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Biomedical subjects

F K Goodwin

Publications and source records attributed to F K Goodwin.

At least 163 records · Page 9Linked to original sources
PubMed1980

Preliminary report of a simple animal behavior model for the anxiolytic effects of benzodiazepines.

A simple system is described to analyze the possibility that increased exploratory behavior is an index for the anxiolytic effects of benzodiazepines in laboratory rodents. Mice were allowed free run in a two-chambered arena, where two-thirds of the area was illuminated and one-third was darkened. The two chambers were separated by a black partition equipped with photocells across the opening, and the entire cage rested on an Animex activity monitor. Transitions across the partition between the light and dark chambers, and total Animex locomotor activity, were increased by clonazepam and chlordiazepoxide, in dose-dependent ranges consistent with previously reported behavior models. The increased exploratory activity with benzodiazepines does not appear to be a non-specific increase in general motor activity, as locomotion in clonazepam and chlordiazepoxide treated mice placed in a bare, undifferentiated cage was not significantly different from vehicle treated mice.

Animals↗
PubMed1980

Monoamine metabolites in cerebrospinal fluid of depressive subgroups.

Lumbar punctures were performed on 69 patients who met Research Diagnostic Criteria (RDC) for major affective disorder, while they were drug-free and depressed. None of the patients met RDC for alcoholism. Cerebrospinal fluid 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured by fluorometry and 3-methoxy-4-hydroxyphenylglycol (MHPG) by gas chromatography. Family histories were ascertained by systematic interviews of patients and their relatives, and diagnoses were made by family history diagnostic criteria (Andreasen et al., 1977). Depressed patients with alcoholism in a first degree relative had significantly lower levels of 5-HIAA and MHPG than patients without a family history of alcoholism (p < 0.05). No difference in HVA levels was found. The metabolite differences remained significant when the influence of sex ratio was considered. These results are in agreement with previous work linking alcoholism to abnormal serotonin metabolism. They provide further biochemical evidence of distinct genetic subtypes of affective disorder along lines suggested by Winokur (1979a, 1979b), and illustrate the usefulness of the family history method in defining patient subgroups.

Adult↗
PubMed1980

Urinary MHPG in subgroups of depressed patients and normal controls.

3-Methoxy-4-hydroxyphenylglycol (MHPG), the urinary metabolite thought best to reflect brain norepinephrine metabolism, was studied in a large group of hospitalized depressed patients with primary affective disorder and in normal controls, as part of an ongoing effort to evaluate the role of central amine dysfunction in affective illness. Overall there was no difference in MHPG between the depressed patients and controls. Hosever, within the depressed population the bipolar patients excreted significantly less MHPG than the unipolars and, as a group, the male bipolar patients had significantly lower MHPG than male controls. MHPG correlated positively with age, age of onset, rating of anxiety and psychosis and, most importantly, with systolic blood pressure. These data support the concept of biological heterogeneity among individuals with major depressive disorders. However, the relationship between MHPG excretion and various psychological and physiological parameters is both intriguing and complex and warrants careful interpretation.

Adult↗
PubMed1980

Failure of naloxone to reduce manic symptoms.

The authors conducted a double-blind placebo-controlled study in which patients with a wide range of manic symptoms were administered 20 mg of naloxone subcutaneously. Naloxone failed to improve manic severity, activation-arousal, or elation-grandiosity for intervals up to 3 hours. Global nurse ratings of mania did not improve over an 8-hour period. The authors suggest that the question of endorphin involvement in mania has not been resolved and recommend clinical studies with longer acting oral narcotic antagonists such as naltrexone.

Affective Disorders, Psychotic↗
PubMed1980

Pinealectomy abolishes plasma melatonin in the rat.

Using gas chromatography-negative ionization mass spectrometry, plasma melatonin levels in pinealectomized and sham-operated rats were assessed. The pinealectomized rats consistently demonstrated an absence of plasma melatonin while the intact animals showed detectable amounts. This suggests that although melatonin may be formed in tissues other than a pineal gland, the contribution to plasma is of pineal origin. Thus, plasma melatonin levels can be used as a marker of circadian melatonin secretion by the pineal gland and of its beta-adrenergic regulation.

Animals↗
PubMed1980

Brain-specific benzodiazepine receptors and putative endogenous benzodiazepine-like compounds.

The recent demonstration of high-affinity binding sites for the benzodiazepines in the mammalian CNS has provided new information on the mechanism of action of this important class of drugs. The presence of these binding sites has prompted studies on their pharmacological and physiological significance, including attempts at isolating an endogenous ligand. The results presented here support the pharmacological importance of these binding sites as receptors, since there is a highly significant correlation between the occupation of these sites by various benzodiazepines and their clinical effects. Our results further support the physiological significance of the benzodiazepine receptor since brain-specific receptors can be demonstrated in the intact animal under physiological conditions. The isolation of a number of substances from bovine brain that competitively inhibit 3H-diazepam binding to synaptosomal membranes suggests the presence of an endogenous ligand. Two of these substances have been identified as the purines inosine and hypoxanthine. Pharmacological studies of these purines suggest that they may have diazepam-like effects in vivo. These results support the existence in brain of endogenous benzodiazepine-like compounds that could normally be involved in ameliorating anxiety and (or) seizure activity.

Animals↗
PubMed1979

Effects of 1-desamo-8-D-arginine vasopressin on behaviour and cognition in primary affective disorder.

DDAVP (1-desamino-8-d-arginine vasopressin), a synthetic analogue of vasopressin with prolonged half-life and high antidiuretic and low pressor activity, was given in a double-blind placebo-controlled trial to four patients with major affective illness. Three of four patients showed highly significant and consistent improvements in tests designed to measure the formation, encoding, and organisation of long-term trace events in memory. Two patients also showed a significant but less consistent amelioration of other depressive symptoms during DDAVP treatment. These findings implicate central vasopressin function in the processing of information and possibly other aspects of affective illness.

Affective Symptoms↗
PubMed1979

Phase advance of the circadian sleep-wake cycle as an antidepressant.

Sleep in depressed patients resembles sleep in normal subjects whose circadian rhythms of temperature and rapid-eye-movement sleep are phase-advanced (shifted earlier) relative to their sleep schedules. If this analogy is relevant to the pathophysiology of depressive illness, advancing the time of sleep and awakening should temporarily compensate for the abnormal timing of depressed patients' circadian rhythms. Four of seven manic-depressive patients studied longitudinally spontaneously advanced their times of awakening (activity onset) as they emerged from the depressive phase of their illness. In a phase-shift experiment, a depressed manic-depressive woman was twice brought out of depression for 2 weeks by advancing her sleep period so that she went to sleep and arose 6 hours earlier than usual. The antidepressant effect of the procedure was temporary and similar in duration to circadian desynchronization induced by jet lag in healthy subjects. This result supports the hypothesis that abnormalities of sleep patterns in some types of depression are due to abnormal internal phase relationships of circadian rhythms.

Bipolar Disorder↗