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A. Monfardini,
C. Arnaboldi,
C. Brofferio,
S. Capelli,
F. Capozzi,
O. Cremonesi,
C. Enss,
E. Fiorini, A. Fleischmann,
L. Foggetta, [......],
M. Pedretti,
D. Pergolesi,
G. Pessina,
F.S. Porter,
M. Prest,
E. Previtali,
P. Repetto,
M. Ribeiro-Gomez,
S. Sangiorgio,
M. Sisti
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ABSTRACT: Neutrino oscillation experiments have proved that neutrinos are massive particles, but cannot determine their absolute mass scale. Therefore the neutrino mass is still an open question in elementary particle physics. An international collaboration is growing around the project of Microcalorimeter Arrays for a Rhenium Experiment (MARE) for directly measuring the neutrino mass with a sensitivity of about 0.2 eV/c2. Many groups are joining their experiences and technical expertise in a common effort towards this challenging experiment. We discuss the different scenarios and the impact of MARE as a complement of KATRIN.
Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment. 09/2005;
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ABSTRACT: Recently, a method for transcranial magnetic stimulation (TMS) of the brain has been developed. Thus, it is possible to explore neurochemical and behavioral effects of TMS in rats. Repeated TMS (9 days) reduced beta-adrenergic receptor binding in cortex, as does electroconvulsive shock (ECS) and other antidepressant treatments. Thus TMS appears to be a potential antidepressive treatment.
Acta Neurovegetativa 02/1996; 103(11):1361-6. · 2.73 Impact Factor
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ABSTRACT: Magnetic stimulation of the brain in unanesthetized humans and animals can painlessly induce motor movements and has recently been reported to have antidepressant properties. In behavioral models of depression and electroconvulsive therapy including enhancement of apormorphine-induced stereotypy, reduction of immobility in the Porsolt swim test and increases in seizure threshold for subsequent stimulation, magnetic stimulation of rat brain had effects similar to those of electroconvulsive shock.
Brain Research 12/1995; 699(1):130-2. · 2.73 Impact Factor
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ABSTRACT: The effect of GABA receptor agonists on release in vitro of radiolabeled GABA and glutamate was studied using a crude preparation of isolated nerve terminals (neurosomes). GABA agonists were incubated (2 min, 37 degrees C) with neurosomes prepared from hypothalamus, preoptic area (POA) and frontal cortex tissues. Under these conditions, GABA and the GABAA receptor agonist muscimol, but not the GABAB receptor agonist baclofen, stimulated 3H-GABA and 3H-glutamate release from POA but not hypothalamic or cortical neurosomes of gonadally intact male rats. These effects were inhibited by the GABAA receptor antagonists picrotoxin, bicuculline and SR-95531. Significant efflux of 3H-glutamate could be elicited from cortical neurosomes following longer (5 min) incubations with 500 microM GABA and 400 microM muscimol. Muscimol-induced release of 3H-glutamate and 3H-GABA was dependent on extracellular calcium. Muscimol and GABA failed to release 3H-GABA or 3H-glutamate from POA neurosomes of ovariectomized female rats. However, administration of estradiol and progesterone to ovariectomized females prior to sacrifice caused the appearance of muscimol induced-release of amino acids from POA neurosomes comparable to that obtained in male rats. GABA-induced release of 3H-glutamate was similarly dependent on pretreatment of ovariectomized rats with ovarian steroids. GABAA receptor-induced release of amino acids is therefore brain region-specific and modified by hormonal status.
