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Biomedical subjects

J D Vincent

Publications and source records attributed to J D Vincent.

At least 145 records · Page 8Linked to original sources

Substance P: evidence for diverse roles in neuronal function from cultured mouse spinal neurons.

Mouse spinal neurons grown in tissue culture were used to examine the membrane mechanisms of action of the peptide substance P. Two functionally distinct actions were observed, one being a rapidly desensitizing excitation, and the other being a dose-dependent, reversible depression of excitatory responses to the putative amino acid neurotransmitter glutamate. These effects on excitability suggest that substance P may play more than one role in intercellular communication in the nervous system.

Animals↗

Membrane effects of thyrotropin-releasing hormone and estrogen shown by intracellular recording from pituitary cells.

The effects of thyrotropin-releasing hormone and 17 beta-estradiol on the electrical membrane properties of a prolactin-secretin pituitary cell line (GH3/B6) were studied with intracellular microelectrode recordings. Of the cells tested, 50 percent were excitable and displayed calcium-dependent action potentials when depolarized. When injected directly on the membrane of an excitable cell, thyrotropin-releasing hormone and 17 beta-estradiol induced action potentials within 1 minute. The spiking activity was preceded by a progressive increase of the input resistance without any detectable change in the resting membrane polarization. The results reveal a rapid effect of both substances on the membrane of GH3/B6 cells. In the case of thyrotropin-releasing hormone, which has both a short-term effect on release of prolactin and a long-term effect on its synthesis, the induced electrical activity may be associated with the stimulation of prolactin production. The physiological implication of 17 beta-estradiol-induced, calcium-dependent spiking activity remains to be elucidated.

Action Potentials↗

Vasopressin release and drinking induced by intracranial injection of angiotensin II in monkey.

The effects of intracerebral injection of angiotensin II (AII) on both water intake and arginine-vasopressin (AVP) release were tested on unanesthetized rhesus monkeys (Macaca mulatta). Injection of 10(-10) mol of peptide was administered with a cannula microinjection system stereotaxically implanted into different diencephalic structures. The preoptic area, anterior part of third ventricle, caudate nucleus, and septum appeared to be the injection sites most effective in eliciting both drinking behavior and AVP release when the animal did not have access to water. On the contrary, when water was presented, AVP release was blocked after AII microinjections in the preoptic area and the third ventricle. No drinking was observed after microinjection in the supraopticus nucleus although AVP release was stimulated. These data suggest that AII might be effective in the regulation of water balance by centrally controlling both the input (drinking) and the output (ADH secretion) of water.

Angiotensin II↗

Chronic methods to study the release of catecholamines from the neostriatum in nonanaesthetized monkeys (Macaca mulatta).

The present report describes two methods allowing the chronic collection of catecholamine (CA) released from the neostriatum in the nonanaesthetized monkey (Macaca mulatta). In both methods the monkeys were placed in a restraining chair. Indwelling electrodes allowed the correlation of behavioural observations with polygraphic recordings. The first method uses a special superfusing cup permanently implanted on the lateral surface of the caudate nucleus, which permits the demonstration of spontaneous and D-amphetamine-induced release of (3H)-dopamine (DA) newly synthesized from L-(3,5-3H)-tyrosine over a period of six days. In the second method the collection of unlabelled CA is carried out by a localized ventricular perfusion. A radio-enzymatic estimation enabled the measurement of unlabelled DA and noradrenaline. With this second method the animals were kept for 25 to 30 days.

Amphetamine↗

[Electrophysiological study of hypothalamic neurons and gonadotropin regulation in rhesus monkey (author's transl)].

