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A Verna

Publications and source records attributed to A Verna.

At least 37 records · Page 2Linked to original sources
PubMed1990

Effects of metabolic inhibitors and hypoxia on the ATP, ADP and AMP content of the rabbit carotid body in vitro: the metabolic hypothesis in question.

The effects of metabolic inhibitors (cyanide, antimycin) and hypoxia on the nucleotide content of the carotid body were investigated in vitro. The mean ATP content of carotid bodies superfused for 1 h in normoxic conditions was around 200 pmol/organ. Whereas metabolic inhibitors induced a decrease in ATP and an increase in AMP, hypoxia (10% O2 in N2, either 4 or 30 min) did not induce any significant change in nucleotide content. The significance of these results is discussed with regard to the metabolic hypothesis.

Adenosine Diphosphate↗
PubMed1989

Modifications in number and morphology of dendritic spines resulting from chronic ethanol consumption and withdrawal: a Golgi study in the mouse anterior and posterior hippocampus.

Using Golgi-impregnated mice brains, the effects of 2.5, 6.5, and 9.5 months of chronic ethanol consumption were investigated with regard to morphology and number of dendritic spines of CA1 hippocampal pyramidal neurons. The posterior part of the hippocampus was more sensitive to the effects of ethanol consumption than the anterior one. In the posterior part of the structure, the number of dendritic spines was reduced by 25 and 33% after 6.5 and 9.5 months of treatment, respectively, as compared to age-matched controls. Moreover, the remaining spines appeared shorter than normal. After 9 months of ethanol treatment followed by 0.5, 1, and 2 months of withdrawal, the number of dendritic spines was reduced by 24, 19, and 7.5% in the posterior hippocampus, respectively. In the anterior part of the hippocampus, a significant loss of dendritic spines (-20.5%) was observed only after 9.5 months of ethanol consumption. After 1 month of withdrawal, both number and morphology of dendritic spines appeared normal in the anterior hippocampus. These results demonstrate that chronic alcohol consumption leads to morphological alterations and loss of dendritic spines in the hippocampus. However, both dendritic spine number and morphology progressively return to normal values after 2 months of withdrawal. This phenomenon is another example of neuronal plasticity in adult animal brain.

Alcoholism↗
PubMed1987

Neuroanatomical effects of chronic ethanol consumption on dorsomedial and anterior thalamic nuclei and on substantia innominata in mice.

Quantitative analysis, using histological sections, showed that chronic ethanol consumption for 7 months produced a weak but significant cellular loss in the dorsomedial thalamic nucleus, anterior thalamus and substantia innominata in the mouse. These results are in agreement with patterns of neuroanatomical damage observed in human alcoholics.

Animals↗
PubMed1987

Build-up and release from proactive interference during chronic ethanol consumption in mice: a behavioral and neuroanatomical study.

Male mice of the BALB/c strain were given a solution of 15% ethanol as their only source of fluid during either 24 or 48 weeks. They were submitted to a sequential alternation (SA) task in a T-maze (6 successive trials). It was found that 48 but not 24 weeks of alcohol administration lead to a deficit as compared to pair-fed or tap-water controls. Whereas experimental mice performed as well as controls on the first 3 choices, they exhibited a gradual decrease in the SA rate on subsequent trials. We suggest that this deficit might result from an exaggerated vulnerability to proactive interference (PI). In order to further test this hypothesis, a second experiment investigated whether a between-trials variation of context of the maze would increase performance. It was found that the SA rate improved as soon as the variation was provided (5th trial). We suggest that the deficit of experimental mice results from an impairment of retrieval processes. A neuroanatomical study was conducted to quantify cell losses resulting from 8, 24 or 48 weeks of ethanol treatment in the mammillary bodies (MM) or the hippocampus (HPC). At the time of appearance of the deficit, MM exhibited a -32% cellular loss, whereas this was only -18% in the HPC. This result emphasises the importance of MM lesion in memory deficits resulting from long-term alcohol consumption.

Alcohol Amnestic Disorder↗
PubMed1986

Effects of long-term ethanol consumption on GABAergic neurons in the mouse hippocampus: a quantitative immunocytochemical study.

