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A Pisani

Publications and source records attributed to A Pisani.

At least 91 records · Page 5Linked to original sources
PubMed1997

Morphological differentiation of the conjunctival goblet cells in the chick (Gallus domesticus).

BACKGROUND: These is no consensus in the literature regarding the differentiation of conjunctival goblet cells in vertebrates. METHOD: The conjunctival epithelium of the chick was studied before and after hatching in order to demonstrate the morphological evolution of the goblet cells. The entire conjunctiva was processed for light microscopy either on semithin sections stained with toluidine blue-pironine or on traditional sections stained with Alcian blue pH 2.5-PAS. RESULTS: It was possible to demonstrate that goblet cells underwent remarkable changes in their secretory activity. At 12 h after hatching, isolated Alcian blue-positive cells were present in the fornix. At 24 h after hatching, cells positive for both Alcian blue and PAS were scattered among epithelial cells. Two days after hatching, cells which reacted positively only to PAS were also present. CONCLUSION: It is suggested that the differentiation of conjunctival goblet cells occurs first in the fornix, probably due to the particular vascular environment of this region, and then spreads all over the conjunctiva.

Alcian Blue↗
PubMed1997

Activation of group III metabotropic glutamate receptors depresses glutamatergic transmission at corticostriatal synapse.

Intracellular recordings were performed from a rat corticostriatal slice preparation in order to characterize the effects of group III metabotropic glutamate receptor (mGluR) agonists on excitatory transmission at corticostriatal synapses. The amplitude of excitatory postsynaptic potentials (EPSPs), evoked by cortical stimulation, was significantly decreased by agonists acting at group III metabotropic glutamate receptors. Both L-2-amino-4-phosphonobutanoate (L-AP4) and L-serine-O-phosphate (L-SOP) were effective in reducing the amplitude of cortically evoked EPSPs, in a dose-dependent manner. The EC50 value for the effect of L-SOP and L-AP4 was 0.89 microM and 9.95 microM, respectively. Both L-AP4 and L-SOP had negligible effects on the intrinsic membrane properties of the recorded neurons and did not alter the postsynaptic response to focal application of glutamate, suggesting a presynaptic site of action. The presynaptic inhibition of both L-SOP and L-AP4 was fully antagonized by 250 microM (s)-2-methyl-2-amino-4-phosphonobutanoate (MAP4), whilst it was unaffected by 500 microM RS-methyl-4-carboxyphenylglycine (MCPG). Conversely, the presynaptic inhibitory effect on the EPSP amplitude exerted by 10 microM 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) was antagonized by 500 microM MCPG, whilst it was not blocked by 250 microM MAP4. Finally, the reduction of the EPSP amplitude produced by a saturating dose of L-SOP was further increased by 10 microM 1S,3R-ACPD, suggesting an additive effect of these compounds. The present results are consistent with the idea that group III mGluRs exert a presynaptic inhibitory modulation of the excitatory glutamatergic transmission at corticostriatal synapses.

Aminobutyrates↗
PubMed1997

Synaptic plasticity and physiological interactions between dopamine and glutamate in the striatum.

Several electrophysiological studies have addressed the interaction between glutamate and dopamine within the striatum. Although the results obtained from these studies were often conflicting, more recently the characterization of new forms of synaptic plasticity in the basal ganglia provided a possible integrative explanation of the different electrophysiological data regarding the interaction between these transmitters. In this review we will try to summarize and discuss the available data concerning the possible impact of the functional role of D1 and D2 receptor activation on the modulation of the glutamatergic corticostriatal pathway. Moreover, we will also describe the function of the striatum in the integration of glutamatergic and dopaminergic inputs to produce long-term changes of synaptic efficacy (long-term depression, long-term potentiation). Finally, we will consider the implication of the interaction between dopamine and glutamate in the regulation of energetic metabolism whose failure is responsible for neuronal death.

Animals↗
PubMed1997

Enhancement of NMDA responses by group I metabotropic glutamate receptor activation in striatal neurones.

