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At least 19 recordsLinked to original sources
PubMed1976

DDC-induced retrograde amnesias prevented by injections of dl-DOPS.

Injection of a dopamine beta-hydroxylate inhibitor, diethyldithiocarbamate (DDC) in rats 30 min prior to training of a step-down passive avoidance task impaired performance of the task 24 hr later. Similarly, injection of DDC 30 min prior to testing blocked retrieval of a passive avoidance habit trained in normal rats the previous day. Injection of a direct norepinephrine (NE) precursor, dl-thero 3,4-dihydroxyphenylserine (DOPS) 60 min before DDC prevented both amnesias. These data support the hypothesis that reduced levels of NE are responsible for DDC-induced amnesias.

Amnesia, Retrograde↗
PubMed1979

Significance of central noradrenergic system on harmaline induced tremor.

Since there is degeneration of substantia nigra concomitant with that of locus coeruleus (LC) in patients with Parkinson's disease, the study was performed to determine the role of central norepinephrine (NE) on harmaline induced tremor. The duration of harmaline (10 mg/kg IP) induced tremor was significantly reduced by intraventricular administration of L-thero-3,4-dihydroxyphenylserine (200 micrograms/rat) and 1-NE (50 micrograms/rat) was increased NE levels in the cerebral cortex, striatum, diencephalon, cerebellum and brain stem. Electrical stimulation of bilateral LC suppressed harmaline-induced 10-12/sec EMG activities in the neck muscle. Bilateral LC lesion upon electrocoagulation and 6-hydroxydopamine treatment resulted in a significant prolongation of the duration of harmaline induced tremor, reducing NE levels in the brain. These data suggest that central NE originating in the LC neurons has an inhibitory effect on the development of the tremor induced by harmaline.

Alkaloids↗
PubMed1977

Nature of the stimulation of biogenesis of cholesterol in the liver by noradrenaline.

1. Administration of noradrenaline increased the incorporation of [1-14C]acetate into hepatic sterols and the activity of liver microsomal 3-hydroxy-3-methylglutaryl-CoA reductase. 2. The stimulation was observed at short time-intervals with a maximum at 4h and was progressive with increasing concentrations of noradrenaline. 3. Protein synthesis de novo was a necessary factor for the effect. 4. The stimulatory effect was not mediated through the adrenergic receptors, but appears to involve a direct action of the hormone within the hepatocyte.

Animals↗
PubMed1975

The actions of dihydroxyphenylalanine and dihydroxyphenylserine on the sleep-wakefulness cycle of the rat after peripheral decarboxylase inhibition.

1. The actions of dihydroxyphenylalanine (DOPA) and dihydroxyphenylserine (DOPS) were assessed on the sleep-wakefulness cycle of male Wistar rats. 2. In comparative studies the extracerebral decarboxylase was inhibited with serinetrihydroxybenzylhydrazide (RO 4-4602) before injection of DOPA or DOPS. 3. DOPA (80-160 mg/kg, i.p.) with or without previous inhibition of the peripheral decarboxylase gave rise to an initial significant increase of slow wave activity, which may be related to a release of 5-hydroxytryptamine. 4. During the subsequent 8 h sessions, DOPA significantly decreased slow wave sleep and rapid eye movement sleep (REM) and increased wakefulness. 5. DOPS (80-160 mg/kg, i.p.) did not significantly modify the sleep-wakefulness cycle apart from a decrease of the latency for the first REM episode after 160 mg/kg in the RO 4-4602 pretreated animals.

Activity Cycles↗
PubMed1979

A comparative study on the uptake and subsequent decarboxylation of monoamine precursors in cerebral microvessels.

The endothelial cells and pericytes of brain microvessels (capillaries and small veins) are equipped with an enzymatic barrier, impeding the passage of circulating amino acids, such as amine precursors, into the brain. The properties of this mechanism was studied in brain slices and isolated microvessels from various species including man and also fetal material, following incubation in dihydroxyphenylalanine (DOPA), 5-hydroxytryptophan (5-HTP) and dihydroxyphenylserine (DOPS). A stereospecific, energy-dependent uptake leading to accumulation in the brain microvessel walls was found in all species studied; this process was found to exist already prenatally. The capacity of decarboxylation, the second step in the trapping mechanism at the blood-brain interphase, showed considerable species variation. The enzyme was present also in fetal brain microvessels. Inhibition experiments provided support for the presence of monoamine oxidase, but absence of catechol-O-methyl transferase, in the microvessel walls.

5-Hydroxytryptophan↗
PubMed1975

The role of dopamine and noradrenaline in temperature control of normal and reserpine-pretreated mice.

Drugs with the common property of stimulating dopamine receptors, have been tested for their effects on core temperature in control and reserpine-pretreated mice. Apomorphine, amantadine, amphetamine, L-dopa and atropine all produced a fall in mouse oesophageal temperature, their efficacy correlating with their ability to activate central dopamine receptors. Amphetamine and L-dopa had a biphasic effect the initial fall being followed by a rise. In reserpine-pretreated mice only amphetamine, apomorphine, L-dopa and D.L-threo-dihydroxyphenyl-serine effectively reversed hypothermia. Amphetamine had the highest efficacy of all the drugs tested. The sum of the effects of apomorphine and D.L-threo-dihydroxyphenylserine was equivalent to the effect of amphetamine alone. It is suggested that in control mice dopaminergic mechanisms mediate the hypothermia and noradrenergic mechanisms the hyperthermia. In reserpine-pretreated mice both systems are involved in the mechanisms restoring body temperature to normal.

