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F Crespi

Publications and source records attributed to F Crespi.

13 recordsLinked to original sources

Isolation rearing of rats alters release of 5-hydroxytryptamine and dopamine in the frontal cortex: an in vivo electrochemical study.

The effects of rearing hooded Lister rats either in groups of seven or singly on 5-hydroxytryptamine (5-HT) and dopamine (DA) release in the frontal cortex were investigated using in vivo voltammetry together with Nafion coated carbon fibre micro-electrodes. The selective detection of basal extracellular levels of 5-HT with this technique (Peak B) was confirmed with parallel experiments using intracranial microdialysis to measure 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels in vivo. The DA voltammetric signal (Peak A) was observed in vivo only following pharmacological or electrical stimulation of DA release. Enhanced efflux of cortical DA and 5-HT in response to local application of KCl and that of 5-HT following parentelar fenfluramine were selectively detected by the association: differential pulse voltammetry (DPV)-Nafion coated microbiosensors, supporting the capability of this electrochemical method to selectively monitor release of these amine neurotransmitters in vivo and in situ. The locomotor behaviour data indicated that isolation rearing resulted in augmented locomotor activity in a novel environment. In addition, the in vivo voltammetric results showed that following KCl or fenfluramine treatment cortical 5-HT release is prolonged while that of DA is increased in rats reared in isolation when compared with socially reared rats. This imbalance between extracellular levels of DA and 5-HT recorded in the frontal cortex of rats exposed to isolated housing conditions may contribute to the behavioural differences reported between isolation and group reared rats.

Animals

In vivo selective monitoring of basal levels of cerebral dopamine using voltammetry with Nafion modified (NA-CRO) carbon fibre micro-electrodes.

The electrochemical technique of differential pulse voltammetry (DPV) with micro-biosensors has been used for a number of years to monitor in vivo and in situ changes in the extracellular concentration of cerebral ascorbic acid, as well as that of the metabolites of dopamine (DA) and serotonin (5-HT). We have recently prepared a carbon fibre micro-electrode (mCFE) which specifically pretreated and coated with Nafion (a negatively charged polymer which repels acids such as 3,4-dihydroxyphenylacetic acid (DOPAC)) allows the direct selective detection of the oxidation of DA and 5-HT in nanomolar concentration in vitro and that of extracellular basal levels of cerebral 5-HT in vivo (peak B at +240 mV). We describe here a modified version of this micro-biosensor now called NA-CRO mCFE as its active tip (30 microns in diameter) is coated with a 50/50 (v:v) mixture of Nafion and dibenzo-18-crown-6 (Aldrich). In vitro this newly reported electrode shows insensitivity to acids (e.g., DOPAC) up to 100 microns and sensitivity to 0.5-1 nM DA. In vivo, in the striatum of anaesthetised rats, a basal oxidation peak at +80 mV (peak A, on average 0.6 nA in height), which corresponds to the oxidation potential of DA in vitro, is consistently detectable with the NA-CRO mCFE (corresponding to an estimated concentration of 1.5 nM). Experiments performed in vivo in anaesthetised rats implanted in the striatum with uncoated (normal) mCFE to measure extracellular DOPAC or with NA-CRO mCFE have been performed in order to analyse the chemical nature of peak A in vivo. It is concluded that the addition of the crown-ether compound to the Nafion coat improves the sensitivity of the micro-biosensor for DA in vitro and allows the detection of its basal extracellular levels in vivo.

3,4-Dihydroxyphenylacetic Acid

Effects of idazoxan on dorsal raphe 5-hydroxytryptamine neuronal function.