1. The interactions between N-methyl-D-aspartate (NMDA) and metabotropic glutamate receptors (mGluRs) were investigated in striatal slices, by utilizing intracellular recordings, both in current- and voltage-clamp mode. 2. Bath-application (50 microM) or focal application of NMDA induced a transient membrane depolarization, while in the voltage-clamp mode, NMDA (50 microM) caused a transient inward current. Following bath-application of the non-selective mGluR agonist 1S,3R-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD, 10 microM), NMDA responses were reversibly potentiated both in current (197 +/- 15% of control) and voltage-clamp experiments (200 +/- 18% of control). 3. Bath-application of the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (3,5-DHPG, 10-300 microM) resulted in a dose-dependent potentiation of NMDA-induced membrane depolarization (up to 400 +/- 33% of control). This potentiation was either prevented by preincubation with (RS)-alpha-methyl-4-carboxyphenylglycine (RS-alpha-MCPG, 300 microM), or blocked when applied immediately after 3,5-DHPG wash-out. 4. Neither (2S,1'S,2'S)2-(2'-carboxycyclopropyl)glycine (L-CCG I, up to 100 microM) nor (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)-glycine (DCG-IV, 1 microM), agonists for group II mGluRs caused any change in NMDA responses. Likewise, L-serine-O-phosphate (L-SOP, 30 microM), agonist for group III mGluRs, did not affect the NMDA-induced depolarization. 5. The enhancement of the NMDA responses was mimicked by phorbol-12,13-diacetate (PDAc, 1 microM) which activates protein kinase C (PKC). The 3,5-DHPG-mediated potentiation of the NMDA-induced depolarization was prevented by preincubation with staurosporine (100 nM) or calphostin C (1 microM), antagonists of PKC. 6. Electrophysiological responses to alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor activation were not affected by agonists for the three-classes of mGluRs. 7. The present data suggest that group I mGluRs exert a positive modulatory action on NMDA responses, probably through activation of PKC. This functional interaction in the striatum appears of crucial importance in the understanding of physiological and pathological events, such as synaptic plasticity and neuronal death, respectively.

Animals↗
PubMed1997

Anatomic distribution of melanocytes in normal nail unit: an immunohistochemical investigation.

Very few histologic reports describe normal melanocytes of the nail unit. Previous studies predominantly address the distal nail matrix melanocytes; we found no review of nail-bed melanocytes in the literature. The proximal nail matrix melanocytes are difficult to identify; the cells cannot be identified by L-DOPA staining. More recently, their scarcity was confirmed by immunohistochemistry with a large panel of antibodies directed against melanocytes. We wished to detect the proximal nail matrix dormant melanocytes and compare their density and distribution with that of the other melanocytes in the distal matrix and nail bed and to establish criteria of normality that may help clarify the pathologic features of benign nevoid melanonychia in the nails of whites. A panel of five monoclonal antibodies (MoAbs), including HMB45 and TRP1 directed against antigens localized in early melanosomal vesicles, was investigated in frozen sections of six nail specimens from whites. Both vertical and horizontal sections were assessed to determine the presence of dormant melanocytes. Results showed that the proximal nail matrix melanocytes were clearly identified with MoAbs HMB45 and tyrosinase-related protein-1 (TRP-1). By contrast, melanocytes stained by MoAb against tyrosinase and L-DOPA reaction were evident, especially in the distal matrix. With MoAb TRP-1, the epithelial sheets showed counts of approximately 217+/-84/mm2 in the proximal matrix and of 132+/-34/mm2 in the distal matrix; the nail bed counts were only 45+/-25/mm2. The split epithelial sheets had 103+/-17/mm2 L-DOPA-positive melanocytes in the distal third of the matrix, but only a few of them were detected in the proximal matrix and none were noted in the nail bed. We clearly identified proximal nail melanocytes using MoAb HMB45 and TRP1. The total number of matrix melanocytes can be estimated as approximately 217/mm2. In proximal matrix, the dormant melanocytes compartment was predominant. In the distal matrix, two compartments were identified: a functionally differentiated and a dormant compartment. Contrary to classical opinion, longitudinal melanonychia originates more frequently in the distal matrix, not secondary to the larger melanocyte density but because only the distal matrix contains an active melanin synthesis compartment. Furthermore, the superficial distribution of proximal nail melanocytes in vertical sections showed a histologic feature that may simulate the pagetoid pattern of melanoma in situ.