Amantadine↗
PubMed1976

Effects of drugs that modify brain biogenic amine concentrations on thyroid activation induced by exposure to cold.

L-Dihydroxphenylalanine (L-DOPA) significantly inhibited intrathyroidal colloid droplet formation induced by exposure to cold in the rat. Diethyldithiocarbamate (DDC) also inhibited colloid droplet formation in response to cold. The combined administration of L-DOPA and DDC produced an additive inhibition of the thyroidal endocytotic response to exposure to cold. Pretreatment with chlorpromazine (CPZ) ameliorated the inhibitory effect of L-DOPA. DL-alpha-methyl-p-tyrosine (alpha-MT) also signficantly depressed the thyroidal response. Inhibition of colloid droplet formation induced by alpha-MT was not altered by the administration of DL-dihydroxyphenylserine (DL-DOPS). On the other hand, treatment of the alpha-MT-treated rats with L-DOPA to normalize dopamine synthesis resulted in a dramatic recovery from the inhibition. Blockade of serotonin biosynthesis with p-chlorophenylalanine (p-CPA) failed to produce a significant inhibition of colloid droplet formation. However, 5-hydroxytryptophan (5-HTP) markedly inhibited the thyroidal response to cold. Brocresine phosphate (BP) was another inhibitor of the thyroidal endocytotic response to exposure to cold. Oxotremorine also markedly depressed the thyroidal response to cold. Since these drugs did not interfere with pituitary thyroid responsiveness to exogenous thyrotropin-releasing hormone (TRH), it seems that the throidal endocytotic response to exposure to cold as a reflection of TSH secretion was directly influenced by alterations of brain biogenic amine concentrations or turnover rates.

5-Hydroxytryptophan↗
PubMed1976

Neurotransmitter regulation of growth hormone and ACTH in the rhesus monkey: effects of biogenic amines.

In an attempt to clarify the role of central neurotransmitters in GH and ACTH regulation, chair-adapted unanesthetized adult male rhesus monkeys and chronic indwelling intratrial cannulae were given 30 min infusions of various agonists known to affect central amines, and plasma samples were withdrawn for GH and cortisol determinations. Infusion of acid-saline vehicle alone had no significant effect on plasma GH or cortisol (P less than 0.05). L-Dihydroxyphenylalanine (L-Dopa) (4.5 and 45 mg/kg), but not apomorphine (7 mug/kg), a specific dopaminergic agonist, produced significant elevations of GH. Both noradrenergic (clonidine HCl, 1.5, 15, and 150 mug/kg, and D,L-threodihydroxyphenylserine (D,L-threodops) 90 mg/kg) and serotoninergic (5-hydroxy-L-tryptophan (5-HTP), 45 mg/kg) agonists induced significant GH responses. These findings suggest that GH is regulated in the rhesus monkey by noradrenergic and serotoninergic neurons, whereas participation of dopaminergic neurons has not been established. Significant cortisol responses were only observed following infusion of 5HTP (45 mg/kg). Dopaminergic and noradrenergic agonists not only failed to alter resting cortisol levels but also did not affect the cortisol response to 5-HTP. In the rhesus monkey serotoninergic mechanisms appear to be responsible for the regulation of resting cortisol levels. A catecholamine inhibitory mechanism was not demonstrated in this species.

5-Hydroxytryptophan↗
PubMed1976

Studies of connections between locus coeruleus and cerebral cortex.

Small tracking electrodes were inserted into the cat locus coeruleus (LC), and the effects of LC stimulation were determined on the transcallosal potential (TCP) evoked in cerebral cortex on the same side. LC stimulation at 8 volts inhibited TCP amplitude an average of 11%. Rostral LC placements appeared most effective. LC stimulation, without drugs, did not affect the peak latency of the TCP. dl-Propranolol and FLA-63 blocked LC inhibition of the TCP and also increased TCP amplitude per se. Propranolol first increased the latency of the TCP during LC stimulation, then decreased decreased it, while also prolonging the latency of the TCP per se. Phenoxybenzamine increased rather than blocked the LC inhibitory effect and also increased TCP amplitude. dl-Erythro-DOPS slightly increased the LC inhibitory effect, and substantially increased TCP amplitude. dl-Threo-DOPS produced somnolence in unanesthetized animals, led to increased norepinephrine levels in cortex and brain stem, and caused cortical potentials to fluctuate widely. A midbrain lesion of the dorsal ascending NE bundle blocked the LC inhibitory effect. LC stimulation alone, or in combination with evoked cortical stimulation, did not affect the interstimulus electrocorticogram or the heart rate. In the transcallosal system of the cortical regions studied, the LC appears to play mainly an inhibitory role.

Animals↗