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Biomedical subjects

R Isola

Publications and source records attributed to R Isola.

11 recordsLinked to original sources
PubMed2006

High resolution scanning electron microscopy of the intracellular surface of intercalated disks in human heart.

The three-dimensional architecture of human cardiac intercalated disks was examined by high resolution scanning electron microscopy of osmium-macerated specimens. This methodology permits viewing of in situ intercalated disks from a vantage point inside individual cardiomyocytes. The erose nature of these structures was rendered in stark relief. Areas covered with clusters of particles were present on some membranous projections--these may represent a combination of desmosomes and fasciae adherentes. On the other hand, areas devoid of particles may correspond to gap junctions.

Adherens Junctions↗
PubMed2001

Intra- and intercellular distribution of mitochondrial probes and changes after treatment with MDR modulators.

Fluorescent probes are currently used to evaluate the mitochondrial transmembrane potential in situ. However, in parallel experiments using the probes JC-1 and TMRM in different cell types (human astrocytes, HEp-2, Vero, KB, and HeLa cells), we found that the distribution of JC-1 and TMRM is highly variable not only in different cell types but also in different cells of the same cell type, a condition that has never been documented until our work. This phenomenon depends on a hidden, widespread multidrug resistance (MDR) phenotype that can be recognized only by comparative assays with MDR inhibitors (progesterone, verapamil, and cyclosporin A) and represents a serious risk of error in the evaluation of the mitochondrial potential.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Glutamate receptors participate in the nicotine-induced changes of met-enkephalin in striatum.

A single dose of nicotine given to mice induces first a rapid decrease (presumed release/enhanced degradation) and then a rise (presumed synthesis/enhanced accumulation) of met-enkephalin (Met-Enk) in dorsal and ventral striatum observed at 30 and 60 min post-treatment, respectively. These studies investigated whether the nicotine effect on Met-Enk was mediated indirectly, in part, via other neurotransmitters known to be released by nicotine. Based on the ability of selective antagonists of dopamine (Sch 23390, D1; Sulpiride, D2), glutamate (CPP, competitive NMDA; dizocilpine, non-competitive NMDA; NBQX, AMPA) and GABA (bicuculline, GABA(A); Sch 50911, GABA(B)) receptors, to inhibit or enhance the response to nicotine, we conclude that nicotine alters striatal Met-Enk, in part, via glutamate NMDA and AMPA receptors. These findings further support the notion that glutamate might play a role in the pharmacology of nicotine.

Animals↗
PubMed2000

Homogeneous longitudinal profiles and synchronous fluctuations of mitochondrial transmembrane potential.

This study reports for the first time (a) the longitudinal profile of the transmembrane potential (mDeltapsi) of single mitochondria using a Nernstian fluorescent probe and (b) the distribution of mDeltapsi fluctuations of mitochondria undergoing permanent depolarization. Our findings show that (1) mitochondria in different energetic conditions coexist in the same cell, (2) mDeltapsi is rather homogeneous along the entire length of single mitochondria, (3) mDeltapsi is not influenced by the surrounding cytoplasmic environment and (4) mDeltapsi fluctuations occur simultaneously in groups of mitochondria connected in a network. Taken together, these findings provide further evidence for a functional relationship between mitochondrial arrangement and energetic condition.

Astrocytes↗
PubMed1999

Nicotine abstinence in the mouse.

We present evidence that intermittent administration of nicotine, 2 mg/kg s.c., four times daily to mice for 14 days produces a somatic abstinence syndrome after discontinuing treatment. The nicotine abstinence was mild and protracted, lasting more than 92 h. The constellation of abstinence signs was characterized by rearing, jumping, shakes, abdominal constrictions, chewing, facial tremor and scratching. No autonomic symptomatology was observed. Nicotine abstinence was attenuated with a single dose of nicotine administered at 24 or 48 h into withdrawal. The nicotinic antagonist mecamylamine, 3 mg/kg, induced a small increase in the total abstinence score when given 60 min after the last nicotine injection. Nicotine-abstinent mice displayed reduced locomotor activity. Finally, mice lost weight during the nicotine treatment which was not recovered during the withdrawal. Along with the rat nicotine abstinence model, the mouse model of intermittent nicotine administration and abstinence might be useful for studying the pharmacological and biochemical mechanisms of nicotine addiction and tobacco use.

Animals↗
PubMed1999

Subcellular heterogeneity of mitochondrial membrane potential: relationship with organelle distribution and intercellular contacts in normal, hypoxic and apoptotic cells.

The subcellular heterogeneity of mitochondrial membrane potential (mDelta psi) was investigated in confluent and sub-confluent cultures of four cell types (human astrocytes, HEp-2, MDCK and Vero cells) in normal growth conditions, hypoxia and apoptosis. The distribution of high-polarized mitochondria, detected by the potential-sensitive probe JC-1, was found to depend on: (1) the proximity to the cell edge; (2) the local absence of cell-cell contacts; and (3) the local absence of acidic vesicles. Both hypoxia and apoptosis produced a general mDelta psi increase with different redistributions of high-polarized mitochondria. Hypoxic cells maintained high-polarized mitochondria for over 24 hours, until cells underwent necrosis. On the other hand, apoptotic cells showed an unexpected convergence of high-polarized mitochondria into an extremely packed mass at one side of the nucleus, in a stage preceding nuclear condensation, but correlated to the retraction of cell-cell contacts.

Animals↗
PubMed1993

Ethanol prevents the glutamate release induced by N-methyl-D-aspartate in the rat striatum.

The administration of ethanol (2 g/kg, i.p.) or of the non-competitive antagonist(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloepten-5,1 0-imine maleate (MK-801; 1 mg/kg, i.p.) induced a decrease in the extracellular concentrations of glutamate, as studied by microdialysis in the striatum of awake rats. Moreover, ethanol and MK-801 completely prevented the increase in extraneuronal glutamate concentration induced by the focal application of N-methyl-D-aspartate (NMDA). The present results suggest that ethanol suppresses glutamate release through an inhibition of NMDA glutamate receptors in the rat striatum.

Animals↗