Aged↗
PubMed1997

A possible mechanism for the aglycemia-induced depression of glutamatergic excitation in the striatum.

We have studied the possible mechanisms underlying the decrease of excitatory transmission induced by glucose deprivation by using electrophysiological recordings in corticostriatal slices. Extracellular field potentials were recorded in the striatum after cortical stimulation; these potentials were progressively reduced by glucose deprivation. The reduction started 5 minutes after the onset of aglycemia. The field potential was fully suppressed after 40 minutes of glucose deprivation. After the washout of the aglycemic solution only a partial recovery was observed. Aglycemia also induced a delayed inward current during single-microelectrode voltage-clamp recordings from spiny neurons. This inward current was coupled with an increased membrane conductance. The A1 adenosine receptor antagonists, 8-cyclopentyl-1,3-dimethylxanthine (CPT, 1 micromol/L) and 1,3-dipropyl-8-cyclopentylxanthine (CPX, 300 nmol/L), significantly reduced the aglycemia-induced decrease of field potential amplitude. Moreover, in the presence of CPT and CPX, a full recovery of the field potential amplitude after the interruption of the aglycemic solution was observed. Conversely, these antagonists affected neither the inward current nor the underlying conductance increase produced by glucose deprivation. The ATP-sensitive potassium channel blockers glibenclamide (10 micromol/L) and glipizide (100 nmol/L) had no effect on the aglycemia-induced decrease of the field potential amplitude. We suggest that endogenous adenosine, but not ATP-dependent potassium channels, plays a significant role in the aglycemia-induced depression of excitatory transmission at corticostriatal synapses probably through a presynaptic mechanism. Moreover, adenosine is not involved in the postsynaptic changes induced by glucose deprivation in spiny striatal neurons.

Adenosine Triphosphate↗
PubMed1997

Gadolinium enhanced MRI predicts clinical and MRI disease activity in relapsing-remitting multiple sclerosis.

The aim of the study was to evaluate the predictive power of baseline gadolinium (Gd) enhanced MRI in relation to subsequent clinical and MRI activity. Sixty eight patients with clinically definite relapsing-remitting multiple sclerosis had a baseline Gd enhanced MRI and were followed up clinically and by monthly Gd enhanced MRI for six months. The occurrence of relapses during the follow up period was predicted by the presence of at least one enhancing lesion on the baseline MRI (P < 0.05). The number and volume of enhancing lesions at baseline were significantly associated with both enhancing lesions observed during the follow up period (P < 0.0001) and the accumulation of abnormality on T2 weighted images (P < 0.0001). Moreover, the presence of three or more enhancing lesions at baseline scan was consistently associated with the development of permanent abnormalities on T2 weighted images six months later. The study suggests that the number and volume of Gd enhancing lesions at a single examination are strong short term predictors of subsequent clinical and MRI activity.

Adult↗
PubMed1997

Predictive value of clinical indices in detecting aspiration in patients with neurological disorders.

