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Biomedical subjects

J J Taljaard

Publications and source records attributed to J J Taljaard.

At least 73 records · Page 4Linked to original sources

Evidence that the stimulatory effect of neurotensin on dopamine release in rat nucleus accumbens slices is independent of dopamine D2-receptor activation.

Neurotensin (NT, 10(-9) M and 10(-7) M) increased the electrically stimulated release of [3H]dopamine (DA) in rat nucleus accumbens slices. This effect was not altered by activation of DA D2-receptors with high or low concentrations of quinpirole (10(-6) M and 10(-8) M) or blockade of DA D2-receptors with near maximal concentrations of sulpiride (10(-6) M and 10(-5) M). The sulpiride-mediated increase in [3H]DA release and the release induced by NT were additive. These results suggest that NT functions independently of DA D2-receptor activation to modulate DA release in the nucleus accumbens. NT did not modulate the simultaneous release of [14C]acetylcholine.

Acetylcholine↗

The beta-adrenoceptor and endocrine abnormalities in juvenile depression.

Neuro-endocrine disturbances were determined in juvenile depressives and possible correlations with biochemical abnormalities investigated. It was established that, as in adult depressives, the young also showed a high incidence of cortisol non-suppression after dexamethasone administration. In addition, a positive correlation observed between lymphocyte beta-adrenoceptor maximal number of binding sites and basal cortisol levels stresses the involvement of the noradrenergic neurotransmission system.

Adolescent↗

Inappropriate antidiuretic state in long-term psychiatric inpatients.

To investigate the occurrence of an inappropriate antidiuretic state in a long-term psychiatric inpatient population, 690 patients underwent serum sodium determination. Forty-four patients (6.4%) had levels less than 133 mmol/l. Fifteen of these patients could be investigated further and the biochemical findings in all were consistent with an inappropriate antidiuretic state. Evidence of previous episodes of water intoxication was found in 80% of these patients. Although more than one possible cause was present in most patients, the two factors most strongly incriminated in the pathogenesis of the inappropriate antidiuretic state were the drugs carbamazepine and hydrochlorothiazide.

Adult↗

Rat brain monoamine and Serotonin S2 receptor changes during pregnancy.

The concentrations of noradrenaline (NA), dopamine (DA), serotonin (5-HT), and their metabolites were determined in 5 brain areas of non-pregnant, 15 and 20 day pregnant and 4 day post-partum rats. Striatal 5-HT content was significantly lower in 15 and 20 day pregnant rats than in estrous controls. A significant decrease in striatal and frontal cortex 5-hydroxyindole-3-acetic acid (5-HIAA) concentration was observed in 15 day pregnant rats. Significant increases in hypothalamic and hippocampal NA levels were observed at 4 days post-partum. Frontal cortex serotonin S2 receptor KD was reduced in 4 day post-partum rats. There was no significant change in S2 receptor Bmax during pregnancy. Levels of progesterone were negatively correlated with striatal DA, homovanillic acid (HVA), 5-HT, and 5-HIAA levels, hypothalamic DA, hippocampal 5-HT, and frontal cortex 5-HIAA values as well as striatal HVA to DA, and HVA to 3,4-dihydroxyphenylacetic acid (DOPAC) ratios and amygdaloid HVA to DOPAC ratios. The limbic neurotransmitter changes might possibly contribute to mood changes which occur during pregnancy and post-partum.

3,4-Dihydroxyphenylacetic Acid↗

The effect of intrahippocampal injection of kainic acid on corticosterone release in rats.

The aim of the present study was to investigate whether the hippocampus exerts a modulatory effect on the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Kainic acid was stereotaxically injected into the CA1 pyramidal cell layer of the dorsal hippocampus, causing histological and behavioural changes typical of kainic acid toxicity. The CA3 pyramidal cells of the dorsal hippocampus were selectively lesioned. Rats treated with kainic acid were hyperactive, executed clockwise rotatory movements and displayed epileptic seizures. The acute excitatory effect of kainic acid on glutamatergic receptors in the hippocampus resulted in an elevation in plasma corticosterone levels, suggesting a stimulation of HPA axis activity. Direct or indirect stimulation of the CA1 pyramidal cells of the dorsal hippocampus appeared to have caused the increase in corticosterone secretion.

Adrenal Glands↗

The effect of selective noradrenergic denervation on thyrotropin secretion in the rat.

The effect of DSP4 [N-(2-chloroethyl)-N-ethyl-2 bromobenzylamine], a neurotoxin which selectively lesions noradrenergic projections from the locus coeruleus, on thyrotropin (TSH) secretion was investigated in the rat. DSP4 treatment (60 mg/kg injected i.p. 10 days prior to experimentation) significantly decreased the noradrenaline (NA) content of the hippocampus, frontal cortex and hypothalamus of the rat brain. DSP4 treatment did not affect the clonidine (250 micrograms/kg, i.p ) or TSH-releasing-hormone (TRH 5 micrograms/kg i.v.) induced stimulation or the isoproterenol induced inhibition of TSH secretion in the rat. These results suggest that the noradrenergic projection from the locus coeruleus to the hypothalamus does not play a significant role in the regulation of TSH secretion. Furthermore, the noradrenergic deficiency did not give rise to the development of the abnormal TSH response to TRH administration which is frequently observed in depression.