The electrical activity of various hypothalamic areas was recorded in anesthetized (sodium pentobartital) (n = 3) and unanesthetized (n = 3) ovariectomized rhesus monkeys. The plasma gonadotropin levels of the animals during the recording sessions were obtained by a chronic cardiac catheter. 1. Sodium pentobarbital greatly affected the electrical activity of most hypothalamic neurons (84%). The mean spontaneous electrical unit activity of neurons in the unanesthetized animals (n = 30) was 1.5 spike/sec. This value decreased to 0.1 spike/sec in the anesthetized group (n = 30). However, a small number of hypothalamic neurons were insensitive to the anaesthetic. 2. The multiunit electrical activity recorded in the median eminence showed marked periodic increases, about 200 sec before LH was observed to rise in the plasma (10/12). This increased firing lasted about 10 min (Fig. 1A). 3. In a few cases (2/12), however, increased firing was not associated with LH release. Since, in this area, multiunit activity represents the summation of a large number of axon terminals, the release of a hypothalamic hormone other than Gn-RH is put foreward as a possible hypothesis. 4. Of 51 neurons recorded in various hypothalamic areas, 3 showed periodic increases of electrical unit activity which corresponded to a rise in plasma LH levels (Fig. 1 B). These neurons are located in the arcuate area. 5. These results are consistent with the hypothesis of a relation between the electrical activity of some hypothalamic neurons and the periodical LH discharges observed in the ovariectomized rhesus monkey.

Animals↗

Responses of central neurones to piribedil and 2-bromo-alpha-ergocryptine: comparison with dopamine and apomorphine.

The effects of two putative dopamine receptor agonists, piribedil and 2-bromo-alpha-ergocryptine were studied by means of microiontophoresis. Their effects were compared with those of dopamine and apomorphine on neurones of the frontal cortex and of the caudate nucleus both of which are rich in dopaminergic terminals. Piribedil and S. 584, its dihydroxyphenyl derivative, displayed a potent dopamine-like inhibition in both these areas. 2-Bromo-alpha-ergocryptine exerted significant inhibition on cortical neurones which were spontaneously active but only weak or negligible inhibition on cortical and caudate glutamate-driven units. These observations raise the possibilities that 2-bromo-alpha-ergocryptine (1) mediates its inhibitory effect via a predominant presynaptic action; (2) acts preferentially on cortical neurones.

Animals↗

Effects of protein synthesis inhibitors on the negative feed-back effect of estrogen on LH release.

Ovariectomized female rabbits were pretreated with actinomycin D (80 microgram/100 g body weight) cycloheximide (300 microgram/100 g body weight) or chloramphenicol (300 microgram/100 g body weight) 4 h before an intravenous injection of 25 microgram of estradiol benzoate. Actinomycin D, cycloheximide and chloramphenicol decreased basal gonadotropin levels, but actinomycin D was less active than chloramphenicol and cycloheximide. Despite this effect on basal levels, such treatment did not prevent the effect of estradiol benzoate on LH release. Moreover, no significant impairment of the LH response to LH-RH was found. The interpretation of experiments using drugs such actinomycin D, cycloheximide or chloramphenicol requires caution; however, one cannot disregard the possibility that the negative feed-back effect of estrogen, in contrast to the positive effect, may not be mediated by RNA-dependent DNA and the protein-synthesizing systems.

Animals↗

Sources of serum [14C]-octanoate in cirrhosis of the liver and hepatic encephalopathy.

Serum octanoate levels of patients with liver cirrhosis and hepatic encephalopathy have been shown to be three to 15 times higher than those of controls. Assays for octanoate have been modified to permit isolation of pure octanoate after GLC. Patients with these conditions were given intravenously differently labeled [14C]-palmitates; serum [14C]-octanoate was isolated in each case and shown by mass spectrometry to be authentic octanoate. [1-14C]-oleate and [1-14C]-stereate were also shown to serve as precursors of serum [14C]-octanoate. When differently labeled palmitates (1-[14C]; omega [14C]; and [14C]-uniformly labeled) were used, different yields of serum [14C]-octanoate were recovered. Octanoate samples were chemically degraded to yield individual carbons or groups of carbons. In this manner it was possible to determine the percentage distribution of the [14C] label within the octanoate carbon chain. The data obtained from these studies suggest that 60% to 80% of the serum octanoate was obtained from the incomplete beta-oxidation of long-chain fatty acids and that 20% to 40% of the octanoate may have been formed de novo.

Caprylates↗