OBJECTIVES: (1) To evaluate the predictive value of a detailed clinical screening of aspiration in patients with neurological diseases, both with and without symptoms of dysphagia taking videofluoroscopy as the gold standard; (2) to assess the existence of risk factors for silent aspiration, measuring the cost-benefit ratio of radiological examination. METHODS: 93 consecutive patients meeting the diagnostic criteria for a neurological disease with a risk of swallowing dysfunctions (cerebrovascular accidents, brain injury, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, myotonic dystrophy, and abiotrophic diseases) underwent a detailed clinical assessment using a 25 item form to check for symptoms of dysphagia and impairment of the oropharyngeal swallowing mechanism. The 3 oz water swallow test was also performed to assess the aspiration risk. Sensitivity, specificity, positive predictive, and negative predictive values (NPV) of dysphagia, history of cough on swallowing, and 3 oz test positivity, versus videofluoroscopy documented aspiration, taken as the gold standard, were measured in all the patients and in subgroups with different neurological disorders. RESULTS: Non-specific complaints of dysphagia showed a very poor predictive value, whereas the symptom "cough on swallowing" proved to be the most reliable in predicting the risk of aspiration, with 74% sensitivity and specificity, 71% positive predictive, and 77% negative predictive value. The standardised 3-oz test had a higher predictive potential than the clinical signs, but had low sensitivity. The association of cough on swallowing with the 3 oz test gave a positive predictive of 84%, and an negative predictive value of 78%. In cases where the clinical tests failed to detect any impairment, videofluoroscopy documented only a low risk (20%) for mild aspiration. CONCLUSIONS: The association of two clinical items (such as history of cough on swallowing and 3 oz test positivity) provides a useful screening tool, the cost:benefit ratio of which seems very competitive in comparison with videofluoroscopy in aspiration risk evaluation.

Adolescent↗
PubMed1997

Role of dopamine receptors in the short- and long-term regulation of corticostriatal transmission.

Several studies have tried to clarify the role of different dopamine (DA) receptors in the control of membrane excitability of striatal neurons. Activation of DA receptors influences both synaptic and intrinsic membrane properties of striatal neurons. More recently it has been reported that endogenous DA plays an important role in the expression of striatal synaptic plasticity. In this review we will try to summarize and discuss the available data concerning the possible impact of the functional role of D1 and D2 receptor activation on the short- and long-term modulation of the excitatory glutamatergic corticostriatal transmission. Moreover, we will also describe the function of the striatum in the integration of glutamatergic and DAergic inputs to produce long-term changes of synaptic efficacy: long-term depression (LTD) and long-term potentiation (LTP).

Animals↗
PubMed1997

Effect of Helicobacter pylori eradication on gastric epithelial proliferation. Relationship with ras oncogene p21 expression.

BACKGROUND: Impaired changes in gastric epithelium proliferation have been described in Helicobacter pylori infection, and a progressive increase of proliferating cells has been shown with the progression of mucosal lesions. AIMS: Purpose of this investigation was to study the effect of eradication on bacterium-induced proliferative changes, evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI) and its relationship to the ras oncoprotein p21, involved in early events of gastric carcinogenesis. PATIENTS AND METHODS: This retrospective study was performed, before and after therapy, in five different groups of patients with progressive stages of Helicobacter pylori damage (N: normality; HG: histological gastritis with normal endoscopy; EHG: histological gastritis with endoscopic chronic erosions; CIM: complete intestinal metaplasia; IIM: incomplete intestinal metaplasia). RESULTS: Six months after eradication, a normalization of PCNA LI was observed in the areas of gastritis, but not in those of intestinal metaplasia, which showed on unchanged type. Moreover, immunohistochemical membrane expression of ras oncoprotein p21 was only associated to intestinal metaplasia. The protein was also expressed in the cytoplasm in 3 patients with incomplete type. CONCLUSIONS: These results suggest that the development of intestinal metaplasia may be associated with an alteration in the control of gastric epithelium proliferation and could represent an initial stage in gastric carcinogenesis. Nevertheless, further genetic changes are necessary for a complete progression to neoplastic disease. A long-term follow-up on extension, type, proliferative situation and oncoprotein expression in areas of intestinal metaplasia may be helpful to explain whether the present data provide new information on the mechanism of Helicobacter pylori induced gastric carcinogenesis.

Adult↗
PubMed1996

The modulation of calcium currents by the activation of mGluRs. Functional implications.

