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Biomedical subjects

G M Tyce

Publications and source records attributed to G M Tyce.

At least 109 records · Page 6Linked to original sources
PubMed1981

Release of endogenous catecholamines from slices of hypothalamus of rats.

The release of endogenous catecholamines from superfused slices of rat hypothalamus was studied under basal conditions and during release evoked by 40 mM K+. Catecholamines in superfusates, and in extracts of the tissue after stimulation, were isolated by column chromatography and quantitated by liquid chromatography with electrochemical detection. Norepinephrine (NE) was not consistently demonstrable in superfusate collected under basal conditions, but 40 mM K+ caused the release of from 2 to 4 ng/g of tissue per min. The addition of cocaine to the superfusate caused increases in basal and evoked release of NE. Epinephrine (E) could be measured in superfusates of slices from male but not female rats and then only when cocaine was added to the superfusate. Accordingly, the concentration of E in hypothalamus was greater in male rats than in female rats. Dopamine (DA) was not consistently measurable in the spontaneous overflow from slices either in the presence or absence of cocaine. K+-evoked release of DA could be demonstrated in slices from female rats. The addition of cocaine increased the evoked release of DA from slices from both sexes. Corticosterone, added to cocaine, had no effects on the efflux of any of the catecholamines. The experiments suggest that neuronal reuptake of all catecholamines is very efficient in the hypothalamus both under basal conditions and during evoked release.

Animals↗
PubMed1981

Free and conjugated dopamine in human ventricular fluid.

Free dopamine and an acid hydrolyzable conjugate of dopamine were measured in human ventricular fluid specimens with a radioenzymatic assay and by high performance liquid chromatography (HPLC) with electrochemical detection. Only trace amounts of free norepinephrine and dopamine were detected in ventricular fluid from patients with movement disorders. When the ventricular fluid was hydrolyzed by heating in HClO4 by lyophilization in dilute HClO4, however, a substantial amount of free dopamine was released. Values for free plus conjugated dopamine in ventricular fluid from patients who had never taken L-DOPA ranged from 139 to 340 pg/ml when determined by HPLC and from 223 to 428 pg/ml when measured radioenzymatically. The correlation coefficient for values obtained by the two methods in the same sample of CSF was 0.94 (P less than 0.001). Patients who had been treated with L-DOPA had higher levels of conjugated dopamine in their ventricular CSF which correlated inversely with the time between the last dose of L-DOPA and withdrawal of the ventricular fluid. Additionally, one patient with acute cerebral trauma had elevated levels of free norepinephrine and both free and conjugated dopamine in his ventricular fluid. Conjugation may be an important inactivation pathway for released dopamine in man.

Chromatography, High Pressure Liquid↗
PubMed1981

Metabolism of acetate to amino acids in brains of rats after complete hepatectomy.

The concentration of glutamine increases in the brain after hepatectomy. In the present studies the conversion of intravenously given [14C]acetate to [14C]glutamate and [14C]glutamine was studied in control rats and in rats at 6 h after complete hepatectomy. The incorporation of label into glutamate was only slightly inhibited, but the further incorporation into glutamine was greatly inhibited, after hepatectomy. These data, and previous data using [14C]glucose as precursor, indicate that synthesis of glutamine in brain is inhibited after hepatectomy, and suggest that its concentration must increase because degradation is inhibited to an even greater extent.

Acetates↗
PubMed1981

Presence of conjugated 5-hydroxytryptamine in in vivo superfusates of rat spinal cord.

The presence of an acid-hydrolyzable conjugate of 5-hydroxytryptamine, presumably 5-hydroxytryptamine-O-sulfate, was demonstrated in in vivo superfusates of rat spinal cord by HPLC with electrochemical detection. In untreated rats, the concentration of the 5-hydroxytryptamine conjugate measured during the basal efflux of 5-hydroxytryptamine did not differ from that measured during the release of 5-hydroxytryptamine evoked by DL-p-chloroamphetamine. Pretreatment of the rats with clorgyline, an inhibitor of the enzyme monoamine oxidase (EC 1.4.3.4), or with probenecid did not alter the concentrations of conjugated 5-hydroxytryptamine measured during the basal efflux of 5-hydroxytryptamine, but did elevate the concentrations of conjugate measured during the evoked release of 5-hydroxytryptamine.

Animals↗
PubMed1981

Monoamine release from cat spinal cord by somatic stimuli: an intrinsic modulatory system.

