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J J Taljaard

Publications and source records attributed to J J Taljaard.

At least 91 records · Page 5Linked to original sources
PubMed1988

Characterization of the effects of serotonin on the release of [3H]dopamine from rat nucleus accumbens and striatal slices.

The effect of serotonin agonists on the depolarization (K+)-induced, calcium-dependent, release of [3H]dopamine (DA) from rat nucleus accumbens and striatal slices was investigated. Serotonin enhanced basal 3H overflow and reduced K+-induced release of [3H]DA from nucleus accumbens slices. The effect of serotonin on basal 3H overflow was not altered by the serotonin antagonist, methysergide, or the serotonin re-uptake blocker, chlorimipramine, but was reversed by the DA re-uptake carrier inhibitors nomifensine and benztropine. With the effect on basal overflow blocked, serotonin did not modulate K+-induced release of [3H]DA in the nucleus accumbens or striatum. The serotonin agonists, quipazine (in the presence of nomifensine) and 5-methoxytryptamine, did not significantly affect K+-induced release of [3H]DA in the nucleus accumbens. This study does not support suggestions that serotonin receptors inhibit the depolarization-induced release of dopamine in the nucleus accumbens or striatum of the rat brain. The present results do not preclude the possibility that serotonin may affect the mesolimbic reward system at a site which is post-synaptic to dopaminergic terminals in the nucleus accumbens.

5-Methoxytryptamine↗
PubMed1988

Effect of ethanol on [3H]dopamine release in rat nucleus accumbens and striatal slices.

Ethanol (10-200 mM) transiently increased tritium overflow from superfused rat nucleus accumbens slices previously incubated with [3H]dopamine (DA) and [14C]choline. The effect was greater in striatal tissue and did not appear to be a non-specific membrane effect since [14C]acetylcholine (ACh) release was not affected. Lack of antagonism by picrotoxin suggested that gamma-aminobutyric acid (GABA) receptors were not involved. Calcium was not a requirement and the DA uptake blocker, nomifensine, was without effect. Ethanol appeared to be causing [3H]DA release into the cytoplasm. K+ -stimulated release of [3H]DA and [14C]ACh from nucleus accumbens and striatal slices was not affected. Clonidine-mediated inhibition of the K+-evoked release of [3H]DA remained unaltered. Ethanol attenuated the isoproterenol-induced enhancement of [3H]DA release. Ethanol therefore appeared to interact with components of the DA terminal causing a transient increase in the release of neurotransmitter without impairing K+-evoked release but apparently interfering with the isoproterenol-induced effect.

Animals↗
PubMed1988

Biological markers in juvenile depression.

3H-p-Aminoclonidine binding to platelets of children and adolescents with major depressive disorder was compared to that of a healthy control population. Significantly higher alpha 2-adrenoceptor Kd and Bmax values were observed in the patient population. 3H-Dihydroalprenolol binding to lymphocyte membranes of the same patient population showed significantly higher beta-adrenoceptor Bmax values than controls. Control females had significantly higher beta-adrenoceptor Kd values than control males, and the female patients had significantly lower beta-adrenoceptor Kd values than control females. 3H-Imipramine binding to platelets of these patients showed significantly higher imipramine Kd values in patients with a suicide attempt, whereas the imipramine Bmax values were significantly increased in patients with major depressive disorder with or without a suicide attempt. We propose that increased platelet alpha 2-adrenoceptor Kd and Bmax values, together with increased platelet imipramine Kd values, may serve as possible biological markers for children and adolescents with major depressive disorder and a tendency toward suicide. Elevated platelet imipramine and lymphocyte beta-adrenoceptor Bmax values may be biological markers for juvenile depression, and decreased beta-adrenoceptor Kd values may be a biological marker for depression in young females.

Adolescent↗
PubMed1987

The modulatory effect of neurotensin on [3H]dopamine release from rat nucleus accumbens slices is enhanced after chronic desipramine treatment.

In the presence of the reuptake blocker, nomifensine (1 microM), neurotensin caused a dose-dependent increase in the 25 mM K+-evoked release of [3H]dopamine ([3H]-DA) from rat nucleus accumbens slices. Chronic desipramine (DMI)-treatment (20 mg DMI/kg/day, orally for 28 days) caused a significant reduction in the K+-stimulated release of [3H]DA from rat nucleus accumbens slices. This could possibly have resulted from increased DA autoreceptor-mediated inhibition of DA release. Superfusion of the DMI-treated rat tissue with buffer-containing neurotensin (100 nM) resulted in an increase in the K+-evoked release of [3H]DA to a level which was higher than that observed with tissue obtained from untreated rats. A similar enhanced effect of neurotensin on DA release was observed when the DA agonist, apomorphine (APO), and ascorbate were included in the superfusion buffer. These findings are consistent with DMI treatment giving rise to impaired DA release possibly due to DA autoreceptor-mediated inhibition of DA release and cancellation of this effect by neurotensin.

