Gonadotropin response to naloxone challenge in female and male psychotic patients: a pilot study.
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Adult↗
Biomedical subjects
D Copolov
Publications and source records attributed to D Copolov.
Psychotic symptoms resulting from intraventricular infusion of dopamine in Parkinson's disease.
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Brain↗
Symptomatic response to antipsychotics differs between recent onset and recurrent chronic schizophrenic patients.
The symptomatic response to standard antipsychotic treatment was assessed over the first 4 weeks of hospitalisation in 39 patients with DSM-III schizophrenia, active phase, using the Brief Psychiatric Rating Scale (BPRS). While highly significant improvement was noted overall, 36% of patients either did not improve or worsened. Furthermore there was no diminution in the withdrawal-retardation factor of the BPRS. Patients experiencing their first admission to hospital, all with recent-onset illness, were then compared with patients who presented with a recurrence and had illness of at least 3 years duration. Despite similarities in overall response, withdrawal-retardation scores did not diminish in recent-onset patients, in contrast to multiple admissions who demonstrated significant improvement. These findings suggest greater responsiveness of negative symptoms to treatment in patients with longstanding illness, and possibly a poorer prognosis in first admission patients with deficit manifestations.
Acute Disease↗
Hypothalamic release of atrial natriuretic factor and beta-endorphin into rat hypophysial portal plasma: relationship to oestrous cycle and effects of hypophysectomy.
The release of beta-endorphin and atrial natriuretic factor (ANF) into hypophysial portal plasma was investigated in male and female Wistar rats. The principal aim of the study was to investigate the possible role of beta-endorphin and ANF in the hypothalamic control of LH and prolactin secretion. In male rats, anaesthetized with urethane, the concentrations of beta-endorphin in portal blood collected immediately after hypophysectomy were within the same range as those in peripheral plasma. Furthermore, electrical stimulation of the median eminence did not increase the portal plasma concentrations of beta-endorphin. In female rats, anaesthetized with alphaxalone, the portal plasma concentrations in long-term (6-8 weeks) or acutely hypophysectomized rats were significantly greater than those in peripheral plasma. In acutely hypophysectomized female rats the concentrations and contents of beta-endorphin in portal plasma collected at 10.00-11.30 h of pro-oestrus were significantly (approximately sixfold) greater than at dioestrus or at 20.00-21.00 h of pro-oestrus, but these changes were not consistently seen in all experiments. In female rats in which the pituitary gland was not removed for portal blood collection, portal plasma contents of ANF remained unchanged throughout the day of pro-oestrus, suggesting that it is unlikely that ANF is involved in the spontaneous LH or prolactin surge. The effects of ovarian steroids on the secretion of hypothalamic ANF and beta-endorphin were determined by measuring the portal plasma concentration of ANF and beta-endorphin on the morning of presumptive pro-oestrus in rats ovariectomized 24 h previously and injected with either oil or oestradial benzoate (OB). Portal plasma contents of ANF were significantly lower in OB- compared with oil-treated rats, suggesting that oestradiol inhibits ANF release into rat hypophysial portal plasma. In contrast, there were no significant between-group differences in the content or concentration of beta-endorphin in portal plasma. Thus, the increased beta-endorphin in the portal plasma of some of the intact animals during the morning of pro-oestrus is not due to the preovulatory surge of oestradiol-17 beta. The output of beta-endorphin into portal blood in long-term hypophysectomized rats was lower than in dioestrous or pro-oestrous rats in which the pituitary gland was removed immediately before portal blood collection.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Evidence for post-translational processing of auriculin B to atriopeptin III immediately prior to secretion by hypothalamic neurons in culture.
In rats, the precursor of atrial natriuretic peptide (ANP) is produced and processed into its smaller congeners in the heart and the brain. We have demonstrated that a congener of ANP, auriculin B (ANP4-28), was present in long term monolayer cultures of neonatal rat hypothalamic neurons. In addition, forskolin and 3-isobutyl-1-methyl-xanthine (IBMX) augmented the cellular content of auriculin B in a dose dependent manner. Thus, cyclic AMP may act as an intracellular signal for modulating the functional development of hypothalamic immunoreactive (ir) ANP producing neurons. Furthermore, our data suggest that the form of ANP released from these cultures, following either forskolin treatment alone or forskolin treatment followed by acute high potassium depolarisation, was atriopeptin III (ANP5-28). Thus atriopeptin III, rather than auriculin B, may represent the endogenous ligand for ANP receptors in the central nervous system.
1-Methyl-3-isobutylxanthine↗
Glucocorticoid receptors and depression.
The number of glucocorticoid receptor sites in lymphocytes was estimated and plasma cortisol concentrations measured in 17 depressed patients, 12 patients with chronic schizophrenia, and 31 healthy control subjects. The number of receptor sites was significantly lower in the depressed patients than in either the controls or the patients with chronic schizophrenia, but there were no differences between the groups in the dissociation constants of the glucocorticoid receptors or the plasma cortisol concentrations. When two control subjects were studied intensively over 28 hours a slight diurnal variation in the number of glucocorticoid receptors was detected. The lower numbers of glucocorticoid receptors in the lymphocytes of depressed patients may explain why such patients, who often have hypercortisolaemia, do not show the clinical features of excess production of cortisol.
Adult↗
The medical and psychological investigation of psychogenic polydipsia: a case study.
