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Biomedical subjects

A S Basile

Publications and source records attributed to A S Basile.

96 records · Page 6Linked to original sources
PubMed1985

Late evolutionary appearance of 'peripheral-type' binding sites for benzodiazepines.

Four classes of non-mammalian vertebrates were examined for the presence of both 'brain-specific' and 'peripheral-type' binding sites for benzodiazepines in the central nervous system. 'Brain-specific' binding sites for benzodiazepines were found in the central nervous systems of all non-mammalian vertebrates studied. However, in contrast to mammals, either very low or undetectable levels of 'peripheral-type' binding sites for benzodiazepines were observed in the central nervous systems of these non-mammalian vertebrates. Furthermore, the density of 'peripheral-type' binding sites for benzodiazepines in non-mammalian vertebrate heart was less than or equal to 2% of that found in mammalian cardiac tissue. These findings suggest a very late evolutionary appearance of 'peripheral-type' binding sites for benzodiazepines, implying that these sites may have (a) highly specialized function(s) in both peripheral tissues and the central nervous system.

Animals↗
PubMed1984

Norepinephrine elicits both excitatory and inhibitory responses from Purkinje cells in the in vitro rat cerebellar slice.

Superfusion of Purkinje neurons in the in vitro rat cerebellar slice with norepinephrine caused increases and decreases of spontaneous Purkinje cell firing. Excitations were evoked by low concentrations of norepinephrine (0.5-10 microM) and by the beta receptor agonist isoproterenol (0.1-5 microM). These excitations were reduced by timolol (1-2 microM), a beta receptor antagonist. Perfusion with higher concentrations of norepinephrine (greater than 16 microM), caused a depression of Purkinje neuron spontaneous activity. This inhibitory response was blocked by the alpha receptor antagonist phentolamine. The alpha 1 selective agonist phenylephrine had no effect on spontaneous activity at concentrations up to 100 microM, but the alpha 2 selective agonist clonidine (1-50 microM) elicited decreases in firing rate. These responses appeared to be due to a direct action on Purkinje cells, because neither the excitation nor the depression of Purkinje neuron activity elicited by norepinephrine was substantially altered when tested in a medium which substantially blocked synaptic transmission within the slice. Under these in vitro conditions, norepinephrine appears to increase the firing rate of Purkinje neurons via an interaction with beta adrenergic receptors, while norepinephrine induced depressions may be linked to alpha adrenergic receptor interactions; both receptors appear to be located directly on the Purkinje neurons.

Action Potentials↗
PubMed1984

Electrophysiological responses to adenosine analogs in rat hippocampus and cerebellum: evidence for mediation by adenosine receptors of the A1 subtype.

Adenosine has profound depressant effects upon the electrophysiological activity of the brain, but the adenosine receptor subtypes which mediate these responses are uncertain. In order to resolve this question, we have characterized the effects of two adenosine analogs which differ in their relative potencies at adenosine A1 and A2 receptors. The effects of these adenosine analogs were examined on spontaneous firing rate of Purkinje neurons in the rat cerebellum in situ, in cerebellar brain slices in vitro, and on synaptic transmission in the rat hippocampus in vitro. Although the A2 agonist appeared to be more potent with local drug application techniques in situ, our in vitro results suggest that the A1 receptor subtype is involved in the electrophysiological actions of these drugs in both rat cerebellum and hippocampus. Furthermore, these data indicate that the physical properties of some adenosine analogs may reduce apparent drug potencies when they are studied with local application techniques.

Adenosine↗
PubMedDate not supplied

Evidence of neuronal degeneration in C57B1/6 mice infected with the LP-BM5 leukemia retrovirus mixture.

Mice infected with LP-BM5 develop a severe immunodeficiency accompanied by learning and memory deficits, gliosis, and neurotransmitter abnormalities. The neurochemical alterations are consistent with elevated excitotoxin levels, suggesting that infected mice may incur neuronal damage. Although the number of neocortical neurons was unchanged in mice 12 wk after LP-BM5 infection, the expression of cytoskeletal proteins declined, particularly in the frontal and parietal cortex as indicated by MAP2, NF-200, and synaptophysin immunoreactivity. In contrast, the number of striatal neurons decreased 19%. The remaining neurons were smaller, with fewer synaptic boutons, and showed decreased synaptophysin and NF-200, immunoreactivity. Immunoblots of cortex and striatum confirmed decreases in MAP2, NF-200 and synaptophysin expression. Finally, although NCAM expression decreased in the striatum, it increased in the cortex. These results indicate that LP-BM5-infected mice sustain significant neuronal damage, which may contribute to their behavioral deficits. Moreover, the increase in cortical NCAM expression suggests active synaptic remodeling to compensate for the persistent excitotoxic environment in these mice, whereas striatal neurons degenerate. These concurrent degenerative and compensatory processes may also occur in the brains of patients with AIDS dementia complex (ADC), who suffer extensive degeneration of the basal ganglia and cerebral cortex.

AIDS Dementia Complex↗
PubMedDate not supplied

Ethanol tolerance of cerebellar purkinje neurons from selectively outbred mouse lines: in vivo and in vitro electrophysiological investigations.

The electrophysiological activity of cerebellar Purkinje neurons was characterized in long sleep (LS: ethanol sensitive) and short sleep (SS: ethanol insensitive) mice made tolerant to ethanol. After 1 to 4 weeks of feeding on a liquid ethanol diet, mice of both lines were less sensitive to the sedative and ataxic effects of parenteral ethanol than were controls. In addition, cerebellar Purkinje cells in ethanol-fed LS and SS mice were less responsive than the controls to the depressant effects of ethanol applied via bath perfusion in vitro and via local pressure ejection application in vivo. Tolerance to the electrophysiological effects of ethanol were already apparent after 7 to 9 days on the ethanol diet, and the degree of tolerance did not increase significantly in either mouse line fed ethanol for an additional 1-3 weeks. Finally, the differences in ethanol sensitivities of naive mice (LS greater than SS) were maintained following the development of tolerance. We conclude that tolerance to both the cellular and behavioral depressant effects of ethanol can be observed after chronic feeding with ethanol in LS and SS mice, and that there are no significant differences in the degree of tolerance developed by these mice. In addition, our data suggest that the inherited differences in ethanol sensitivity between LS and SS mice, and the changes in ethanol sensitivity which occur in these mice with chronic exposure to this depressant agent, are mediated by different mechanisms.

Action Potentials↗