Animals↗
PubMed1987

Value of acetylated haemoglobin assay in fetal assessment.

Acetylation of fetal haemoglobin, probably a post-translational, intracellular, enzyme-mediated reaction, depends upon an adequate supply of glucose and oxygen to the fetus and the nature of the diabetes (if present) in the mother. These complicating factors limit the general usefulness of acetylated fetal haemoglobin assay in fetal assessment.

Acetylation↗
PubMed1987

Effect of chronic antidepressant treatment on noradrenergic modulation of [3H]dopamine release from rat nucleus accumbens and striatal slices.

Unlike desipramine, a potent blocker of noradrenaline uptake, the antidepressant drugs, mianserin and citalopram did not, after chronic administration (28 days), attenuate the clonidine-induced inhibition of [3H]dopamine (DA) release from rat nucleus accumbens slices. Mianserin, like desipramine, failed to alter the isoproterenol-induced enhancement of [3H]DA release from rat nucleus accumbens and striatal slices. These findings suggest that antidepressant action does not necessarily involve desensitization of central alpha 2- or beta-adrenoceptors which influence neuronal transmission.

Adrenergic Fibers↗
PubMed1987

Noradrenergic and dopaminergic modulation of thyrotropin secretion in the rat.

Noradrenergic and dopaminergic regulation of thyrotropin (TSH) secretion was investigated in adult male Wistar rats. TSH secretion displayed a circadian variation with peak serum TSH levels at 10.00 h. The alpha 2-adrenoceptor agonist, clonidine (250 micrograms/kg, i.p.), was found to cause an enhancement of serum TSH levels at 10.00 h (160 +/- 10% of control values, P less than 0.001) which was antagonized by prior administration of the alpha 2-adrenoceptor antagonist, yohimbine (3 mg/kg, i.p.). The alpha-adrenoceptor antagonist phentolamine caused a significant decrease in serum TSH levels at 10.00 h (62 +/- 15% of control values, P less than 0.05) at a dosage of 2 mg/kg, i.p. The alpha 1-adrenoceptor agonist, phenylephrine (0.2 or 2 mg/kg, i.p.), was without effect as were the dopaminergic receptor agonist, apomorphine (1 or 5 mg/kg, i.p.), and the antagonist, sulpiride (20 mg/kg, i.p.). The beta-adrenoceptor agonist, isoproterenol (1 mg/kg, i.p.) was found to cause a decrease in serum TSH levels at 10.00 h (70 +/- 16% of control levels, P less than 0.01), which was completely antagonized by prior administration of the beta-adrenoceptor antagonist, propranolol (10 mg/kg, i.p.). TSH-releasing hormone (TRH, 5 micrograms/kg, i.v.) caused a significant stimulation of TSH secretion (470 +/- 63% of basal levels, P less than 0.001), which was not affected by prior treatment of the rats with yohimbine (0.1 mg/kg, i.p.), phentolamine (2 mg/kg, i.p.), propranolol (10 mg/kg, i.p.) or sulpiride (20 mg/kg, i.p.). There was, however, a tendency towards a decrease in the TRH-stimulated release of TSH in rats pretreated with phentolamine or propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Mseleni disease serum is not harmful to cultured chondrocytes.

The origins of Mseleni disease, an acquired polyarticular degenerative joint disease, are unknown. We examined sera from 12 patients with the disease, 5 unaffected Mseleni residents, and 5 Durban residents. The effects of sera from the 12 patients with Mseleni disease on DNA or sulfated proteoglycan synthesis by cultured rabbit or human infant articular chondrocytes were no different from those of control sera. Cells derived from 2 children contained no stainable DR antigens; coculture had no impact on either of the above measures of cell function.

Adult↗
PubMed1987

Effect of chronic desipramine treatment on neurotransmitter-thyrotropin releasing hormone--thyrotropin interactions in the rat.

