrane properties of neostriatal neurons and spontaneous and evoked synaptic potentials was studied with the use of intracellular recordings from anesthetized rats. Most of these neurons showed regular or irregular spontaneous depolarizing potentials that only in a few cases triggered action potentials at resting level. 2. The stimulation of the ipsilateral substantia nigra or of the sensorimotor cortex produced a relatively fast depolarizing post-synaptic potential (EPSP). In some cells this potential was followed by an inhibitory period that appeared as an hyperpolarization when the cell was depolarized from the resting level (inhibitory postsynaptic potential, IPSP). A late and long-lasting depolarization (LD) followed the EPSP or the EPSP-IPSP sequence. 3. Repetitive discharge with little adaptation was observed during direct depolarization. Most of the neurons tested for current-voltage (I-V) relationship showed nonlinearity of the input resistance in the hyperpolarizing direction. Spontaneous and evoked EPSPs were decreased in their amplitude and duration when the membrane potential was held at levels more hyperpolarized than -85 mV because of the strong rectification at these levels of hyperpolarization. 4. Local microiontophoretic application of bicuculline (BIC) or systemic administration of BIC and pentylenetetrazole (PTZ) produced a reduction of the IPSPs. The reduction of the inhibitory transmission caused a strong increase of the LD. The current-evoked firing pattern was not greatly altered. 5. The intracellular application of cesium increased the amplitude and the duration of the spontaneous depolarizations that triggered bursts of action potentials under this condition. Spikes were broadened and the rectification in the hyperpolarization direction was reduced. 6. Iontophoretically applied cadmium strongly depressed the amplitude of the spontaneous and evoked postsynaptic potentials. During cadmium application, nigral stimulation produced constant latency, all-or-none spikes in the absence of any synaptic potential. 7. Repetitive stimulation of the ipsilateral substantia nigra by electrical shocks (5 Hz, 25 s) produced a progressive and reversible decrease of the spontaneous depolarizing potentials (SDPs) and a decrease of the firing rate. In the same cells, when the train of stimulation was delivered in the ipsilateral cortex, a membrane depolarization coupled with an increase of the firing rate was observed. 8. We conclude that although synaptic circuits mediate a phasic inhibition in neostriatum, the low level of spontaneous firing of most neostriatal neurons is mainly because of the effects that membrane properties exert on the spontaneous and the evoked synaptic depolarizations in the striatum.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1989

Met- and leu-enkephalins inhibit rat cortical neurons intracellularly recorded in vivo while morphine excites them: evidence for naloxone-sensitive and naloxone-insensitive effects.

The action of enkephalin-analogues (D-ala2-D-leu5-enkephalin and D-ala2-D-met-enkephalin) and morphine, iontophoretically applied, was tested on rat cortical neurons intracellularly recorded "in vivo". Inhibition of cellular excitability of 60% of the tested cells followed the iontophoretic administration of opioid peptides. 50% of the inhibited cells were also hyperpolarized. The amplitude of membrane hyperpolarization was related to the value of the membrane potential. In 13 out of the 30 inhibited cells the change in membrane input resistance was measured; the input resistance was decreased by 30%. In 8 cells, hyperpolarized by the opioid peptides, the depolarizing postsynaptic potentials, evoked by cortical stimulation, were also reduced in amplitude. Naloxone, iontophoretically applied, reversed and/or prevented the peptide responses. On the same neurons, morphine induced a bursting pattern of spiking activity and increased the membrane input resistance: this action was naloxone-insensitive. The reported results suggest that opioid peptides and morphine activate, respectively, naloxone-sensitive and naloxone-insensitive mechanisms on the same cortical neurons, leading to different and, in some respect, opposite effects on the neuronal activity.

Animals↗
PubMed1988

Morphine induces a spontaneous and evoked bursting activity in rat cortical neurons by adding a postsynaptic active mechanism to the synaptic input: an intracellular study in vivo.

The action of morphine on spontaneous and stimulus-evoked postsynaptic potentials was investigated in rat cortical neurons recorded intracellularly in vivo. Iontophoretically applied, morphine increased supra-threshold evoked depolarizing postsynaptic potentials inducing bursts of spikes, but only slightly increased weak (subthreshold) potentials. Spontaneous excitatory postsynaptic potentials were affected in a similar way, but their frequency did not change. Inhibitory postsynaptic potentials were only subsequently modified. Membrane hyperpolarization, induced by negative current injection, counteracts the morphine-induced burst generation. We suggest that the action of this alkaloid on threshold postsynaptic events involves a voltage-dependent mechanism, which may be triggered by synaptic currents.