Adrenergic Fibers↗

Quantitative determination of lymphocyte ACTH1-39.

A method was developed for quantitative measurement of ACTH1-39, produced by human lymphocytes. It was shown that pH adjustment to 2 was essential for processing of the precursor molecule proopiomelanocortin (POMC). Linearity between time of incubation and ACTH production was shown. The existence of specific endopeptidases in lymphocytes for processing of the POMC molecule remains doubtful.

Adrenocorticotropic Hormone↗

A novel hypothesis for the psycho-modulating effects of lithium: the role of essential fatty acids, eicosanoids and sub-cellular second messengers.

Evidence is presented for a novel proposal for the mechanism of action of lithium in manic depressive psychosis. Lithium has well established effects on catecholaminergic--and hormone--stimulated adenyl cyclase activity and on cyclic AMP formation. Although there is conflicting evidence in the literature concerning the effects of the ion on cyclic nucleotide phosphodiesterase, not much is known of the effects of lithium on cyclic GMP. These two second messengers have been proposed to be mutually antagonistic in their actions but that a physiological balance between the two is essential for maintaining homeostasis of the human psyche. An in vivo animal study was undertaken to determine the effects of chronic lithium treatment on the dynamics and kinetics of these two cyclic nucleotides and phosphodiesterase in rat cerebral cortex. From these results, a possible functional coupling mechanism between the two second messenger systems and the effects of lithium are proposed. Lithium by means of its specific site of action, is unique among psychoactive drugs in that it can control both phases of bipolar illness. This point of action is proposed to be the metabolism of free fatty acids where lithium, by altering the availability of precursors for eicosanoid metabolism, is able to modulate both noradrenergic- and cholinergic-dependent pathways. By doing this, the ion is able to reestablish lost control over adrenergic and cholinergic balance critical for thought process and mood stability.

Animals↗

Horseshoe kidneys in vervet monkeys.

Two cases of horseshoe kidneys in vervet monkeys are described. Apart from the fusion, the rest of the urogenital system was anatomically normal and renal function was apparently not affected by this condition. The microanatomy was normal in both cases.

Animals↗

Increased dopamine D2 receptor-mediated inhibition of [14C]acetylcholine release in the dorsomedial part of the nucleus accumbens.

Dopamine (DA) D2 receptor-mediated inhibition of the K+-stimulated release of [14C]acetylcholine (ACh) from prelabeled rat dorsomedial nucleus accumbens slices was found to be 1.7 times greater than that observed in dorsorostral and ventromedial slices. This observation is consistent with the 1.9 fold higher DA D2 receptor density found in the dorsomedial area. In contrast, there were no differences in the DA D2 receptor-mediated effects on [3H]DA release in these areas. In addition, DA D2 receptor-mediated effects on [3H]DA and [14C]ACh release could not be demonstrated in the ventrorostral part of the nucleus accumbens consistent with the fact that DA D2 receptors were barely detectable in this area. The results suggest that cholinergic terminals in the dorsomedial part of the nucleus accumbens are under greater inhibitory DA control than in other areas of the nucleus accumbens.

Acetylcholine↗

Lack of effect of chronic desipramine treatment on dopaminergic activity in the nucleus accumbens of the rat.

The binding of [3H]SCH 23390 to dopamine (DA) D1-receptors was measured in the nucleus accumbens of rats treated chronically with desipramine for 14 days. DA D1- and D2-receptor binding using [3H]SCH 23390 and [3H]spiperone, respectively as ligands, was determined in rats treated for 28 days. Neither Bmax nor Kd values were influenced by chronic desipramine treatment. In addition, chronic desipramine treatment (28 days) did not influence the dose dependent, quinpirole (10-1000 nM)-mediated inhibition of the electrically stimulated release of [3H]DA release and [14C]ACh from nucleus accumbens slices or the dose dependent increase in [3H]DA release and decrease in [14C]ACh release in the presence of 1 and 10 microM nomifensine. Therefore, our results suggest that the effect of chronic antidepressant treatment cannot be attributed to changes in either DA D1- or D2-receptor binding or DA D2-receptor function in the nucleus accumbens.

Acetylcholine↗

The effect of partial noradrenergic denervation on corticosterone secretion in the rat.

