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J D Vincent

Publications and source records attributed to J D Vincent.

At least 127 records · Page 7Linked to original sources
PubMed1984

Electrophysiological effects of angiotensin II on cultured mouse spinal cord neurons.

The effects of angiotensin II (AII) on the membrane properties of cultured spinal neurons were investigated using electrophysiological methods. In 26% of neurons tested AII induced changes in membrane potential and input resistance which varied according to the concentration of applied peptide. At low concentrations (10(-6) M), AII increased input resistance by an ionic mechanism which appears to involve a reduction in Cl- conductance. At higher concentration (10(-4) M), AII evoked depolarization associated with a decrease in input resistance. This response appears to depend on an increase in Na+ conductance. Our observations indicate that AII can have multiple effects on neuronal membrane properties dependent on the concentration of applied peptide.

Angiotensin II↗
PubMed1984

Angiotensin II in the central nervous system in the rat.

Characteristics and functional activity of Angiotensin II (AII) neuronal receptors were studied using binding and intracellular recording methods. Characteristics of AII binding allowed definition of two distinct classes of high and low affinity binding sites. The effects of AII on the electrophysiological membrane properties of neurones were investigated using cultured mouse spinal cord (SC). AII induced changes in membrane potential and input resistance which varied according to the applied concentration of peptide. These data agreed with binding results suggesting two classes of AII neuronal receptors. Although angiotensin II-like material is found in the rat brain by RIA and immunochemistry, the presence of authentic angiotensin II (AII) is a point for discussion. Using RIA and radio-receptor assay (RRA), we found AII like peptides. However, chromatographic separation by gel filtration has revealed that this material is not authentic AII but consists of compounds of higher molecular weight. The recognition of the same material, both by AII antibodies (RIA) and AII binding sites (RRA) suggests that precursors containing AII sequences exist in the rat brain. We incubated rat brain with 3H-angiotensin I (AI) at 37 degrees C and analysed the resulting 3H-peptides (HPLC). Authentic 3H-AII was not detected, but two smaller peptides appeared (peak alpha et beta). The same peaks appeared when rat brain was incubated with 3H-AII. We have only been able to reveal 3H-AII formation from 3H-AI by inhibiting AII angiotensinases with excess of AII or low temperature (22 degrees C or 12 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1983

Immunocytochemically identified vasopressin neurons in culture show slow, calcium-dependent electrical responses.

From morphological characterization and intracellular recordings, monolayer cultures derived from fetal mouse hypothalami were found to include functionally differentiated peptide neurons, a number of which appear to contain vasopressin. These cells exhibited particular patterns of slow, calcium-dependent membrane depolarizations, resembling in their periodicity and duration the phasic activity of vasopressin neurons recorded extracellularly in vivo.

Action Potentials↗
PubMed1983

Electrophysiological properties of normal somatotrophs in culture. An intracellular study.

Normal rat pituitary cells were isolated and enriched to obtain a relatively pure population of growth hormone (GH) secreting cells by sedimentation at unit gravity and subsequently grown in culture. The electrophysiological properties of these cells were studied with intracellular recording techniques. 4-6-day-old cells did not show active electrical properties. At 7-9 days the cells were able to generate evoked responses (fast responses) which were blocked by inhibitors of calcium flux and prolonged with tetraethylammonium. The resting potential of these cells was sensitive to external local application of substances known to act on the release of GH. External elevated K+ induced a strong depolarizing response which was associated with an increase of membrane conductance. Somatostatin induced a hyperpolarizing response associated with a decrease of membrane conductance. It is suggested that the fast Ca2+-dependent responses and the slow variations of the resting potential induced by substances which modify hormone release may play an important role in the control of the secretory process of the presumably GH-secreting cells.

Animals↗
PubMed1982

An electrophysiological study of cultured human pituitary cells.

The electrophysiological properties of tumoral pituitary cells were studied in 4 types of human adenomas including prolactinomas, growth-hormone-secreting tumors, adrenocorticotropin-hormone-secreting adenoma and 'non-functioning' tumors. Only 9% of the cells from prolactinomas and ACTH tumors were excitable but they never elicited spontaneous action potentials. These cells did not respond to substances known to act on the hormone-releasing process (thyreoliberin, dopamine). However, 37% of the cells cultured from growth-hormone-secreting adenomas and from 'non-functioning' tumors displayed action potentials. The action potential was calcium-dependent, i.e., it was blocked by cobalt, nickel and methoxyverapamil and could be recorded in a sodium-free medium. Thyreoliberin triggered action potentials, whereas dopamine and gamma-aminobutyric acid inhibited electrical activity. These results show that human tumoral pituitary cells in culture are able to generate Ca2+-dependent action potentials. The data from growth-hormone-secreting tumors are in good agreement with the stimulus-secretion coupling concept; however, differences in the response of cells cultured from other types of human pituitary tumors suggest that each type of adenoma has specialized membrane properties.

Action Potentials↗
PubMed1982

Angiotensin II stimulates prolactin release in the rhesus monkey.

The effect of angiotensin II (AII) on plasma prolactin (PRL) concentrations was evaluated in ovariectomized rhesus monkeys which had been conditioned to chair restraining. Intracerebro-ventricular (i.v.t.) microinjections of AII increased PRL plasma levels in a dose-dependent manner. PRL values peaked at 10 min after injection and declined rapidly thereafter. Peak levels of PRL after 50 micrograms AII were approximately 7 times higher than those of baseline controls and were significantly reduced when 500 micrograms saralasin were injected via the ventricular route 15 min before AII injections. Measurements of vasopressin (AVP) plasma levels in some experiments showed that AVP release occurred following any dose of AII, irrespective of PRL liberation. In 2 animals, central injections of AII induced a dose-related increase in blood pressure. This study shows that, in primates, AII is able to influence PRL secretion via specific AII receptors. This action of AII is independent of AVP release and may be indirectly mediated through vasoactive effects of the octapeptide.