The effects of 6 months' ethanol consumption by mice on hippocampal GABAergic neurons were investigated by means of an immunocytochemical method using GABA antibodies. Although ethanol treatment did not modify body or brain weights in our experimental conditions, two differences were observed in ethanol-treated mice, as compared to controls: a decrease in the labelling intensity of immunopositive neurons and fibers in the dorsal and the ventral parts of the hippocampus; and a decrease in the number of immunopositive neurons. This neuronal loss was statistically significant in the ventral hippocampus only, where it reached about 25% in the stratum radiatum. It is concluded that chronic ethanol consumption leads to a decrease in GABA content of hippocampal neurons and to a loss of GABAergic neurons, mostly in the ventral part of the hippocampus. These alterations in GABAergic transmission could be related to the well known functional deficits observed in chronic alcoholism.

Alcoholism↗
PubMed1985

Effects of chronic ethanol consumption on pyramidal neurons of the mouse dorsal and ventral hippocampus: a quantitative histological analysis.

The effects of a 9-month period of ethanol consumption (followed by 3 or 6 months of withdrawal) on the hippocampus of mice were investigated. Compared with control animals, a loss of hippocampal neurons was observed on histological sections from ethanol-treated mice. This loss was greater in the ventral hippocampus (-18.6% to -18.7%) than in the dorsal hippocampus (-5.2% to -8.5%). However, the nucleus diameter, as well as the number of dendritic spines (studied using the Golgi-rapid impregnation) of the remaining neurons was not significantly affected by chronic ethanol consumption in our experimental conditions.

Alcoholism↗
PubMed1985

Ultrastructure and architecture of the sarcoplasmic reticulum in frog sino-atrial fibres: a comparative study with various preparatory procedures.

Various preparatory procedures were tested to preserve the ultrastructure of the sarcoplasmic reticulum (SR) by the best possible method within frog sino-atrial muscle fibres. These procedures were: conventional aldehyde fixation with or without tannic acid, cryofracture, metallic impregnation and quick-freezing followed by freeze-substitution. Our results illustrated that, when optimally preserved, the SR architecture and ultrastructure of frog sino-atrial fibres were not fundamentally different from those described in many other vertebrate muscle fibres, particularly cardiac fibres. The three-dimensional arrangement of the SR and the structure of its main compartments were situated in a precise fashion: the peripheral SR, located close to the plasma membrane, was made of a tight network of tubules and showed typical couplings; the juxtafibrillar SR was made of a loose network of tubules, small cisternae and some tubules near Z-lines; the intermediary SR, associated with the mitochondria, was made of tubules and fenestrated cisternae. Contacts between SR and mitochondrial membranes were also studied; cryofractures revealed no special intramembrane particles at this level. Collapsed portions of the SR were found after quick-freezing. Because of its relative importance and its three-dimensional arrangement, the SR of frog sino-atrial fibres may have comparable functional significance to the SR of other cardiac muscle fibres.

Animals↗
PubMed1984

Chronic ethanol consumption induces neuronal loss in mammillary bodies of the mouse: a quantitative analysis.

Quantitative analysis, using histological sections, showed that chronic ethanol consumption in the mouse produced neuronal loss in the medial mammillary bodies. This cellular loss was not uniform and was more marked in posterior (-30.1%) than in anterior (-8.8%) parts. Moreover, a reduction of the nucleus diameter of the remaining neurons was found. These results are in agreement with patterns of neuroanatomical damage observed in human alcoholics.

Alcoholism↗
PubMed1984

Distribution of sympathetic nerve endings within the rabbit carotid body: a histochemical and ultrastructural study.

