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Biomedical subjects

S W Tang

Publications and source records attributed to S W Tang.

70 records · Page 4Linked to original sources
PubMed1983

Binding of [3H]Ro 11-2465. Possible identification of a subclass of [3H]imipramine binding sites.

Ro 11-2465 is a cyanide derivative of imipramine. In cerebral cortex homogenates, [3H] Ro 11-2465 displays a binding profile similar to that of [3H]imipramine. Agents compete with binding of [3H]Ro 11-2465 in an order of potency similar to their ability to block serotonin uptake, and raphe lesions greatly decrease the binding of [3H]Ro 11-2465. These observations suggest that the sites labeled by [3H]Ro 11-2465 are presynaptic. The binding of [3H]Ro 11-2465 is sodium ion-dependent, as are both the binding of [3H] imipramine and the serotonin uptake mechanism. In the presence of sodium ions, binding of [3H]Ro 11-2465 to brain tissue or platelets at 4 degrees is apparently irreversible. Binding is not displaced by high concentrations of the displacing agent desipramine or by repeated washing. However, by either removing sodium or increasing the assay temperature to 23 degrees, the ligand dissociates from the tissue. In tissue where [3H]Ro 11-2465 is irreversibly bound to receptor at 4 degrees, subsequent [3H]imipramine binding is decreased by about 50%. At temperatures greater than 23 degrees, [3H]Ro 11-2465 binding displays a temperature dependency similar to that of [3H]imipramine; that is, when temperatures are raised from 23 degrees to 30 degrees or 37 degrees there is no change in the Bmax, but the affinity of the ligand for the receptor is decreased. These data suggest that [3H]Ro 11-2465 binds to a discrete population of [3H]imipramine binding sites, comprising about one-half of the total [3H] imipramine binding sites.

Animals↗
PubMed1982

Reduced presynaptic dopamine receptor density after chronic antidepressant treatment in rats.

Chronic administration of desipramine and nomifensine to rats reduced the number of presynaptic dopamine receptors as labeled by 3H-dopamine in rat striatal tissues, with no change in receptor affinity. This change can only be brought about by continuous daily treatment with antidepressants for a duration of at least 21 days or longer. All antidepressants did not displace 3H-spiperone or 3H-dopamine at low concentrations in vitro, suggesting that the agents may not act on the dopamine receptors directly. A possible interaction between neurotransmitters in the central nervous system for the overall therapeutic effect of antidepressant drugs was proposed.

Animals↗
PubMed1982

Lack of effect of raphe lesions on serotonin S2 receptor changes induced by amitriptyline and desmethylimipramine.

Spiperone binding was studied in rat cortical and striatal homogenates by direct binding assay after chronic (10 mg/kg/day i.p. for 21 days) treatment with the tricyclic antidepressants amitriptyline (AMT) and desmethylimipramine (DMI). Both AMT (a potent serotonin reuptake inhibitor) and DMI (a weak serotonin reuptake inhibitor) treatment were associated with decreased specific binding of 3H-spiperone and 3H-mianserin in the cortex (markers for serotonin S2 receptors) of 31-45% of normal rats, but not the binding of 3H-spiperone in the striatum (a marker for dopamine D2 receptors). The same chronic treatment of raphe-lesioned rats with AMT or DMI produced equivalent (38-40%) decreased specific binding of these ligands in the cortex but no change in striatum. These results suggest that synaptic serotonin concentration may not be the factor responsible for the decreased number of spiperone binding sites observed after chronic antidepressant treatment.

Amitriptyline↗
PubMed1981

Controlled exercise elevates plasma but not urinary MHPG and VMA.

The effect of controlled exercise on plasma and urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) and vanillylmandelic acid (VMA) was investigated in normal subjects. After 3 days of bed rest, six normal volunteers engaged in controlled exercise adjusted to a constant 40% of the individual's maximum oxygen intake. The exercise program consisted of 4 miles of walking and a half-hour each of bicycle ergometry and treadmill walking. Both plasma VMA and MHPG were higher on the exercise day than on the resting day, while urinary VMA and MHPG levels did not differ from rest to exercise. The mean urinary MHPG/VMA ratio (0.46) differed markedly from the mean plasma MHPG/VMA ratio (2.3). Plasma and urinary MHPG apparently represent different indices of norepinephrine metabolism.

Adolescent↗
PubMed1981

Differential effect of chronic desipramine and amitriptyline treatment on rat brain adrenergic and serotonergic receptors.

Serotonergic and adrenergic receptors were examine in rat brains by direct binding assays after chronic treatment with tricyclic antidepressants. Chronic amitriptyline (AMT) treatment (10 mg/kg/day i.p. for 21 days) decreased specific 3H-spiperone binding in the cortex and not in the caudate nuclei. Specific 3H-dihydroalprenolol (3H-DHA) binding was reduced in cerebellar but not in cerebral cortex. Chronic desipramine (DMI) treatment given in the same dose schedule, on the other hand, decreased specific 3H-DHA binding in both cerebellar and cerebral cortex. Specific 3H-spiperone binding in the cerebral cortex was also reduced but to a lesser extent than that in the AMT treated group. Scatchard analysis showed that reductions in 3H-spiperone or 3H-DHA binding in all cases were due to decreases in number of binding sites (Bmax) and not to changes in dissociation constants (KD). No change was observed in 3H-serotonin (3H-5HT), 3H-clonidine, or 3H-WB-4101 binding. The results show that there is no single common change in brain adrenergic and serotonergic receptors after chronic AMT and DMI treatment.

