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Biomedical subjects

J C Garbutt

Publications and source records attributed to J C Garbutt.

51 records · Page 3Linked to original sources
PubMed1986

The TRH test during dopamine receptor blockade in depressed patients.

In an evaluation of the possible role of dopamine on TRH test results, 21 depressed patients were given TRH before and after one week of treatment with a low dose of haloperidol. Haloperidol significantly increased serum prolactin (both basal and after TRH) and cortisol levels, decreased body temperature, and had no effect on serum TSH, growth hormone, or thyroid hormone levels. Five of six patients with initial TSH blunting were retested with TRH; in four patients the TSH response remained blunted. These data render it unlikely that dopamine exerts a major inhibitory input on TSH secretion in depression.

Adult↗
PubMed1986

The prolactin response to thyrotropin-releasing hormone in depressed patients and normal subjects.

The prolactin (PRL) response to thyrotropin-releasing hormone (TRH) was studied in depressed patients (while ill or during remission) and in normal volunteers. Depressed women were shown to have lower basal PRL and lower PRL after TRH, but similar proportional PRL responses, compared to normal women. Depressed women also had basal thyroxine levels that were higher than those of the control women. No significant changes in PRL were noted in depressed men; in fact, there was almost complete overlap of all PRL variables between depressed and normal male subjects. Examination of the responses of PRL and of thyrotropin (TSH) to TRH revealed a significant positive relationship between the two in depressed women, but no association in men.

Adult↗
PubMed1986

Appearance of mania in drug-resistant bipolar depressed patients after treatment with L-triiodothyronine.

L-Triiodothyronine (T3) has been reported to potentiate the antidepressant effects of tricyclic antidepressants (TCAs) in patients who do not respond to these drugs, while thyroxine (T4) has been used to treat rapid-cycling bipolar disorder patients. The development of mania in antidepressant-resistant bipolar depressed patients after T3 was added to their antidepressant treatment is reported. It is speculated that thyroid hormone-catecholamine receptor interaction might underlie these T3-associated clinical manifestations. It is concluded that T3 did not prevent the switch to mania in the bipolar depressed patients reported here. Further study is necessary to determine if T3 plays a role in promoting the switch to mania in depressed patients treated with T3 in conjunction with TCAs, and if bipolar depressed patients are particularly vulnerable to mania from the combined effects of TCAs and T3.

Adult↗
PubMed1985

Urinary biopterin and neopterin excretion and pituitary-adrenal activity in psychiatric patients.

The urinary excretion of biopterin and neopterin, pterin compounds related to tetrahydrobiopterin, the cofactor for the initial steps in monoamine synthesis, was serially measured in a heterogeneous group of psychiatric patients and compared to excretion in control subjects, to state of illness, and to the results of the dexamethasone suppression test. Patients with major depression had increased excretion of biopterin compared to normal subjects. There was no relationship between biopterin or neopterin excretion and postdexamethasone cortisol levels. Pterin excretion did not significantly change with improvement in mood or with conversion from nonsuppressor to suppressor status. The meaning of increased urinary biopterin is presently unclear, although its relation to hormonal state and sympathoadrenal tone deserves further study.

Adult↗
PubMed1984

Urinary excretion of biopterin and neopterin in psychiatric disorders.

Levels of urinary neopterin and biopterin were determined in patients having a diagnosis of schizophrenia, unipolar depression, or bipolar depression. Both neopterin and biopterin levels were significantly higher in the urine of patients with unipolar depression than in the urine of the control group. Subclassification of patients into primary and secondary depression demonstrated a significant elevation of urinary biopterin in both groups, whereas urinary neopterin was elevated only in those patients with primary depression. In patients with bipolar depression, neopterin excretion was elevated, but biopterin excretion did not differ from controls. No significant differences were found in schizophrenic patients.

Adult↗
PubMed1984

A dramatic behavioral response to thyrotropin-releasing hormone following low-dose neuroleptics.

A dramatic improvement in mood and behavior after TRH occurred during treatment with low-dose neuroleptics in a patient with major depression and borderline personality disorder. This response was observed during both open and double-blind trials. The administration of TRH alone or with higher dosages of neuroleptics, was ineffective. Twenty other patients with major depression, including several with borderline personality disorder, were studied in an identical design but did not show similar improvement.

Adult↗
PubMed1983

The TRH test in patients wih borderline personality disorder.

Fifteen patients with a primary diagnosis of borderline personality disorder were studied with the thyrotropin-releasing hormone (TRH) test. Twelve carried the additional diagnosis of depression, substance abuse, or both. A blunted thyroid-stimulating hormone (TSH) response to TRH was found in seven patients, two of whom were neither depressed nor had the additional diagnosis of depression and/or substance abuse. TSH blunting was unrelated to such factors as thyroid status, serum cortisol, weight, height, or body surface. Since TSH blunting occurs in about 25% of patients with major depression but not in schizophrenia, the findings suggest that some patients with borderline personality disorder share a neuroendocrine abnormality with some affective disorder patients.

Adolescent↗
PubMed1983

Is there a tardive dysmentia?