Life Sciences 02/1995; 56(20):1665-78. · 2.53 Impact Factor
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ABSTRACT: Noxious pinch to the scruff of the neck using a metal clip produces profound immobility and analgesia. Noxious pinch delivered to the tail fails to induce immobility and results in nociceptive behavior directed at the pinched tail. However, when administered shortly after neck-clip removal, noxious tail-pinch reinstated immobility without any nociceptive response. Prior neck-clip also enhanced the antinociception induced by the tail-pinch as measured by nociceptive response to a leg pinch. Immobility, as well as antinociception, decreased as the time interval between neck-clip removal and the tail-pinch application increased. Pharmacological manipulations which reduce nociception produced a similar alteration in the response to tail-pinch. Thus, following local injections antinociceptive doses of lidocaine to the base of the tail and systemic morphine administration tail-pinch produced marked immobility. Transection of the brain at the intercollicular level provides evidence for supraspinal involvement in post-neck pinch effects. Not only was the ability of prior neck-pinch to confer antinociceptive properties on tail-pinch abolished, but increased responsiveness to noxious tail-pinch was seen. We, therefore, propose that prior neck-pinch confers new stimulus properties on noxious pinch of other body regions resulting in an enhanced antinociceptive effect, which affects both remote regions and the site of stimulation, and the ability to induce immobility.
Brain Research 02/1993; 601(1-2):28-33. · 2.73 Impact Factor
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ABSTRACT: Treatment of ovariectomized rats in vivo with ovarian steroids has been found to influence the efflux of glutamate and gamma-aminobutyric acid from preoptic area synaptosomes incubated in vitro. Since these studies indicated a possible role of the glutamate carrier in steroid-modulated release of amino acids, the present studies examined the characteristics of efflux of glutamate and of the carrier system for glutamate in synaptosomes of the preoptic area derived from ovariectomized hormone-treated rats. The efflux of [3H]glutamate from preoptic area synaptosomes, was induced by glutamate and by the glutamate carrier agonist, D-aspartate; the putative glutamate carrier antagonist dihydrokainate failed to block this efflux. Dihydrokainate inhibited the uptake of glutamate but it was less effective than D-aspartate. The excitatory amino acid receptor agonists, N-methyl-D-aspartate and kainate were without effect while quisqualate modestly stimulated the efflux of [3H]glutamate. Efflux of [3H]glutamate, induced by glutamate itself or by D-aspartate was not blocked by the excitatory amino acid receptor antagonists, D-2-amino-5-phosphonovaleric acid, 6,7-dinitroquinoxaline-2,3-dione or kynurenate. Glutamate-induced efflux of [3H]glutamate did not require external Ca2+. Glutamate altered neither the basal nor the potassium-induced increases in the intrasynaptosomal concentration of Ca2+ as measured by the fura-2 method. Glutamate-induced efflux of [3H]glutamate was blocked by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. It is concluded that the glutamate-induced efflux of [3H]glutamate in synaptosomes of the preoptic area is a carrier-mediated process that does not require activation of receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
Neuropharmacology 12/1992; 31(11):1171-8. · 4.81 Impact Factor
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ABSTRACT: Treatment of ovariectomized rats with both estradiol and progesterone in vivo resulted in a marked enhancement of glutamate-induced release of newly synthesized [3H]gamma-aminobutyric acid (GABA) from synaptosomes of the preoptic area in vitro. With this treatment, as little as 0.01 nM glutamate, in vitro, enhanced release of GABA. In contrast, glutamate, in vitro, did not stimulate release of GABA from synaptosomes, obtained from rats treated with either estradiol or progesterone alone and only large concentrations of glutamate (1.0 and 10 mM) caused a modest release of GABA from synaptosomes from ovariectomized, vehicle-treated rats. Also, treatment with estradiol plus progesterone did not alter glutamate-induced release or exchange of [3H]glutamate. Glutamate-induced release of GABA was calcium-independent and attenuated by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-DL-disulfonic acid. Thus, glutamate-induced, steroid-enhanced release of GABA may occur through a chloride-dependent carrier rather than by exocytosis. In addition to enhancement by glutamate, release of GABA was also enhanced by D-aspartate, an agent that is transported by the neuronal glutamate carrier. It is postulated that enhancement of glutamate-induced release of GABA, by estradiol plus progesterone in the preoptic area, represents one process by which these steroids modulate reproductive function in female rats.