Amitriptyline↗
PubMed1981

Depression associated with cimetidine.

Over the past three years we have seen twelve patients who have become depressed while taking cimetidine. Clinically the depression is similar to that seen in a Primary Affective Disorder. Two representative cases are presented. It is suggested that cimetidine has precipitated a depressive reaction is vulnerable patients. Tricyclic antidepressants are effective in relieving the depression. It is postulated that cimetidine, by blocking H2 receptors in the CNS, produces an imbalance between H1 and H2. This imbalance may be an etiological factor in precipitating the depression. Tricyclic antidepressants have little effect on H2 but are potent H1 receptor blockers. This H1 blockade could restore the balance between H1 and H2, thereby relieving the depression.

Adult↗
PubMed1979

The effect of clonidine withdrawal on total 3-methoxy-4-hydroxyphenylglycol in the rat brain.

The effect of clonidine withdrawal on the brain norepinephrine system was studied in the rat. Clonidine suppresses brain total 3-methoxy-4-hydroxyphenylglycol (MHPG) significantly and no tolerance to this effect was observed up to 21 days. Cessation of clonidine treatment resulted in an elevation in the level of brain total MHPG. The suitability of the clonidine withdrawal syndrome as a model of bipolar depression is discussed.

Animals↗
PubMed1979

Interaction of antidepressants with clonidine on rat brain total 3-methoxy-4-hydroxyphenylglycol.

The effects of some antidepressants on brain total 3-methoxy-4-hydroxyphenylglycol (MHPG) were studied in the rat. Desipramine decreased and mianserine increased the brain total MHPG concentration while the other antidepressants had no effect. They were also the only antidepressants that attenuated the lowering action of clonidine on brain total MHPG, but possibly through different mechanisms. Two tertiary amine tricyclic antidepressants, amitriptyline and imipramine, appeared to enhance the lowering action of clonidine on brain total MHPG. The results suggest that antidepressants are heterogeneous in their action on brain noradrenergic mechanisms in the rat.

Animals↗
PubMed1978

The effect of acute and chronic desipramine and amitriptyline treatment on rat brain total 3methoxy-4-hydroxyphenylglycol.

The effect of acute (single dose), short-term (4 days), and chronic treatment (21 days) with two tricyclic antidepressants desipramine and amitriptyline on brain 3-methoxy-4-hydroxyphenylglycol (MHPG) was examined in the rat. Amitriptyline had no effect on brain total MHPG irrespective of the duration of the treatment and did not interfere with the lowering effect of clonidine on brain total MHPG. Acute and short-term desipramine treatment decreased brain total MHPG in rats, while chronic desipramine treatment increased it. The differential effect of acute and chronic treatment of desipramine on the brain total MHPG was further demonstrated by the lack of interference with the lowering effect of clonidine on brain total MHPG by one single dose of desipramine; partial interference after 4 days and complete interference after 21 days of desipramine treatment.

Amitriptyline↗
PubMed1978

A radiotracer method for the measurement of central nervous system catecholamines in vivo.

A new strategy for measurement of brain catecholamines was tested in an animal model. [3H]Norepinephrine was infused intravenously in rabbits to label the peripheral norepinephrine pools. The specific activity of urinary 3-methoxy-4-hydroxymandelic acid was consistently higher than that for 3-methoxy-4-hydroxyphenyglycol (MHPG). Central sympathectomy with 6-hydroxydopamine abolished this difference. Using the formula we propose, it is estimated that 30-50% of urinary MHPG originates from the central nervous system.

Animals↗
PubMedDate not supplied

CNS 3-methoxy-4-hydroxyphenylglycol: its peripheral assessment by isotopic dilution and theoretical significance.

An isotope dilution model for the peripheral measurement of CNS catecholamine metabolism was examined in rabbits. 3H-norepinephrine (3H-norepinephrine (3H-NE) infusions were performed on rabbits before and after central sympathectomy via intraventricular 6-hydroxydopamine (6-OHDA) treatment. Urine samples were obtained 72 hr after 3H-NE infusion and analysed for specific activities (SAs) of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3-methoxy-4-hydroxymandelic acid (VMA). The SA of MHPG was lower than that of VMA in all animals suggesting a source of unlabelled MHPG. The difference between the SAs of VMA and MHPG was abolished when the brain MHPG was markedly lowered by 6-OHDA injections. In animals which received 6-OHDA but retained moderate levels of brain MHPG, the difference between SAs of VMA and MHPG was maintained. The proposed model is able to predict and differentiate between rabbits that have severe depletion of CNS catecholamines and normal controls. The results suggest important relationships between CNS and peripheral NE metabolism and the compensatory capacity of the CNS to insult.

Animals↗