Glutamatergic transmission in the central nervous system (CNS) is mediated by ionotropic, ligand-gated receptors (iGluRs), and metabotropic receptors (mGluRs). mGluRs are coupled to GTP-binding regulatory proteins (G-proteins) and modulate different second messenger pathways. Multiple effects have been described following their activation; among others, regulation of fast synaptic transmission, changes in synaptic plasticity, and modification of the threshold for seizure generation. Some of the major roles played by the activation of mGluRs might depend on the modulation of high-voltage-activated (HVA) calcium (Ca2+) currents. Some HVA Ca2+ channels (N-, P-, and Q-type channels) are signaling components at most presynaptic active zones. Their mGluR-mediated inhibition reduces synaptic transmission. The interference, by agonists at mGluRs, on L-type channels might affect the repetitive neuronal firing behavior and the integration of complex events at the somatic level. In addition, the mGluR-mediated effects on voltage-gated Ca2+ signals have been suggested to strongly influence neurotoxicity. Rather different coupling mechanisms underlie the relation between mGluRs and Ca2+ currents: Together with a fast, membrane-delimited mechanism of action, much slower responses, involving intracellular second messengers, have also been postulated. In the recent past, the relative paucity of selective agonists and antagonists for the different subclasses of mGluRs had hampered the clear definition of the roles of mGluRs in brain function. However, the recent availability of new pharmacological tools is promising to provide a better understanding of the neuronal functions related to different mGluR subtypes. The analysis of the mGluR-mediated modulation of Ca2+ conductances will probably offer new insights into the characterization of synaptic transmission and the development of neuroprotective agents.

Animals↗
PubMed1996

The corticostriatal projection: from synaptic plasticity to dysfunctions of the basal ganglia.

Corticostriatal transmission has an important function in the regulation of the neuronal activity of the basal ganglia. The firing activity of corticostriatal neurones excites striatal cells via the release of glutamate. Presynaptic receptors that are located on corticostriatal terminals and that regulate the release of glutamate in the striatum have been postulated for dopamine and glutamate. Activation of these receptors may exert a negative feed-back on the striatal release of glutamate. High-frequency activation of corticostriatal fibres causes either long-term depression or long-term potentiation of excitatory transmission depending on the subclass of glutamate receptor that is activated. These forms of synaptic plasticity could be involved in motor learning. Alterations in striatal synaptic plasticity might be implicated in Parkinson's disease and Huntington's disease.

Animals↗
PubMed1996

Vla and alpha 6 beta 4 integrin expression in neuroendocrine carcinomas of the skin (their xenografts on nude mice and a corresponding primary culture).

Immunohistological expression of VLA1-5 and alpha 6 beta 4 integrins have been studied in 21 cases of primary neuroendocrine carcinomas of the skin (NECS), three xenografts on nude mice and one NECS cell culture. The phenotypic properties of NECS cells were largely maintained in NECS grafted on athymic nude-mice and in the corresponding cell line. Our results indicate that alpha 1 beta 1 and to a lesser extent alpha 3 beta 1, alpha 5 beta 1 are the main integrins expressed in NECS. In addition, VLA2, 4 and alpha 6 beta 4 are heterogeneously expressed in the same group of tumors and very sparsely present. These data suggest that like neuroblastoma and primitive peripheral neuroectodermal tumor (pPNET) the absence or the heterogeneous distribution of such integrins is correlated with the aggressive behaviour of NECS although long-term follow-up was not available for our cases. On the other hand, the alpha 1 expression could be regarded as a novel marker for differential diagnosis between NECS (alpha 1+) and pPNET (alpha 1-). The alpha 1 beta 1, alpha 2 beta 1, alpha 3 beta 1, alpha 5 beta 1 heterodimers in the 21 NECS studied showed an uniform pericellular staining of both the peripheral cells and central cells of the tumor islands. The predominant expression of alpha 1 beta 1 is consistent with the hypothesis of a primitive epithelial totipotential origin in NECS.