The distribution of sympathetic (noradrenergic) nerves within the rabbit carotid body was investigated by fluorescence microscopy and electron microscopy. With the Falck-Hillarp method, fluorescent nerve fibres were found associated with blood vessels and type I/type II cell groups. After the injection of 6-hydroxydopamine, degenerating nerve profiles were found near blood vessels, near type I/type II cell groups and in contact with type II cells. Following the administration of [3H]noradrenaline, labelled nerve profiles were observed in close association with blood vessels and around cell groups; a few labelled nerve profiles were observed in contact with type II cells. With a modified chromaffin method, chromaffin nerve profiles were found around blood vessels, around type I/type II cell groups and their sensory nerve supply and in contact with type II cells. It was shown that for about one-third of the chromaffin nerve profiles, the nearest structure (in the plane of section) was a type I/type II cell group. Furthermore, the mean distance between chromaffin nerve profiles and blood vessels and between chromaffin nerve profiles and type I/type II cell groups was about the same (2.2 microns and 2.7 microns respectively). These results suggest that the carotid body sympathetic innervation might have, in addition to its vasomotor function, a direct action on the chemosensory structures. This hypothesis is discussed in the light of currently available physiological data and a comparison is made with the role of the sympathetic innervation in other sensory systems.

Animals↗
PubMed1983

Effects of ion-containing liposomes upon the chemoafferent activity of the rabbit carotid body superfused in vitro.

The effects of calcium concentration changes in carotid body cells on the chemoreceptor discharges were studied in vitro on carotid bodies removed from anaesthetized rabbits. Addition of calcium-containing liposomes to the superfusing medium increased the chemoreceptors' discharges. This effect was abolished by hyperoxia or when EGTA-containing liposomes were simultaneously added with the calcium-containing liposomes. A histological control with ferritin-enriched liposomes showed that the liposome content was transferred into the cellular elements of the preparation except the nerve endings. Results suggest a relationship between calcium concentration changes in carotid body cells and chemoafferent activity.

Animals↗
PubMed1983

In vitro recording of chemoreceptor activity in catecholamine-depleted rabbit carotid bodies.

Carotid bodies, together with Hering's nerves, were excised from anesthetized rabbits 24, 48 or 72 h after single reserpine injections (5 mg kg-1, i.v. or i.p.) and were superfused in vitro. Some carotid bodies were processed for formaldehyde-induced fluorescence microscopy to assess catecholamine depletion. Twenty-four hours after reserpine treatment, most of the type I cell islets had lost their fluorescence and the number of spontaneously active chemoafferent units was dramatically reduced. Forty-eight hours after reserpine injection, both the fluorescence of type I cells had partially recovered and the number of chemoreceptor units was almost normal. A significant reduction of both the normoxic and hypoxic frequencies of discharge was demonstrated in carotid bodies examined 24 or 48 h after reserpine pretreatment. Superfusions with dopamine (1, 10, 100 microM) transiently restored the response to hypoxia. It is proposed that catecholamines contained in type I cells play a prominent role in the genesis of chemoafferent activity and in the chemoreceptor response to hypoxia.

Animals↗
PubMed1981

Ultrastructural features of the carotid body after in vitro experiments: correlation with physiological results.

We have studied the ultrastructure and physiological properties of the rabbit carotid body superfused in vitro. After 3 h superfusion, the ultrastructural features of the carotid body cells, nerve fibres and nerve endings are similar to those observed after in vivo perfusion with fixative. After 5 h superfusion, the fluorescence of type I cells and sympathetic post-ganglionic nerve fibres appears normal, as demonstrated by the Falck method. After 6 h superfusion, some type I cells are characterized by a highly vacuolated cytoplasm whereas most of the nerve fibres and nerve endings still show a normal ultrastructure. Damaged cells are not more abundant in the centre of the organ than in the surface layer. Recordings from chemoafferent units demonstrate the possibility of superfusing the carotid body with an air-equilibrated medium without any noticeable excitation. Large and reproducible responses to hyperoxic and hypoxic superfusions are recorded. It is concluded that the in vitro superfused rabbit carotid body is a reliable and useful preparation for studying the mechanism of chemoreceptor excitation.

Animals↗
PubMed1980

Role of the carotid body cells: long-term consequences of their cryodestruction.

Rabbit carotid bodies were frozen in situ to destroy type I cells. After a one-year period of recovery allowing the sensory nerve fibres to regenerate, the animals were reexamined. Results showed that type I cells were not all destroyed in many instances but also that the presence of ventilatory reactions to chemoreceptor stimuli was always related to the presence of type I cells.

Animals↗