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Biomedical subjects

A A Mathé

Publications and source records attributed to A A Mathé.

At least 73 records · Page 4Linked to original sources
PubMed1990

Electroconvulsive treatment attenuates behavioral response to SKF 38393 in reserpine-treated mice.

Electroconvulsive treatment (ECT) of mice, once daily for 7 days, significantly reduced the stimulation of motor activity induced by the selective dopamine (DA) D1-receptor agonist SKF 38393 (15 mg/kg IP), but significantly increased the motor stimulation by the unselective DA-receptor agonist apomorphine (1.5 mg/kg IP) in reserpine-treated (10 mg/kg IP) mice, when compared to control mice, receiving sham ECT. The results provide a functional correlate to previously observed ECT-induced down-regulation of D1 receptor sites in DA-rich regions of the rodent brain. Such an effect may be significant for clinical actions of ECT in affective disorders and, possibly, in Parkinson's disease.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Hypothalamic-pituitary-adrenal axis interaction with prostaglandins.

1. The major PGE2 plasma metabolite, 15-keto-13, 14-dihydro-PGE (PGEM) was measured during metyrapone, dexamethasone and ACTH tests in order to elucidate if plasma PGE was affected by short term changes of the hypothalamic-pituitary adrenal axis function in man. 2. Plasma PGEM, serum cortisol and serum 11-deoxycortisol were determined by RIA. 3. Metyrapone (an inhibitor of adrenal 11 beta-hydroxylase), 250-1000 mg was given orally at 4 hour intervals for 20 hours. PGEM, cortisol and 11-deoxycortisol were measured before and 10 and 22 hours after the start of metyrapone in 10 patients evaluated for pituitary disease. 4. Dexamethasone, 1 mg orally, was given at 23 hours on day one and 25 IU (1-24) ACTH were given iv at 8 hours on day two. Blood was drawn for determination of PGEM and cortisol at 8 hours day one, and 8 hours day two. After the ACTH injection, blood was drawn at 90 minutes (for PGEM) and at 120 minutes (for PGEM and cortisol). 10 subjects aged 21-62 years were studied. 5. Plasma PGEM levels were significantly increased after metyrapone, concomitantly with the lowering of serum cortisol levels. 6. No difference in the PGEM increase between patients with normal or subnormal 11-deoxycortisol response was found. 7. A significant increase in plasma PGEM levels was found when serum cortisol was suppressed 9 hours after dexamethasone administration. 8. Glucocorticoids inhibit synthesis of eicosanoids and the present results suggest that short term decrease in cortisol may stimulate PG synthesis.

17-Hydroxycorticosteroids↗
PubMed1990

Brain neuropeptides: tachykinins, neuropeptide Y, neurotensin and vasoactive intestinal polypeptide in the rat brain: modifications by ECT and indomethacin.

1. The effects of electroconvulsive treatment (ECT) and indomethacin on brain regional and right-left hemispheric distribution of tachykinins (TK), neuropeptide Y (NPY), neurotensin (NT) and vasoactive intestinal polypeptide (VIP) were studied in the rat. 2. Differences in peptide concentration between brain regions (frontal cortex, striatum, occipital cortex, hippocampus and hypothalamus) were found for all five peptides measured (all P values less than 0.001). 3. Furthermore, concentration differences between the hemispheres were found for SP, NKA and VIP (P less than 0.001, P less than 0.001 and and P less than 0.005, respectively), but not for NT and NPY. Peptide concentrations were generally higher in the right than the left hemisphere; e.g., SP levels in the frontal cortex, striatum, occipital cortex and hippocampus were 194, 390, 335 and 136 percent higher, respectively, in the right compared to the left hemisphere. The results are consistent with other findings of right-left brain asymmetries in distribution of some neurotransmitters. 4. One ECT had no detectable effects on concentrations of SP, NKA, NT or VIP. However, the mean concentration of NPY was higher in all regions (except the striatum) and both hemispheres (P = 0.004). 5. In the rats pretreated with indomethacin, levels of SP, NKA and NT were decreased (P less than 0.001, P less than 0.001 and P = 0.039 respectively), whereas the concentrations of VIP and NPY were not affected. For SP and NKA the decrease was apparent in all brain regions and both in the right and left hemispheres. For NT, the effect was more prominent in the left than in the right hemisphere.

Animals↗
PubMed1989

Effect of repeated electroconvulsive treatment on regional concentrations of tachykinins, neurotensin, vasoactive intestinal polypeptide, neuropeptide Y, and galanin in rat brain.