Animals↗
PubMed1996

A field potential analysis on the effects of lamotrigine, GP 47779, and felbamate in neocortical slices.

We studied the action of the new antiepileptic drugs lamotrigine (LTG), GP 47779 (the active metabolite of oxcarbazepine), and felbamate (FBM) on stimulus-evoked field potentials recorded from rat prefrontal and frontal cortical slices. In the presence of physiologic concentrations of extracellular magnesium (1.2 mM) the field potential amplitude was not affected by the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, 2-amino-5-phosphonovalerate (APV), while it was blocked by the non-NMDA glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). When magnesium was removed from the bathing medium, there was a significant NMDA-mediated component of the field potential. LTG and GP 47779 decreased, in a dose-dependent manner, the field potential amplitude under both experimental conditions. FBM caused a dose-related decrease of the field potential amplitude only in the absence of external magnesium, suggesting a selective interaction with an NMDA-mediated component of this potential. These findings indicate that the reduction of cortical excitatory transmission might represent a common target for new antiepileptic drugs.

Animals↗
PubMed1996

Felbamate inhibits dihydropyridine-sensitive calcium channels in central neurons.

The effect of the antiepileptic drug felbamate (FBM) on high-voltage-activated Ca++ currents was studied in cortical and neostriatal neurons acutely isolated from adult rats. Patch-clamp recordings in the whole-cell configuration were performed. Ba++ ions as the charge carrier for Ca++ channels were used. In pyramidal cortical cells, FBM dose-dependently reduced high-voltage-activated Ca++ currents in all the tested neurons. At concentrations of 30 to 100 nM, FBM already produced a significant inhibition of high-voltage-activated Ca++ currents (-6/-15%). At saturating concentrations (1-3 microM), FBM-mediated inhibition averaged 44%. The responses were fully reversible. The dose-response curves revealed IC50 of 504 nM. In striatal neurons, FBM decreased the same conductances by about 28%; the threshold dose was 1 to 2 microM, with an IC50 of 18.7 microM. In both structures, the observed inhibitions were unaffected by omega-conotoxin GVIA and omega-agatoxin IVA, suggesting that N-like channels and P-Like channels were not involved in the FBM-mediated responses. In addition, when omega-conotoxin GVIA and omega-agatoxin IVA (100 nM) were coapplied, the FBM-mediated inhibition on the remaining Ca++ currents averaged 87%. The FBM responses were occluded by micromolar concentrations of nifedipine, supporting a direct interference with dihydropyridine-sensitive channels. It is concluded that the described effect of FBM might represent an efficacious mechanism for either controlling spike discharge from epileptic foci or protecting neurons from excessive Ca++ loading. In both cases, FBM would act as a broad spectrum neuroprotective agent.

Animals↗
PubMed1995

Actions of glycine on non-dopaminergic neurons of the rat substantia nigra.

The effects of glycine on non-dopaminergic cells in rat substantia nigra pars compacta and pars reticulata maintained in vitro were investigated using intracellular recording techniques. Glycine, superfused at a concentration between 30 microM and 1 mM, reversibly blocked the spontaneous firing of these neurons. The inhibition of firing discharge was associated with a hyperpolarization of the membrane (potassium acetate-filled electrodes) and an increase in conductance. Under voltage-clamp experiments (holding potential between -57 and -65 mV), glycine produced an outward response which reversed polarity at about -74 mV. However, when the recording electrodes were filled with KCl, the glycinergic response was mainly depolarizing/inward and reversed at about -43 mV. Thus, it appeared to be due to an increase in chloride permeability. Furthermore, the effects of glycine were reversibly antagonized by strychnine (between 300 nM and 1 microM). Our findings demonstrate that glycine is a potent inhibitory agent on non-dopaminergic cells of the substantia pars compacta and par reticulata that acts by activating strychnine-sensitive receptors.

Animals↗