The case of a 17 year-old female with psychogenic polydipsia is reported; 13 out of 18 members of her maternal family were known to have had polydipsia and polyuria, but only two had undergone endocrine investigations--one had diabetes insipidus and one also had psychogenic polydipsia. There are probable contributions of non-genetic family factors including imitation and identification to the development of this patient's condition. Detailed family and developmental histories may be of particular assistance in the understanding of the psychogenesis of the disorder in some patients.
Adolescent↗
Naloxone inhibits both glucocorticoid and [D-Ala2,Met5]enkephalinamide reversal of behavioural effect of adrenalectomy.
Intact rats treated immediately after a 15-min swimming exposure with i.m. 1 or 10 mg/kg naloxone (but not with 10 mg/kg of MRZ2593, a quaternary analogue) showed significant reduction in immobility (55, 30%) compared with controls (70%) during a 5-min retest 24 h later. This effect of naloxone was seen when administered 1 h prior to retest. Adrenalectomized rats, as previously shown, are only approximately 30% immobile on retest; administration of [D-Ala2,Met5]enkephalinamide (50 micrograms i.m.) or dexamethasome (6 micrograms i.m.) elevated immobility to 66 and 69% respectively. Administration of naloxone (0.1-10 mg/kg) progressively antagonized the effect of both [D-Ala2,Met5]enkephalinamide and dexamethasone, to 36 and 41% immobility on retest at 10 mg/kg. We conclude that the incorporation of information post-stress normally involves at least two opioidergic pathways, and that the integrity of one of these pathways is an absolute requirement for such incorporation to occur, based on the naloxone studies. In contrast, either glucocorticoids or enkephalin analogues are sufficient to restore behaviour post-adrenalectomy, suggesting that corticosteroid-dependent neural mechanisms may substitute for this second opioidergic pathway.
Adrenalectomy↗
Behavioural effect of adrenalectomy: reversal by glucocorticoids or [D-Ala2,Met5]enkephalinamide.
Rats adrenalectomized 4-6 d before a 15-min swimming test showed levels of immobility indistinguishable from controls. Retested 24 h later, adrenalectomized rats showed significantly reduced (28%) immobility compared with controls (70%) or hypophysectomized rats (60%), but not hypophysectomized-adrenalectomized rats (41%). The effect of adrenalectomy was reversed by the administration (within 1 h of initial test, but not subsequently) of dexamethasone (6-20 micrograms; 65% immobility) and corticosterone (6 mg; 74%), but not by the mineralocorticoid deoxycorticosterone (6 mg; 33%). [D-Ala2,Met5]enkephalinamide (5-50 micrograms) also restored immobility (66%). We postulate that hormones from both adrenal medulla and cortex are involved in the retention of information post-stress, and that these hormones act directly on the CNS rather than via the pituitary, since the response to adrenalectomy is not dependent on the presence of the pituitary gland.
Adrenalectomy↗
Insulin hypoglycaemia and cholinergic blockade: response of plasma immunoreactive beta-endorphin.
Six normal subjects were studied to investigate the mechanisms involved in the release of immunoreactive beta-endorphin (ir-beta EP) in response to insulin hypoglycaemia. Insulin alone (0.2 U/kg body weight) was followed after a 30 min lag period by a congruent to 2.5 fold elevation of plasma ir-beta EP, with a return to basal levels by 90 min. Concurrent infusion of 10% dextrose at 250 ml/h for 2 h prevented the increase in plasma ir-beta EP levels, suggesting an effect of hypoglycaemia rather than a direct effect of insulin. Premedication with atropine 0.6 mg at -30 min was followed by hypoglycaemia equivalent to that seen with insulin alone, but no increase in plasma ir-beta EP, suggesting the involvement of cholinergic mechanisms in the neural mediation of ir-beta EP release in response to hypoglycaemia.
Adult↗
Brain amines and peptides--their relevance to psychiatry.
The amine theory of affective disorder and the dopamine and endorphin theories of schizophrenia are controversial but heuristically valuable concepts that have emerged from the psychobiological revolution of the last decade. That revolution stemmed largely from the development of techniques for localizing and assaying neuroregulators and their receptors in the brain under normal, pathological and experimental conditions. The data thus obtained are reviewed here, and the current status of the emergent psychobiological hypotheses assessed.
Amines↗
Decreased serotonin2A receptors in Brodmann's area 9 from schizophrenic subjects. A pathological or pharmacological phenomenon?
There have been repeated reports of a decrease in serotonin2A receptors in the frontal cortex from subjects with schizophrenia. Similarly, in rats treated with antipsychotic drugs, it has been shown that many antipsychotic drugs decrease cortical serotonin2A receptors, an affect not seen with the antipsychotic drug haloperidol. We therefore compared the density of serotonin2A receptors in frontal cortex from schizophrenic subjects treated with haloperidol, schizophrenic subjects treated with other antipsychotic drugs, and nonschizophrenic subjects. Independent of antipsychotic drug treatment, serotonin2A receptors were decreased in the frontal cortex from schizophrenic subjects. Importantly, the density of serotonin2A receptors was not different in schizophrenic subjects whether or not they had been treated with haloperidol. This study suggests that data obtained from treating rats with antipsychotic drugs cannot be simplistically extrapolated to studies on tissue obtained postmortem from schizophrenic subjects treated with the same drugs.
Adolescent↗