1. Superfusates taken from spinal cords of cats anaesthetized with chloralose and urethane were assayed for endogenous serotonin and noradrenaline by high-pressure liquid chromatography with electrochemical detection. 2. Stimulating the dorsolateral funiculus, caudal to a spinal transection, enhanced in a frequency-dependent manner the levels of monoamines in the spinal superfusate. 3. Tyramine added to the superfusate enhanced the release of noradrenaline and serotonin. 4. In cats with intact neuraxes, stimulation of the sciatic nerve at high, but not low intensities produced a 2- to 3-fold increase in the levels of monoamines in the spinal superfusate. This evoked monoamine efflux was attenuated by cold block of the cervical spinal cord. 5. Stimulation of the infraorbital branch of the trigeminal nerve evoked the release of noradrenaline and serotonin from the lumbar cord in animals with intact neuraxes. Cold block of the cervical cord blocked trigeminal-evoked release of lumbar serotonin and noradrenaline. 6. That the monoamine efflux was not due to elevations in blood pressure was indicated by the failure of vasoxyl, an alpha-agonist producing hypertension, to evoke any changes in spinal monoamine levels. 7. The monoamine release was not dependent upon either an opiate-sensitive link or upon the activation of the sympathetic ganglia, because systemic administration of naloxone (an opiate antagonist) and chlorisondamine (a ganglionic blocking agent) failed to antagonize the evoked release of amines. 8. These results suggest the existence of a spinopetal monoamine system which is activated by peripheral stimuli. The modulatory influence associated with increasing monoamine tone in the spinal cord clearly indicated that somatic stimuli may activate a descending monoamine pathway which serves to modulate the magnitude of the ascending sensory message.

Animals↗
PubMed1981

Effects of 5-hydroxytryptamine on neuroeffector junction in human pulmonary artery.

The effects of 5-hydroxytryptamine on release of norepinephrine and on contraction of smooth muscle in human pulmonary artery were studied. Helical strips were prepared from intra-parenchymal arteries removed 3-18 h after death. The strips were labeled with L-[7-3H]norepinephrine and mounted for superfusion and isometric tension recording. Electrical stimulation (10 V, 2 ms, 2 Hz) of the strips increased the release of total radioactivity; this release was blocked by tetrodotoxin. 5-Hydroxytryptamine (10(-5) M) exerted a cocaine-sensitive, indirect sympathomimetic effect on the overflow of norepinephrine from resting strips. This action was not blocked by methysergide. No effect of 5-hydroxytryptamine on release of norepinephrine from electrically stimulated tissue could be demonstrated. 5-Hydroxytryptamine (10(-5) M) also caused contractions of pulmonary smooth muscle, not blocked by phentolamine (10(-5) M) but mediated in part through methysergide-sensitive 5-hydroxytryptamine receptors.

Adolescent↗
PubMed1981

Prejunctional inhibition of norepinephrine release caused by acetylcholine in the human saphenous vein.

We performed experiments to determine whether or not acetylcholine exerts a prejunctional inhibitory effect on adrenergic neurotransmission in the human blood vessel wall. Rings of human greater saphenous veins were prepared 2 to 15 hours after death and mounted for isometric tension recording in organ chambers filled with Krebs-Ringer solution. Acetylcholine depressed contractile responses to electric activation of the sympathetic nerve endings significantly more than those to exogenous norepinephrine; the relaxations caused by the cholinergic transmitter were antagonized by atropine. Helical strips were incubated with [3H]norepinephrine and mounted for superfusion. Electric stimulation augmented the fractional release of labeled norepinephrine. Acetylcholine caused a depression of the evoked 3H release which was antagonized by atropine but not by hexamethonium. These experiments demonstrate that, as in animal cutaneous veins, there are prejunctional inhibitory muscarinic receptors on the adrenergic nerve endings in the human saphenous vein. By contrast, the human vein also contains postjunctional inhibitory muscarinic receptors.

Acetylcholine↗
PubMed1981

Functional aspects of bulbospinal monoaminergic projections in modulating processing of somatosensory information.

Descending monoamine pathways have been shown to modulate the processing of nociceptive information. Several lines of evidence support this hypothesis: 1) stimulation of brain-stem sites by intracerebral electrodes or the local application of opiates inhibits spinal reflex activity, this effect being antagonized by intrathecal monoamine antagonists; 2) the iontophoretic administration of monoamines in the spinal cord will antagonize the discharge of dorsal horn nociceptors; and 3) the intrathecal administration of monoamines will elevate the pain threshold in the unanesthetized animal. One natural mode of activating this intrinsic circuit appears to be through the activation of small-diameter afferents. Recent evidence has shown that such somatic stimulation causes the release of 5-hydroxytryptamine and norepinephrine. The role of this system appears to be in modulating the properties of sensory processing at the spinal cord level.

5-Hydroxytryptophan↗
PubMed1981

Effects of fentanyl on adrenergic function in canine coronary arteries.

The effects of fentanyl on sympathetic nerve endings in canine coronary arteries have been examined. Measurements were made of change in endogenous norepinephrine in isolated coronary artery in the presence of fentanyl, and of the effects of fentanyl on norepinephrine release and metabolism using superfused strips of coronary arteries in which transmitter stores had been prelabeled with [3H]norepinephrine. [3H]Norepinephrine and its 3H metabolites were separated from samples of superfusate (physiologic salt solution flowing continuously over the prelabeled coronary artery) by column chromatography and measured by scintillation spectrometry. The addition of fentanyl (2 x 10(-6) and 8 x 10(-6) M) caused the overflow of total radioactivity (radiolabeled norepinephrine and radiolabeled metabolites of norepinephrine entering the superfusate) to increase significantly above basal levels in both unstimulated and electrically stimulated arteries. The increased overflow could be accounted for by a small increase in norepinephrine and a sizeable increase in 3,4-dihydroxyphenylglycol, the metabolite arising from the intraneuronal metabolism of norepinephrine. Because this metabolite is without agonist activity and the increases in norepinephrine were small, fentanyl in the concentrations studied had minimal effects on adrenergic neurotransmission in this vascular bed.