Long-term administration of the antidepressant drug, desipramine (20 mg/kg/day, orally for 28 days), decreased the stimulatory effect of the alpha 2-adrenoceptor agonist, clonidine (250 micrograms/kg, i.p.) on thyrotropin (TSH) secretion in the rat, but did not alter basal TSH secretion. beta-Adrenoceptor-mediated inhibition of TSH secretion by isoproterenol (1 mg/kg, i.p.) was unaffected by chronic desipramine treatment, as were the stimulatory effect of TSH-releasing hormone (TRH, 5 micrograms/kg, i.v.) on TSH release and its inhibition by the alpha-adrenoceptor antagonist, phentolamine (2 mg/kg, i.p.). These findings suggest that chronic desipramine treatment induces subsensitivity of alpha 2-adrenoceptors which modulate TSH secretion in the rat while not affecting beta-adrenoceptor-mediated inhibition of TSH release. These findings suggest that pituitary TRH receptors are unchanged but that changes occurred at the hypothalamic level in alpha 2-adrenoceptor-mediated stimulation of TRH release. Although cerebral beta-adrenoceptors have been shown convincingly to be down-regulated after chronic desipramine treatment, their function in the hypothalamic TRH system after 28 days of treatment with desipramine appears to be unimpaired.

Animals↗
PubMed1987

Diets realistic for westernized people significantly effect lipoproteins, calcium, zinc, vitamins C, E, B6 and haematology in vervet monkeys.

This report describes measurements of 50 variables in adult, female, reproductively inactive Vervet monkeys during prolonged nutrition realistic for westernized people. Dietary treatments consisted of an atherogenic Western diet (WD) and a prudent Western diet (PD). Ingredients were normal foods for man and no extra cholesterol was added. Fortification of both diets with vitamin C after cooking was necessary to prevent deficiency. Randomised groups of Vervet monkeys received either the PD or WD for 47 months, while a third group was fed WD for 20 months and then PD for 27 months (WD-PD). Before the dietary treatments nourishment was by a high carbohydrate diet (HCD) and baseline and reference values (RV) apply to this nutritional status. Plasma total cholesterol (mg/dl) was increased from 147 (HCD) to 174 (PD) and 376 (WD). Individual cholesterolaemio response ranged from mild to severe and was stable (PD and WD). Dietary reversal (WD-PD) reduced cholesterolaemia promptly. Statistically significant increases in calcium, zinc and vitamin E and decreased vitamin B6 were associated with the WD relative to the PD (in serum and plasma). Two cholesterol metabolising microsomal enzymes in liver were notably increased and one unchanged (WD). There were no dietary effects on triglycerides, vitamin A and glucose in plasma; insulin, glucagon, electrolytes, copper, magnesium or enzymes reflecting liver, muscle or brain cell damage in serum. Red blood cells, platelets and directly associated parameters increased (WD), haemoglobin was the same and haemoglobin per red cell decreased. Bleeding time was not affected. Bivariate correlations across the diets confirmed that Western nutrition promoted inherent individual susceptibility to cholesterolaemia. There were notable differences from RVs in total cholesterol, calcium, packed cell volume and haemoglobin, which emphasise excesses and deficiencies of the WD and PD.

Animal Nutritional Physiological Phenomena↗
PubMed1987

Hepatitis in vervet monkeys caused by Fusarium moniliforme.

The fungus Fusarium moniliforme Sheldon is a common contaminant of maize (Zea mays L.) intended for human and animal consumption throughout the world. Culture material of F. moniliforme MRC 826, isolated from home-grown maize in an area in Transkei, southern Africa, with a high rate of human oesophageal cancer, was highly toxic to vervet monkeys (Cercopithecus pygerythrus). Ten monkeys were fed a standard primate diet which contained various amounts of culture material for 180 days. Two control monkeys received the standard diet without culture material. Pathological changes observed in liver biopsies taken by laparotomy were characterized by focal disturbance of the trabecular structure, degeneration and necrosis of hepatocytes, mononuclear infiltration, and in severe cases by cirrhosis. Biochemical changes, particularly increases in liver enzyme activities in serum, paralleled the liver damage seen by light microscopy. The acute, subacute and chronic toxic hepatitis induced in various degrees in all the monkeys fed fungal culture material showed close similarity with human viral hepatitis. The lesions also have some similarities to those induced in primates by aflatoxin, but differ in several respects. Ultrastructural nuclear and nucleolar changes caused by F. moniliforme, i.e. marginal clumping of chromatin and large nucleoli with segregation of fibrillar and granular components, suggested some similarity with the changes reported to be caused by aflatoxin and some other hepatocarcinogens. A long-term feeding experiment in vervet monkeys with F. moniliforme MRC 826 and attempts to isolate and chemically characterise the hepatotoxic metabolite(s) produced by this fungus are being continued.

Alanine Transaminase↗
PubMed1987

Estrogen-2/4-hydroxylase activities in rat brain and liver microsomes exhibit different substrate preferences and sensitivities to inhibition.