DSP4(N-(-2-chloroethyl)-N-ethyl-2-bromobenzylamine) treatment significantly decreased the noradrenaline content in the hippocampus, frontal cortex and hypothalamus of the rat brain. DSP4 treatment did not affect plasma corticosterone levels. Clonidine, an alpha2-adrenoceptor agonist, had no effect on corticosterone secretion in either DSP4- or saline-treated rats. Isoproterenol, a beta-adrenoceptor agonist, significantly stimulated corticosterone secretion. This effect was inhibited by the prior administration of the beta-adrenoceptor antagonist propranalol. DSP4 treatment did not alter the isoproterenol-induced stimulation of corticosterone secretion. The administration of a high dose of dexamethasone (100 micrograms/kg, i.p.) significantly decreased the plasma corticosterone concentration of saline-treated controls, while an intermediate dose (25 micrograms/kg, i.p.) did not suppress corticosterone release significantly. DSP4-treatment did not influence dexamethasone-induced suppression of corticosterone secretion. These results show that significant decreases in noradrenaline content in the hippocampus, frontal cortex and hypothalamus appear to have no effect on the regulation of corticosterone secretion and that corticosterone secretion may be stimulated by catecholamines via beta-adrenoceptors.

Adrenergic Fibers↗

Effect of selective noradrenergic denervation on noradrenaline content and [3H]dopamine release in rat nucleus accumbens slices.

DSP4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine) treatment (50 mg/kg i.p., 10 days previously) significantly decreased the noradrenaline (NA) content of the rostral part of the nucleus accumbens. The medial and caudal areas were not affected. The nucleus accumbens appears to receive noradrenergic innervation predominantly from subcoeruleus nuclei of the pons-medulla while the locus coeruleus neurons project to the rostral area. The isoproterenol-induced enhancement of the K+-evoked release of [3H]dopamine (DA) was not affected by DSP4 treatment. Noradrenergic denervation does not appear to have been sufficient to cause up-regulation of postsynaptic beta-adrenoceptors.

Animals↗

Increased peripheral lymphocytes, lymphoid hepatitis and anaemia in African vervet monkeys seropositive to retroviruses.

Wild-caught African Vervet monkeys are commonly infected by Simian T-lymphotropic virus I (STLV1) and Simian immunodeficiency virus (SIV), yet the natural histories of these infections are largely unknown. Seropositivity was associated with increased total, T and atypical lymphocytes. In seropositive females there was mild, normocytic, normochromic anaemia. Lymphoid hepatitis was present in seven seropositive cases. African Vervets used in biomedical research, vaccine production and organ transplantation research are often infected by exogenous retroviruses which can be oncogenic and immunosuppressive in captive monkeys. Elimination of these infections may be possible by breeding Vervets in captivity.

Anemia↗

Noradrenergic function and hypothalamic-pituitary-adrenal axis activity in adolescents with major depressive disorder.

Levels of plasma norepinephrine (NE), free 3-methoxy-4-hydroxyphenylglycol (MHPG), and cortisol in adolescents with major depressive disorder (10 girls, 1 boy; mean +/- SD age = 16.4 +/- 1.6 years, range = 14-19 years) did not differ significantly from those in a group of healthy adolescents (17 girls, 12 boys; mean +/- SD age = 15.9 +/- 1.5 years, range = 12-18 years). No correlations were observed between these variables and age within the adolescent groups. However, when the adolescent data were viewed in combination with data previously obtained for an adult population (De Villiers et al., 1987), significant positive correlations between the variables were observed within the patient group. A moderate positive correlation with age was also observed for patients' NE and free MHPG levels. No such correlations were observed for the combined control group. When groups were partitioned into three age categories, it became apparent that differences in the three variables between the patient and the control groups were restricted to elderly subjects (greater than 50 years). In adults (21-50 years old), only the patients' NE levels were significantly elevated. These findings suggest that duration of illness may be important in determining the full expression of the biochemical abnormality in major depression.

Adolescent↗

Self-induced water intoxication. A case report.

A 19-year-old female schizophrenic with self-induced water intoxication is described. Factors of pathogenic significance included primary polydipsia and non-maximal urinary diluting capacity.

Adult↗

Regional distribution of monoamines in the nucleus accumbens of the rat.

Monoamine concentrations were low in the rostral area of the nucleus accumbens. Their distributions were not identical. Differences were observed in the medial area. DA concentrations were high in both medial and caudal areas. Noradrenaline (NA) and serotonin (5-HT) concentrations were considerably lower than the dopamine (DA) concentration. The NA concentration was highest in the caudal area of the nucleus accumbens and the (5-HT) concentration was highest in the ventrocaudal area. There was a rostrocaudal decrease in the 3,4-dihydroxyphenylacetic acid (DOPAC)/DA and 5-hydroxyindole-3-acetic acid (5-HIAA)/5-HT ratios. Uptake of [3H]DA and [14C]choline was lowest in the rostral area. The K+-stimulated release of [14C]acetylcholine (ACh) was also lowest rostrally, but there was no rostrocaudal difference in the K+-stimulated release of [3H]DA. These results provide further evidence of the heterogeneity of the nucleus accumbens.

Animals↗