Action Potentials↗
PubMed1987

Intracellular studies on the dopamine-induced firing inhibition of neostriatal neurons in vitro: evidence for D1 receptor involvement.

Intracellular recordings were obtained from rat neostriatal slices. Bath-applied dopamine (1-10 microM) produced a reversible inhibition of the action potentials evoked by direct stimulation and a decrease in the amplitude of the intrastriatally evoked depolarizing postsynaptic potentials. No change in membrane potential was detected during the application of 1-10 microM dopamine. Dopamine application also produced a decrease in anomalous rectification in the depolarizing direction. This subthreshold inward rectification was abolished by tetrodotoxin, but not by calcium-free and cadmium (0.1-1 mM)-containing solutions. The dopamine-induced decrease in excitatory postsynaptic potential amplitude was evident at resting membrane potential or at more positive levels, but was absent at hyperpolarized values of the membrane potential. Addition of bicuculline (50-500 microM) to the medium did not affect the inhibitory action of dopamine. The inhibitory action of dopamine also persisted in calcium-free and cadmium-containing solutions. The adenosine 3',5'-cyclic monophosphate analogue, 8-bromo-adenosine 3',5'-cyclic monophosphate (0.1-1 mM), mimicked the effects produced by D1 receptor activation. Bath application of 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) (1-10 microM), a selective D1 dopaminergic agonist, mimicked the effects of micromolar concentrations of dopamine. The D2 dopaminergic agonists, 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline (LY 171555) and bromocriptine (both at 10 nM-10 microM), had no effects on neostriatal cells. The inhibition induced by micromolar doses of dopamine or SKF 38393 was antagonized by bath applications of R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin++ +-7-ol (SCH 23390; 0.1-10 microM), a D1-selective antagonist, but not by sulpiride (10 nM-10 microM), a D2 antagonist. We conclude that the inhibitory effect of dopamine on rat striatal neurons is postsynaptically mediated by the activation of D1 dopaminergic receptors via the reduction of a voltage-dependent tetrodotoxin-sensitive inward conductance.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1975

Small intestinal sucrase and isomaltase split the bond between glucosyl-C1 and the glycosyl oxygen.

The products of the hydrolysis of sucrose and palatinose by the sucrase-isomaltase complex from rabbit small intestine were investigated by persilylation followed by gas-liquid chromatography and mass spectrometry. If the hydrolysis is carried out in H218O, the heavy oxygen is found exclusively at the Ci of the alpha-glucopyranose formed. The 18O enrichment equals that of the incubation medium. The oxygen exchange between the monosaccharides and water is not accelerated by the sucrase-isomaltase complex. These observations show that the bond split by the sucarse and the isomaltase moiety of the complex is the one between glucosyl-Ci and the glucosyl oxygen. They agree with the mechanism proposed for these carbohydrases in the accompanying paper (Cogoli, A., and Semenza, G. (1975) J. Biol. Chem. 250, 7802-7809) involving the formation of an oxocarbonium ion.

Animals↗
PubMedDate not supplied

Clinical and electrophysiological effects of apomorphine in Parkinson's disease patients are not paralleled by amino acid release changes: a microdialysis study.

We performed a microdialysis investigation of extracellular amino acid (glutamate and GABA) concentrations during sterotaxic neurosurgery (the implantation of permanent electrodes in the internal globus pallidus (GPi) or subthalamic nucleus (STN) for deep brain stimulation in advanced Parkinson's disease (PD) patients, after prolonged therapy wash-out). Electrophysiological single unit recordings and perioperative clinical status assessments were also performed. Amino acid levels were measured in the GPi and GPe (external globus pallidus) of three PD patients and in the STN of another three PD patients. Stable basal release values of the examined amino acids were obtained within one hour. In clinical "off" state, the basal levels of GABA in the GPi were double those in the GPe in all the three patients. This finding could represent a biochemical marker for GPi target identification in PD surgery. Acute subcutaneous apomorphine administration induced electrophysiological changes and clinical amelioration but did not change amino acid concentrations. This result could be due to methodological limitations of the microdialysis technique. Alternatively, it could suggest that the clinical effects of acute apomorphine might also be mediated by direct activation of dopaminergic receptors located in the output nuclei.

Aged↗