NADPH-dependent estrogen-2/4-hydroxylase activities in rat brain and liver microsomes were compared with respect to the utilization of different estrogens as substrates and the inhibitory effects of alpha-naphthoflavone, metyrapone and steroids. Of 6 different estrogens used as substrates, only 17 beta- and 17 alpha-estradiol were transformed relatively effectively by brain microsomes. In contrast liver microsomes utilized these two estrogens as well as ethynyl estradiol, estrone and diethylstilbestrol effectively. Estriol was a poor substrate for estrogen-2/4-hydroxylase activity in both tissues. With 40 microM 17 beta-estradiol as substrate the estrogen-2/4-hydroxylase activities in brain and liver were inhibited by alpha-naphthoflavone, metyrapone, progesterone, 17 alpha-hydroxyprogesterone and testosterone. The brain enzyme activity appeared to be more sensitive than the liver enzyme to inhibition by alpha-naphthoflavone and metyrapone. Testosterone propionate (50-100 microM) stimulated the brain enzyme activity significantly. Progesterone and 17 alpha-hydroxyprogesterone were the most effective steroidal inhibitors of brain estrogen-2/4-hydroxylase activity. In the liver the inhibitory potencies of 3 different steroids varied, depending on the estrogen used as substrate. With 17 beta-estradiol, for example, progesterone was the most potent steroidal inhibitor, while corticosterone was the most potent inhibitor when diethylstilbestrol was used as substrate. These findings indicate that rat liver microsomes can utilize a wider range of different estrogens for catecholestrogen formation than brain microsomes and suggest that the profiles of catecholestrogen-forming P-450 isozymes in the two organs differ.

Animals↗
PubMed1987

Beta-adrenoceptors on lymphocytes of patients with major depressive disorder.

3H-Dihydroalprenolol binding to lymphocyte membranes of patients with primary, unipolar major depressive disorder was compared to that of a normal, healthy control population. No significant difference could be demonstrated between the Kd values of the two different groups, but the Bmax values of the depressed patients were significantly lower than those of the controls. Positive correlations were observed between the lymphocyte beta-adrenoceptor Bmax values of the patients and their Beck self-evaluation and Hamilton depression ratings. We propose that decreased lymphocyte beta-adrenoceptor Bmax values may be used as a biological marker for major depressive disorder.

Adult↗
PubMed1987

Noradrenergic function and hypothalamic-pituitary-adrenal axis activity in primary unipolar major depressive disorder.

Plasma levels of cortisol, norepinephrine (NE), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were found to be significantly higher in 16 drug-free patients with primary, unipolar major depressive disorder than in 20 controls. Plasma free MHPG and basal cortisol levels showed a significant positive correlation in the controls, but not in the patients. There were, however, significant positive correlations between cortisol and NE, as well as between NE and free MHPG levels in the patients. No correlations were observed between patient plasma NE levels and platelet alpha 2-adrenoceptor or lymphocyte beta-adrenoceptor Kd or Bmax values. These peripheral measures of noradrenergic function are proposed as useful markers for patients with primary, unipolar major depressive disorder with melancholia.

Adult↗
PubMed1987

Impaired water excretion and elevated plasma vasopressin in patients with alcohol-withdrawal symptoms.

Reports describing the fluid balance status of alcoholics in withdrawal are varied, and conflicting. We examined this question by recording values for a variety of parameters in response to a standard water load test. Compared with age and sex matched healthy volunteers (n = 14), alcoholics in withdrawal (n = 17) exhibited lower cumulative urine output (p = 0.0001), higher minimum urine osmolality (p = 0.0001), lower serum sodium (p = 0.0024 before loading) and elevated plasma arginine vasopressin levels (p = 0.0045 before loading). We believe that these findings are best explained by a resetting of osmoreceptors, a supposition in keeping with contemporary views on the pathogenesis of alcohol dependence and withdrawal. This additional evidence of an antidiuretic state in alcohol withdrawal leads us to question the practice of fluid supplementation in its management and we suggest that this policy be revised.

Adult↗
PubMed1986

Mseleni joint disease. Part II. Low serum calcium and magnesium levels in women.

Low calcium and magnesium levels were found in serum from women domiciled in an area where an osteo-arthrosis with a female preponderance is endemic. Despite decreased serum calcium, the methodology used indicated low circulating parathyroid hormone, while values for phosphorus, total alkaline phosphatase and the serum proteins were not remarkable. Alcoholism was excluded as a factor influencing the measured variables. The results reported, together with previous findings, justify intensified investigation into the link between diet-induced mineral deficiencies and endemic osteo-arthrosis at Mseleni.

Adult↗