Neuropharmacology 09/1992; 31(8):799-807. · 4.81 Impact Factor
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ABSTRACT: MK-801 and dextrorphan, selective non-competitive antagonists at N-methyl-D-aspartate (NMDA) receptors, were used to evaluate the effect of NMDA receptor blockade on sexual and motor behaviors in female rats. Ovariectomized rats were treated with estradiol benzoate (EB) for 48 or 72 h followed by progesterone (P) 3.5-4 h before testing the animals for sexual receptivity. After testing for estrous responsiveness, the effect of NMDA antagonists on several motor behaviors was also assessed. Lordosis frequency and intensity were inhibited in animals that received 0.5 mg/kg MK-801 30 min before EB; the same dose of MK-801 was relatively ineffective when administered 24 h after EB. In neither case did MK-801-treated females differ from controls when motor behaviors were assessed after mating tests. When 30 mg/kg dextrorphan, a short-acting NMDA antagonist, was administered 15 min before P, sexual behavior was not blocked. However, both 0.05 mg/kg MK-801 and 30 mg/kg dextrorphan suppressed ongoing female sexual behavior within 30 min in animals made receptive with EB and P. These deficits in sexual behavior were associated with changes in motor performance. MK-801 (0.1 mg/kg) and dextrorphan (30 mg/kg) abolished movement in the vertical dimension (e.g. jumping and rearing). By contrast, the drugs increased movement in the longitudinal (locomotion) and lateral (circling) dimensions. At 0.2 mg/kg, MK-801 blocked movement in both the vertical and longitudinal dimensions; however, it failed to block circling. Only at 0.4 mg/kg did MK-801 inhibit lateral movements and righting reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain Research 01/1992; 568(1-2):138-46. · 2.73 Impact Factor
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ABSTRACT: In vivo treatment of ovariectomized rats with estradiol benzoate plus progesterone, but not with either steroid alone, produced a large increase in veratridine-induced release of radiolabeled glutamate and newly synthesized GABA from preoptic area synaptosomes in vitro. Neither basal nor KCl-evoked release of amino acids was altered. Thus gonadal steroids appear to be involved in the control of amino acid neurotransmitter release in a brain region of importance for regulation of female reproductive physiology and behavior.
Brain Research 02/1990; 507(1):161-3. · 2.73 Impact Factor
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ABSTRACT: Pinch of the nape of the neck, of mice, with a serrated clip, produces immobility and lack of responsiveness to noxious stimulation. In this study we attempted to determine whether clip application produces true blockade of nociception, independent of its immobilizing effect, and examined the level of the neuroaxis at which such an effect takes place. To this end nociception was measured using indices not requiring a motor response. Neck pinch eliminated the elevation of heart rate induced by noxious pinch of the tail without affecting heart rate by itself providing evidence for its analgesic effect. Direct evidence that neck pinch suppresses the transmission of noxious information is also provided. Neck pinch inhibits neural activity evoked by noxious peripheral stimulation while exerting minimal effects on the effects of nonnoxious stimuli. Thus, sensory evoked activity in the periaqueductal gray area, elicited by noxious electrical stimulation, but not innocuous stimuli, is inhibited by neck pinch. Similarly, neck pinch inhibits the response of spinal cord neurons to noxious but not nonnoxious stimulation. It, therefore, appears that neck pinch produces true analgesia by activating supraspinal systems which in turn acts to inhibit the transmission of nociception both at spinal and supraspinal levels.
Physiology & Behavior 09/1989; 46(2):151-7. · 2.87 Impact Factor
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ABSTRACT: Noxious pinch of the neck and the base of the tail can produce equipotent analgesia as measured by the tail flick method. However, noxious stimulation of the neck can suppress pain responsiveness both at the site of stimulation and at sites remote from the stimulated area while noxious stimulation of the tail produces analgesia only at sites remote from the stimulated area. Thus, neck pinched animals are immobile and completely unresponsive to the noxious pinch whereas pinch to the base of the tail, which results in tail flick suppression, causes vocalization and well organized biting behavior directed at the pinched area. The analgesia elicited by noxious stimulation applied to both body regions is eliminated by spinalization, the administration of intermediate doses of barbiturates (30 and 45 mg/kg) and transection at the midcollicular, but not more rostral, brain level. Concurrent with the elimination of the analgesic effect of noxious pinch on tail flick is the emergence of responses to noxious neck pinch with vocalization and intense motor reactions now elicited by noxious stimulation of the nape of the neck. These results indicate that different analgesic systems are activated by noxious tail and neck pinch both requiring the integrity of mesencephalic structures for their normal function. Furthermore, these systems can be distinguished by their ability to produce recurrent, inhibitory, supraspinal effects on nociceptive information originating at different body regions.