The effects of single and repeated electroconvulsive treatments (ECTs) on brain regional distribution of substance P (SP), neurokinin A (NKA), neurotensin (NT), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), and galanin (GAL) were studied in the rat. Rats were divided into four groups receiving one of the following treatments: one ECT, one sham ECT, six ECTs, or six sham ECTs. After sacrifice by focused microwave irradiation, brains were dissected into frontal cortex, striatum, occipital cortex, hippocampus, hypothalamus, and pituitary sections. Peptides were extracted by boiling the tissues in 1 mol/l acetic acid and measured in extract aliquots by specific radioimmunoassays. Marked regional differences (P = .0005) were found for each of the peptides measured. The highest concentrations of SP and NKA were found in the hypothalamus and, in descending order, in striatum, pituitary, frontal cortex, occipital cortex, and hippocampus. For NT, the highest level was found in the hypothalamus and, in descending order, in pituitary, striatum, hippocampus, frontal cortex, and occipital cortex. The highest VIP concentrations were measured in frontal and occipital cortex, followed by pituitary, hypothalamus, striatum, and hippocampus. The highest NPY and GAL concentrations were found in the hypothalamus and the pituitary; in frontal and occipital cortex, as well as in the striatum and hippocampus, the peptides levels were rather evenly distributed. Repeated handling (stress?) decreased both NT and GAL in frontal (P = .05 and .04) and occipital cortex (P = .09 and .07). ECT, one or six treatments, had no effect on SP, NKA, NT, VIP, or GAL concentrations in different brain regions. However, an increase in NPY concentrations in hippocampus (six sham ECTs vs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Modification of guinea pig lung anaphylaxis by central nervous system (CNS) perturbations.

Since several studies indicate that protection from lethal anaphylaxis is mediated by anterior hypothalamic (AH) lesions, we investigated the hypothesis that central nervous system perturbations can modify release of mediators from antigen-challenged sensitized lungs. Three types of perturbations were made in guinea pigs: AH perturbation (electrodes inserted and the current was applied), anterior hypothalamic sham (AS) (electrodes placed as in the AH group but no current was passed), and posterior hypothalamic (PH) perturbation (electrodes placed and the current was applied). A control group was sham operated (electrodes not inserted). Eleven days after the operation, guinea pigs receiving brain perturbations and half the control group were sensitized to the antigen ovalbumin. The other half of the control group received vehicle only (nonsensitized). Twenty-five days after this procedure, lungs were perfused in situ, and the outflows were collected before and after injection of antigen. The perfusates were assayed for immunoreactive prostaglandin and histamine, and the lungs were assayed for cAMP, guanosine monophosphate, and histamine. Release of mediators and changes in lung cyclic nucleotides after perfusion with antigen were significantly greater in all the antigen-sensitized compared to the nonsensitized animals. Within the anaphylactic groups, significant reductions in mediators and in cyclic nucleotides were found in the animals with perturbations of the AH region compared to the CO animals. The time course of mediator release was not altered. The results extend to the biochemical level, the observation that the perturbation of the AH region can markedly modify the anaphylactic response, and indicate that this effect may be due to altered release of mediators.

Anaphylaxis↗
PubMed1986

Plasma prostaglandin E2 metabolite--measured as 11-deoxy-15-keto-13,14-dihydro-11 beta,16 xi-cyclo-PGE2--in twins with schizophrenic disorder.

Blood samples were obtained from 18 twin pairs, and the major prostaglandin E2 (PGE2) plasma metabolite 15-keto-13,14-dihydro-PGE2 was measured by RIA after its conversion to 11-deoxy-15-keto-13,14-dihydro-11 beta,16 xi-cyclo-PGE2. Significant positive correlations were found in all the twin pairs, in 11 pairs diagnosed as DSM-III schizophrenic disorder and schizoid/schizotypal personality disorder, and in the 5 nonschizophrenic pairs. These results indicate that synthesis of prostaglandins (PGs) is in part genetically determined. With regard to absolute PGE2 metabolite levels, the data did not support the hypothesis of increased PGE2 in schizophrenia. Thus, seven of eight schizophrenic probands had lower metabolite concentrations than their healthy twin siblings, and in one pair they were similar. Furthermore, schizophrenic probands and their healthy sibling controls, taken as a group, had lower PGE2 metabolite levels than the group comprised of affective disorder probands and their respective controls. These findings raise the possibility that a change in PGE2 may be associated with schizophrenic and also possibly with affective disorders.

Alcoholism↗
PubMed1986

Cortisol and Alzheimer's disease, I: Basal studies.

Patients with Alzheimer's disease and nondemented elderly control subjects participated in studies of cortisol secretion during sleep and at 9:00 a.m. and were given dexamethasone suppression tests (DSTs) and lumbar punctures. Nocturnal and 9:00 a.m. cortisol concentrations were significantly higher in the demented patients. CSF MHPG negatively correlated with mean nocturnal cortisol. The most severely demented patients had the highest 9:00 a.m. and mean nocturnal cortisol concentrations. DST results did not distinguish samples with substantially different nocturnal cortisol concentrations. These results suggest that measurements of basal plasma cortisol concentrations and dexamethasone suppression provide different information but support the notion of somewhat higher than normal cortisol concentrations in Alzheimer's disease patients.