A change in the phenomenology of schizophrenia has been observed over the past several decades; affective disturbances and phasic courses have become more evident. Although there is no obvious single explanation for these changes, several ideas have been considered. The advent and use of antipsychotic drugs over the past 30 years stands out as the most significant change. Because it is well known that chronic treatment with antipsychotic drugs can induce tardive dyskinesia and has been hypothesized to induce a supersensitivity psychosis, it is reasonable to believe that other behavioral changes may occur over time. We here describe a behavioral disorder that we have termed tardive dysmentia, involving changes in affect, activation level, and interpersonal interaction. A relationship between tardive dysmentia and tardive dyskinesia is suggested. It is our hypothesis that tardive dysmentia contributes to the changing course of schizophrenia and occurs after long-term treatment with antipsychotic drugs.

Adult↗
PubMed1983

The interaction between GABA and dopamine: implications for schizophrenia.

A role for gamma-aminobutyric acid (GABA) in the pathophysiology of schizophrenia was first suggested by Eugene Roberts in 1972. Since then considerable work has been accomplished in both the clinical and basic sciences regarding GABA and schizophrenia. Although it was originally thought that GABA might be useful in treating schizophrenia because of its inhibition of dopaminergic activity, recent data have shown that in certain models GABA has the opposite effect on dopaminergic functions. Regardless of the relationships of GABA to dopamine, neither biochemical nor pharmacological studies have been able to demonstrate a clear and reproducible GABA disturbance in schizophrenia. A number of problems contribute to the difficulty in studying GABA in schizophrenia, including the lack of specific and nontoxic GABA agonists as well as the complexity of the GABA system in brain. Interest in GABA research in schizophrenia appears to have waned, but several areas nevertheless appear promising for clinical investigation.

Animals↗
PubMed1983

Is carbamazepine helpful in paroxysmal behavior disorders?

Carbamazepine was used to treat two patients with paroxysmal behavioral episodes and preexisting psychiatric disease. Carbamazepine abolished the paroxysmal episodes. Its effects on the preexisting disease were less clear. These data suggest carbamazepine treatment for paroxysmal behavior.

Adult↗
PubMed1982

Cerebrospinal fluid hydroxylase cofactor in schizophrenia.

Cerebrospinal fluid levels of pterin cofactor were measured in off-medication schizophrenic patients and normal control subjects as one aspect of monoamine physiology in schizophrenia. Pterin cofactor is essential for the hydroxylation of several substances including tyrosine, the rate-limiting step in the synthesis of dopamine and norepinephrine. No significant differences were found. Platelet monoamine oxidase activity correlated significantly with pterin levels in male schizophrenic and in female control subjects.

Adult↗
PubMedDate not supplied

Administration of chlordiazepoxide affects [3H][3-MeHis2]thyrotropin-releasing hormone binding in rat brain.

The effects of acute and subchronic administration of chlordiazepoxide (CDZ) on [3H][3-methyl-histidyl2]thyrotropin-releasing hormone binding to thyrotropin-releasing hormone (TRH) receptors in membrane preparations from various regions of rat brain were examined. Acute administration of CDZ (50 mg/kg x 3 within 24 h) did not alter either the equilibrium dissociation constant (Kd) or the maximum number of binding sites (Bmax) in cerebellum (CB), olfactory bulbs (OB), frontal cortex (Cx), hypothalamus (HT) or corpus striatum (ST). However, the Kds of the pyriform cortex/amygdala (PC/A) (Kd = 3.6 +/- 0.1 nM compared to 1.9 +/- 0.1 nM in the control group; p less than 0.01) and the hippocampus (HP) (Kd = 7.8 +/- 0.7 nM compared to 2.1 +/- 0.1 nM in the control group; p less than 0.01) were increased. There were no changes in Bmax. Subchronic administration of CDZ (50 mg/kg/day for 7 days) increased the Kd of the PC/A complex (p less than 0.05), the OB (p less than 0.05) and the HP (p less than 0.01) without altering in Bmax. These results, showing regional differences in the response of TRH receptors to acute and subchronic CDZ administration, suggest that reduced affinity of TRH receptors in the PC/A complex, OB and HP may be related to some of the neurobiological actions of CDZ and/or its metabolites.

Animals↗
PubMedDate not supplied

Association between preference for sweets and excessive alcohol intake: a review of animal and human studies.

This report reviews a series of studies demonstrating a relationship between the consumption of sweets and alcohol consumption. There is consistent evidence linking the consumption of sweets to alcohol intake in both animals and humans, and there are indications that this relationship may be at least partially genetic in nature. Alcohol-preferring rats have a tendency to consume sucrose and saccharin solutions far beyond the limits of their normal fluid intake and this has been proposed to be a model of the clinical phenomenon known as loss of control. Furthermore, rats and mice, genetically bred to prefer alcohol, tend to choose more concentrated sweet solutions, compared to animals which do not prefer alcohol. Similar tendencies to prefer ultra-sweet solutions have been noted in studies of alcoholic subjects, with most alcoholics preferring sweeter sucrose solutions than do controls. Evidence also exists that those alcoholics who prefer sweeter solutions may represent a familial form of alcoholism. Finally, consumption of sweets and/or sweet solutions may significantly suppress alcohol intake in both animals and in alcoholics. Carbohydrate structure and sweet taste may contribute to this effect through different physiological mechanisms involving serotonergic, opioid, and dopaminergic functions. The possibility that there is concordance between sweet liking and alcohol consumption and/or alcoholism has theoretical, biological, and diagnostic/practical implications.

Alcohol Drinking↗