Brain Research 08/1988; 455(1):49-57. · 2.73 Impact Factor
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ABSTRACT: A pinch to the nape of the neck of mice, by application of a noxious clip, produces analgesia and immobility. Because both opiate and dopaminergic systems are usually implicated in analgesia and immobility, the pharmacological profile of clip-induced effects was compared to those elicited by the dopamine antagonist haloperidol, and by morphine. In addition, the effects of a series of pharmacological agents on clip-induced effects was examined. Haloperidol, but not morphine, produced immobility similar to that seen after application of the clip to the neck. Application of clip completely inhibited righting in all tests utilized. Haloperidol inhibited righting in all tests, except for inversion from a supine position. Righting from this position could also be inhibited in mice treated with haloperidol when a mild pinch, ineffective in a naive animal, was applied. Clip-induced immobility, but not analgesia, was reversed by amphetamine. Administration of the cholinergic antagonist scopolamine, but not methylscopolamine, reversed both the analgesia and immobility. Pinch-induced analgesia was as marked as that elicited by morphine but could not be reversed by the opiate antagonist naloxone. It is proposed that pinch-induced immobility is mediated by both dopaminergic and cholinergic systems. Additional unidentified systems are also involved. Analgesia, induced by a noxious pinch, can be dissociated pharmacologically from the immobilizing effect, is non-opiate in nature, and involves activation of central cholinergic synapses.
Neuropharmacology 07/1988; 27(6):641-8. · 4.81 Impact Factor
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ABSTRACT: In the present study we have attempted to characterize, in mice, a situation which appears to simulate real life predation and elicits simultaneous analgesia and immobility. We utilized pinch produced by clip application to various regions of the body and examined its effect on responsiveness to noxious stimuli and motor behavior. Intense noxious clip was applied to the nape of the neck, back and base of the tail. The area most effective for the elicitation of both clip induced analgesia and immobility was the nape of the neck while tail pinch resulted in analgesia but not immobility. Evidence is provided that different systems are responsible for clip induced immobility and analgesia. Temporal dissociation of clip induced analgesia and immobility could be demonstrated with continuous clip application for 30 min showing a different time course for the analgesic and immobilizing effects. Different stimuli were effective in eliciting clip induced analgesia and immobility with noxious stimuli essential for the induction of clip induced analgesia and innocuous stimuli sufficient for clip induced immobility. Thus, low analgesic doses of local anesthetics injected into the nape of the neck prevented noxious clip from inducing analgesia but immobility was still evident. In contrast, nonnoxious pinch to the nape of the neck elicited immobility but not analgesia and clip induced immobility could still be induced after the administration of high doses of morphine which completely blocked responses to noxious stimuli. These results demonstrate that in a situation resembling natural predation both analgesia and immobility are produced concurrently but that these behavioral phenomena can be elicited differentially and may be mediated by different independent systems.
Physiology & Behavior 02/1988; 44(1):39-45. · 2.87 Impact Factor
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ABSTRACT: Until now there have been only a few attempts to use many scattering angles simultaneously in triple-axis spectrometry with neutrons. We present a novel Multi-Analyzer Detector (MAD) unit for a Triple-Axis Spectrometer (TAS) set up at the Forschungsreaktor München (FRM). The layout is based on the principle of monochromatic defocusing. Up to 61 analyzers are mounted around the sample in the constant final energy mode. This arrangement supplies the flexibility of a TAS with a multi-channel analyzer capacity similar to a Time-of-Flight Spectrometer. The gain in measurement time can be more than an order of magnitude.
Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment.
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ABSTRACT: Treatment of ovariectomized rats with both estradiol and progesterone in vivo resulted in a marked enhancement of glutamate-induced release of newly synthesized [3H]γ-aminobutyric acid (GABA) from synaptosomes of the preoptic area in vitro. With this treatment, as little as 0.01 mM glutamate, in vitro, enhanced release of GABA. In contrast, glutamate, in vitro, did not stimulate release of GABA from synaptosomes, obtained from rats treated with either estradiol or progesterone alone and only large concentrations of glutamate (1.0 and 10 mM) caused a modest release of GABA from synaptosomes from ovariectomized, vehicle-treated rats. Also, treatment with estradiol plus progesterone did not alter glutamate-induced release or exchange of [3H]glutamate. Glutamate-induced release of GABA was calcium-independent and attenuated by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2, 2'-dl-disulfonic acid. Thus, glutamate-induced, steroid-enhanced release of GABA may occur through a chloride-dependent carrier rather than by exocytosis. In addition to enhancement by glutamate, release of GABA was also enhanced by d-aspartate, an agent that is transported by the neuronal glutamate carrier. It is postulated that enhancement of glutamate-induced release of GABA, by estradiol plus progesterone in the preoptic area, represents one process by which these steroids modulate reproductive function in female rats.
Neuropharmacology.
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E. Andreotti,
C. Arnaboldi,
P. de Bernardis,
J. Beyer,
C. Brofferio,
M. Calvo,
S. Capelli,
O. Cremonesi,
C. Enss,
E. Fiorini, [......],
G. Pessina,
S. Petcov,
F.S. Porter,
M. Prest,
E. Previtali,
P. Repetto,
M. Ribeiro-Gomez,
S. Sangiorgio,
D. Schaeffer,
M. Sisti
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ABSTRACT: We describe and discuss the features of MARE, an experiment based on arrays of rhenium low temperature microcalorimeters that have the potential to bring the sensitivity to the neutrino mass down to 0.2 eV, by studying the beta spectrum of (Q-value = 2.47 keV).
Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment.
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ABSTRACT: Treatment of ovariectomized rats in vivo with ovarian steroids has been found to influence the efflux of glutamate and γ-aminobutyric acid from preoptic area synaptosomes incubated in vitro. Since these studies indicated a possible role of the glutamate carrier in steroid-modulated release of amino acids, the present studies examined the characteristics of efflux of glutamate and of the carrier system for glutamate in synaptosomes of the preoptic area derived from ovariectomized hormone-treated rats. The efflux of [3H]glutamate from preoptic area synaptosomes, was induced by glutamate and by the glutamate carrier agonist, d-aspartate; the putative glutamate carrier antagonist dihydrokainate failed to block this efflux. Dihydrokainate inhibited the uptake of glutamate but it was less effective than d-aspartate. The excitatory amino acid receptor agonists, and kainate were without effect while quisqualate modestly stimulated the efflux of [3H]glutamate. Efflux of [3H]glutamate, induced by glutamate itself or by d-aspartate was not blocked by the excitatory amino acid receptor antagonists, d-2-amino-5-phosphonovaleric acid, 6,7-dinitroquinoxaline-2,3-dione or kynurenate. Glutamate-induced efflux of [3H]glutamate did not require external Ca2+. Glutamate altered neither the basal nor the potassium-induced increases in the intrasynaptosomal concentration of Ca2+ as measured by the fura-2 method. Glutamate-induced efflux of [3H]glutamate was blocked by the putative chloride channel antagonist, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. It is concluded that the glutamate-induced efflux of [3H]glutamate in synaptosomes of the preoptic area is a carrier-mediated process that does not require activation of receptors. Furthermore, the glutamate carrier involved is atypical, in that chloride ion transport may be coupled to glutamate transport.
Neuropharmacology.