Angiotensin II↗
PubMed1982

[45Ca flow from cultured pituitary cells: effect of TRH and potassium].

Potassium (KCl: 50 mM) increases the uptake of 45Ca by GH3/B6 pituitary cells whereas TRH (100 nM) does not modify the uptake. On the contrary, 45Ca efflux is quickly and transiently increased by TRH whereas KCl has no influence on the 45Ca outflow. Our results suggest that these two secretagogues act on the GH3 pituitary cells by different processes.

Animals↗
PubMed1981

Effects of estrogens on the responses of caudate neurons to microiontophoretically applied dopamine.

The electrical activity of caudate neurons and their response to iontophoretically applied dopamine (DA) were tested at different time intervals before and after i.m. injection of estradiol benzoate in rats ovariectomized one week previously. One hundred and three neurons were recorded before estradiol injection and, of these, 25% were spontaneously active and 75% were driven by glutamate. The firing activity of the majority (86%) of the neurons was inhibited on application of DA. At 2--6 after the estradiol injections, the proportion of spontaneously active neurons was elevated to 87% and their firing rate was dramatically increased. Concomitantly, the proportion of cells affected by DA decreased to 39%; moreover, the majority of cells responsive to DA was now excited following it. We conclude that estrogens are able to influence the global activity of caudate neurons and to reverse their sensitivity to DA. This action may be partly mediated by the pituitary since it was not observed in ovariectomized rats which were also hypophysectomized.

Action Potentials↗
PubMed1981

Electrophysiological evidence for connections between septal neurones and the supraoptic nucleus of the hypothalamus of the rat.

In order to see whether septal neurones are connected to the hypothalamic neurones secreting vasopressin or oxytocin, neurones in different regions of the septum were recorded during electrical stimulation of the supraoptic nucleus. The position of the stimulating electrode within the latter was verified using lactating rats in which milk ejections could be induced by a train of electrical pulses applied to the nucleus. The responses of septal neurones to single pulse stimulation were then analysed by post-stimulus time histograms. In the septum ipsilateral to the site of stimulation, 42% of the neurones were antidromically invaded, 20% were orthodromically excited and 21% were inhibited following suraoptic stimulation. In the contralateral septum, 2% of the cells tested were antidromically invaded, 3% were excited and 16% inhibited. In the medial septum, 14% of the neurones were orthodromically excited, and 48% were inhibited. These results provide electrophysiological evidence for direct connections between septal neurones and the ipsilateral supraoptic nucleus of the hypothalamus, and give further support to the hypothesis of a septal influence on the activity of vasopressin- or oxytocin-releasing cells in the magnocellular system.

Animals↗
PubMed1981

[Angiotensin II and nigostriatal system (author's transl)].

The central renin-angiotensin system is implicated most importantly in the control of water balance, blood pressure and endocrine function (AVP and ACTH). Several central structures are sensitive to angiotensin II (A II), principally: the subfornical organ, the vascular organ of the lamina terminalis, the area postrema and the preoptic area. Furthermore, binding studies with radio-active ligands and also immunohistofluorescence have shown respectively the presence of A II receptors and immunoreactive material bound by A II antibodies in other central structures, and in particular parts of the motor system. In the present study, a double approach, both electrophysiological and biochemical, was used to investigate the possible role of the peptide A II in the neostriatum of the rat. 1 Microiontophoretic application of A II was shown to modify the spontaneous activity of some neurones (15/68) in the neostriatum. Generally, the action of A II was inhibitory and the inhibition was blocked by Sar1-Ileu8-A II, a specific A II antagonist. 2 Angiotensin II 10(-6) M; 10(-5) M; 5.10(-5) M) stimulated the spontaneous release of 3H-dopamine continuously synthetized from 3H-tyrosine in striatal slices of the rat. The A II-evoked release of 3H-dopamine was prevented when slices were superfused with a calcium-free medium containing EGTA. It was also suppressed in the presence of the specific antagonist Sar1-Ileu8-A II. 3 Kainic acid lesion of the intrastriatal cell bodies produced a moderate decrease of A II in the striatum (38%) whilst the activity of the converting enzyme decreased dramatically (-68%). These results suggest that there are angiotensin-containing nerve endings in the neostriatum, and that the cell bodies of such nerves are located outside this structure. Their functional role is discussed.

Angiotensin II↗
PubMed1980

Evidence of a direct action of angiotensin II on neurones in the septum and in the medial preoptic area.

Angiotensin II (AII) was microiontophoretically applied on neurones located in the septum and the medial preoptic area (MPOA). All the septal neurones sensitive to AII (15/37) responded by an inhibition to the peptide application. Of 44 units tested in the MPOA 21 cells (48%) were sensitive to AII and responded either by an increase (11/21) or decrease (10/21) in their firing. The specificity of these responses were ascertained by simultaneous application of the antagonist Sar-Ile-Angiotensin II. These data suggest that Angiotensin II acts directly on neurones of the septum and medial preoptic area, structures implicated in the control of drinking behaviour.

1-Sarcosine-8-Isoleucine Angiotensin II↗