Animals↗
PubMed1981

Release of norepinephrine and serotonin in cat spinal cord: direct in vivo evidence for the activation of descending monoamine pathways by somatic stimulation.

We sought to examine the likelihood that somatic input into the central nervous system might serve to release serotonin and noradrenaline into the cat spinal superfusate. In these experiments, the lumbar spinal cord of the chloralose-urethanized cat was superfused with a concentric polyethylene catheter. Resting levels of serotonin and noradrenaline were on the order of 0.5 and 0.3 ng/ml, respectively. Following bilateral stimulation of the sciatic nerve at intensities which produced no change in pupil size or blood pressure, there was no change in the resting levels of serotonin and noradrenaline. In contrast, stimulation of the sciatic nerve at intensities which evoked elevations in pupil size and blood pressure, an approximate 3-fold increase in the levels of either monoamine was noted during the interval of stimulation. In other experiments, elevations of blood pressure by intravenous infusion of vasoxyl failed to produce significant changes in the levels of serotonin and noradrenaline in the spinal superfusates. These results suggest that the activation of small diameter, peripheral somatic, afferents activates descending monoamine pathways. One consequence of this activation, as predicted by the effects of the intrathecal administration of these monoamines, would be to modulate the processing of nociceptive information.

Animals↗
PubMed1980

Resting and K+-evoked release of serotonin and norephinephrine in vivo from the rat and cat spinal cord.

Using a spinal superfusion system, the release of serotonin (5-HT) and norepinephrine (NE) from rat and cat spinal cord was measured using a high performance liquid chromatograph with an electrochemical detector. Resting levels of 5-HT and NE in the chloralose-urethanized rat were of the order of 0.8 and 0.4 ng/ml, respectively. Potassium (40 or 80 mM, in excess) produced a dose-dependent increase in the levels of both monoamines in the superfusate. The substitution of cobalt blocked this evoked release. Depletion of spinal 5-HT or NE by the prior intrathecal administration of 5,6-dihydroxytryptamine (5,6-DHT) or 6-hydroxydopamine (6-OHDA) reduced the resting levels of 5-HT and NE, respectively, and prevented the increase produced by excess potassium. These experiments indicate the ability to reliably collect and measure monoamines which overflow from spinal terminals and which reflect the degree of activation of the spinal monoamine system.

5,6-Dihydroxytryptamine↗
PubMed1980

Disposition of norepinephrine during nerve stimulation in dog saphenous vein.

The relative importance of neuronal and extraneuronal uptake in the disposition of norepinephrine (NE) released by electrical stimulation (ES) from adrenergic nerves in isolated dog saphenous vein was determined. Helical strips of vein were incubated in L-[7-(3)H]NE (1 x 10(-6)M) and mounted for superfusion. Superfusate was collected continuously before, during, and after ES (10 V; 2 ms; 1, 2, and 5 Hz). Measurements were made of [3H]NE and its metabolites in vein and in superfusate. Previous studies have established that 3,4-dihydroxyphenylglycol (DOPEG) is of neuronal origin and O-methylated metabolites (OMM) are of extraneuronal origin. Thus, extraneuronal uptake was estimated directly by measuring the amounts of OMM in superfusate, and neuronal uptake followed by metabolism was estimated by measuring [3H]DOPEG. The magnitude of the neuronal uptake fraction that enters vesicles for reuse was estimated from the compensatory increases in [3H]NE and in OMM when neuronal uptake was blocked. Similar amounts of released NE were taken up by neuronal uptake, by extraneuronal uptake, and diffused out of the synaptic cleft. Between 5-20% of the released NE was sequestered in vesicles for reuse.

Adrenergic Fibers↗
PubMed1980

Effects of estradiol on release and disposition of norepinephrine from nerve endings.

Studies were performed to determine whether estradiol (E2) has a direct action on the release and disposition of norepinephrine (NE) from adrenergic nerve endings in isolated superfused canine saphenous veins. [3H]NE and is labeled metabolites were separated by column chromatography with measurement by liquid scintillation spectrometry. An increase in the spontaneous overflow of total 3H, [3H]NE, and [3H]dihydroxyphenylglycol ([3H]DOPEG) that occurred with 1 and 10 microgram/ml E2 in the superfusing medium suggested that E2 either induced NE release or interfered with intraneuronal NE storage. During electrical stimulation (ES), release of [3H]NE and [3H]DOPEG exceeded controls with 1 and 10 microgram/ml E2 in the superfusate, yet total 3H was little changed. The evoked release of [3H]DOPEG showed less of an elevation over its spontaneous efflux in E2-treated veins than in nontreated veins, suggesting that E2 may block neuronal reuptake of released NE. The efflux of O-methylated deaminated metabolites during and after ES was decreased by E2 treatment, suggesting also an inhibition of extraneuronal uptake of NE.

Adrenergic Fibers↗