The effects of the alpha 2-adrenoceptor antagonist idazoxan on 5-hydroxytryptamine (5-HT) neuronal firing and release have been investigated. Idazoxan, administered i.v. (10 micrograms/kg and 0.5 mg/kg) increased dorsal raphe nucleus (DRN)-5-HT neuronal firing rate in a dose-dependent fashion. At the higher dose, a voltammetric study revealed increases in extracellular 5-HT and 5-hydroxyindole acetic acid (5-HIAA) levels, there was no effect with the lower dose. Intra-raphe administration of idazoxan (1 ng) also elevated the firing rate of 5-HT neurones in the dorsal raphe, suggesting that idazoxan may produce the increase in firing by a direct effect in the DRN. However, microiontophoretic application of idazoxan did not increase the firing rate of 5-HT neurones in the DRN. Thus the increase in the firing rate of 5-HT neurones in the DRN observed with systemic and local administration of idazoxan is probably not due to a direct action of idazoxan on the 5-HT neurone. Possibly the idazoxan acted at alpha 2-adrenoceptors located on noradrenergic terminals thus stimulating noradrenaline release and consequently increased 5-HT activity. Chronic administration of idazoxan (0.8 mg/kg per h for 14 days), using osmotic mini-pumps, caused an elevation in basal firing rate and an attenuation of the inhibitory response of DRN 5-HT neurones to the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OHDPAT) (10 micrograms/kg i.v.). This finding suggests that chronic infusion with idazoxan leads to desensitisation of the 5-HT1A somatodendritic autoreceptor.

8-Hydroxy-2-(di-n-propylamino)tetralin

In vivo voltammetric detection of neuropeptides with micro carbon fiber biosensors: possible selective detection of somatostatin.

The electrochemical activity of catechol- and indoleamines, measured by differential pulse voltammetry (DPV) with specifically electrically pretreated carbon fiber microelectrodes, has been utilized to develop sensitive assays for amine neurotransmitters and metabolites. So far, four oxidation peaks have been recorded in vivo between -200 and +500 mV and are well identified. We now report that by increasing the potential sweep range to +950 mV, a further peak, called Peak 5, was detected at +800 mV in vivo in the striatum of anesthetized rats. Neuropeptides containing tyrosine, tryptophan and/or cysteine appear to be electrochemically active between +600 and +900 mV in vitro in a buffered solution at pH 7.4. The present study investigates the chemical nature of Peak 5 and the possible contribution of electroactive neuropeptides to this in vivo voltammetric signal. Experiments performed in vitro and in vivo with amino acids, neuropeptides, or bacitracin (a potent peptidase inhibitor) support the view that Peak 5 is peptidergic. Furthermore, peripheral administration of cysteamine and intrastriatal injection of specific somatostatin antisera both cause the eventual disappearance of Peak 5, suggesting that somatostatin (which oxidases in vitro at approx +800 mV), or a structurally related peptide, could be the principal component of striatal Peak 5.

Animals

In vivo voltammetry with micro-biosensors for analysis of neurotransmitter release and metabolism.

In vivo voltammetry involves the electrochemical detection of central oxidisable substances in situ. In association with this technique micro carbon fibre electrodes (CFE) are able to separate ascorbic acid (Peak 1) from 3,4-dihydroxyphenylacetic acid (DOPAC) plus dopamine (DA) (Peak 2) and 5-hydroxyindoleacetic acid (5-HIAAA) plus serotonin (5-HT) (Peak 3) in vitro. In vivo these biosensors detect the amine metabolites, due to their high extracellular concentration (microM) compared to the amines (nM). In addition homovanillic acid (HVA) (or 3-methoxytyramine (3-MT) in pargyline-pretreated mice) (Peak 4) and somatostatin (Peak 5) were also measured in vivo. However, potassium-stimulated release of DA has been directly monitored in pargyline pretreated mice. In addition, low concentrations (nM) of DA and 5-HT can now be selectively monitored in vitro with new biosensors coated with Nafion which repels negatively charged species including acid metabolites. In vivo, the combination of the Nafion-CFE and normal CFE allowed simultaneous measurements of release and metabolism of 5-HT, respectively. This permitted the observation that changes in 5-HT release are not necessarily reflected by changes in 5-HIAA levels. At present we are developing a Nafion biosensor to monitor basal extracellular DA. Electron microscope studies have shown radical modifications in the surface and structure of carbon fibres following chemical and electrical pretreatments, which may be involved in the development of sensitivity and selectivity displayed by the pretreated CFE towards electroactive compounds. A new approach for selective detection of neuroamines is the analysis of their stimulated fluorescence using LASER. In vitro, the fluorescence of 5-HT is in fact clearly distinguishable from that of 5-HIAA. The feasibility of this methodology in vivo using fiber optic probes will be explored.

Animals

In vivo evidence that 5-hydroxytryptamine (5-HT) neuronal firing and release are not necessarily correlated with 5-HT metabolism.

The relationship between 5-hydroxytryptamine release, metabolism and unit activity has been investigated in the anaesthetized rat. 5-Hydroxytryptamine release and metabolism were monitored in vivo by the measurement of extracellular 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the frontal cortex using in vivo voltammetry combined with nafion-coated and uncoated electrically pretreated carbon fibre electrodes. The monoamine oxidase inhibitor pargyline (100 mg/kg) increased extracellular 5-hydroxytryptamine and decreased 5-hydroxyindoleacetic acid. The 5-hydroxytryptamine releaser fenfluramine (10 mg/kg i.p.) acutely increased extracellular 5-hydroxytryptamine while having no effect on 5-hydroxyindoleacetic acid and the effect on extracellular 5-hydroxytryptamine was markedly reduced in rats pretreated (four weeks) with 5,7-dihydroxytryptamine. 8-Hydroxy-2-(di-n-propyl-amino) tetralin (10 micrograms/kg i.v.), an agonist at the 5-hydroxytryptamine1A somatodendritic autoreceptor, inhibited 5-hydroxytryptamine neuronal firing in the dorsal raphe nucleus and decreased extracellular 5-hydroxytryptamine during the period when firing was inhibited but did not alter extracellular 5-hydroxyindoleacetic acid. In contrast 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridin-4-yl) (RU 24969), which is an agonist at the terminal autoreceptor in the rat, had no effect on 5-hydroxytryptamine neuronal firing but decreased 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. The results support the view that extracellular 5-hydroxyindoleacetic acid is not a good index of 5-hydroxytryptamine release and that under specific circumstances 5-hydroxytryptamine neuronal firing, release and metabolism are independent of one another.

Action Potentials

Esterase activity of rat muscle.

The esterasic capacity of a series of skeletal muscles in response to three hemisuccinate ester drugs was investigated in rats and compared to that on alpha-naphthylacetate as a reference esterase substrate. Marked variations between different muscles and between given muscles of animals of different sex were observed, indicative of a complex heterogeneity in muscular expression of esterase activity.

Animals

Evidence for a relationship between recovery from anaesthesia, modified state of consciousness and striatal voltammetric levels of ascorbic acid.

The effects of various procedures which modify consciousness were studied on the extracellular concentration of ascorbic acid (AA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindolacetic acid (5HIAA) in rat striatum, as measured by differential pulse voltammetry (DPV) with electrically pretreated carbon fibre micro-electrodes (CFE). Recovery from anaesthesia (produced by 500 mg/kg i.p. chloral hydrate) was accompanied by a six-fold increase in extracellular striatal AA levels, while negligible changes in DOPAC and 5HIAA occurred. Following complete recovery from anaesthesia, the animals were re-injected with the same dose of anaesthetic which specifically reduced AA levels by 90% (DOPAC levels were unchanged and 5HIAA concentrations slightly reduced). In conscious rats, the neuroleptic haloperidol (1 mg/kg i.p., n = 5) and the minor tranquillizer diazepam (10 mg/kg i.p., n = 5), both considered as behaviourally depressant drugs, reduced extracellular AA levels to 50% of controls. The psychomotor stimulant D-amphetamine (1 mg/kg i.p., n = 5) increased AA levels by 90% over controls. Stress activation of animals (handling for 10 min, n = 10) also produced a transient, significant increase (180% of control values) in this striatal parameter. Taken together with previous reports, our results suggest a close relationship between the state of consciousness and extracellular AA levels in the rat striatum and that this relationship appears to be more correlated to AA as no such clear interdependence was noted between the levels of consciousness and extracellular striatal DOPAC or 5HIAA.

3,4-Dihydroxyphenylacetic Acid

[A case of degenerated jejunal diverticulum].

Reference is made to a case of jejunal diverticulum that had perforated and degenerated in the course of time. Its manifestation had taken the form of several melaena episodes and the consequent diagnostic difficulties are described.

Diverticulum

[Parietal tumors of the stomach].

The preoperative diagnosis, histopathology, clinical picture and treatment of tumours originating in the muscle and nerves of the stomach wall are described in the light of a series of cases collected over a period of 12 yr at the B Surgery Division, Varese District Hospital. Differential diagnosis and histological assessment of malignancy are not always easy. Transition forms exist in addition to those that are typically malignant or benign. Surgical management must take into account the extent, histological features and progess of the tumour. It can range from simple removal by enucleation to resection of the wall around the point of insertion of the tumour, or to distal, proximal or total gastroresection.

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