Aged↗
PubMed1986

Cortisol and Alzheimer's disease, II: Dexamethasone suppression, dementia severity, and affective symptoms.

The course of Alzheimer's disease can be complicated by depressive illness, often presenting enigmatically. To determine whether the dexamethasone suppression test (DST) can help distinguish patients with coexisting dementia and depression from those with dementia alone, DSTs were conducted with 22 nondepressed Alzheimer's disease patients. Eleven patients were nonsuppressors. The nonsuppressors were older than the suppressors but did not differ in depression or dementia ratings. The 8:00 a.m. postdexamethasone cortisol level correlated with depressive symptoms. A relationship between severity of dementia and depressive symptoms was also demonstrated.

Aged↗
PubMed1986

Correlates of lateral ventricular size in chronic schizophrenia, II: biological measures.

CSF homovanillic acid levels showed a significant negative correlation with ventricle-brain ratios (VBRs) in a group of drug-free chronic schizophrenic male veterans, while CSF 5-hydroxyindoleacetic acid levels showed a similar, nearly significant trend. The response of plasma human growth hormone to 0.75 mg of apomorphine also demonstrated a significant negative correlation with VBR in this group, but other measures of central neurotransmitter activity were unrelated to ventricular size.

Adult↗
PubMed1985

Evaluating prolactin response to dopamine agonists in schizophrenia. Methodological problems.

Serum prolactin (PRL) level was assessed after challenges with apomorphine hydrochloride, saline, dopamine hydrochloride, or levodopa-carbidopa (Sinemet) in 19 control and 38 chronic schizophrenic subjects. Baseline PRL level varied inversely with age. High correlations existed between baseline PRL level and any subsequent absolute measure of PRL after administration of a dopamine agonist or placebo. Percent decrease was not a function of baseline concentrations and was therefore the only independent measure of drug response. Baseline PRL level was generally lower during exacerbation than remission in patients studied during two states of illness. Percent PRL level decrease after apomorphine administration was significantly greater in normal subjects than in schizophrenics. Correction of apomorphine responses for corresponding placebo (saline) values abolished differences between groups. Prolactin responses after dopamine or levodopa-carbidopa did not differ; however, placebo correction was not possible.

Acute Disease↗
PubMed1985

Different pattern of association of beta-endorphin and cortisol responses to dextroamphetamine in postmenopausal women and young men.

A negative correlation between plasma beta-endorphin and cortisol responses to 0.15 mg/kg dextroamphetamine i.v. was found in a group of seven normal postmenopausal women, while the responses of the two hormones were positively correlated in nine normal young men. These results suggest that even though the adrenocorticotropic hormone (ACTH)-cortisol and beta-endorphin are usually regulated by the same mechanism (both ACTH and beta-endorphin are derived from proopiocortin), there are situations in which these systems can be associated in a different pattern. The elucidation of these situations may contribute to the understanding of regulatory mechanisms of the two systems.

Adult↗
PubMed1985

Clinical studies of the cholinergic deficit in Alzheimer's disease. I. Neurochemical and neuroendocrine studies.

Autopsy studies indicating that cholinergic neurons are selectively lost in patients with Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT) suggest that peripheral markers for central cholinergic activity would be useful in diagnosis. The present studies found that cerebrospinal fluid (CSF) concentrations of acetylcholine (ACh) correlated with the degree of cognitive impairment (r = .70) in a sample of carefully diagnosed patients with AD/SDAT, but metabolites of other neurotransmitters were not related to cognitive state; this suggests that CSF ACh may be a valid measure of cholinergic degeneration. Cortisol and growth hormone were measured in plasma samples drawn from patients and controls every 30 minutes from 2100 to 1100 hours the next day. Mean plasma cortisol concentrations were higher in patients with AD/SDAT than in controls and correlated inversely with CSF methoxy-hydroxyphenylglycol (MHPG) (r = .61) and positively with degree of cognitive impairment (r = +.53); as anticholinergic drugs suppress cortisol this finding indicates that cortisol dysregulation may be a marker for abnormalities in other neurotransmitter systems, particularly the noradrenergic system. Growth hormone secretion was not different in patients and controls but was positively correlated with CSF MHPG (r = +.63).

Acetylcholinesterase↗
PubMed1985

Clinical studies of the cholinergic deficit in Alzheimer's disease. II. Psychopharmacologic studies.

Two studies investigated the ability of physostigmine, given both intravenously and orally, to reduce symptoms of Alzheimer's disease. Intravenous physostigmine significantly and reliably enhanced memory in 13 of 16 patients tested, but the dose producing the improvement varied among patients. Oral physostigmine decreased overall symptom severity in a reliable way in seven of 12 patients tested. The extent of improvement was correlated with the increase in mean cortisol secretion produced by physostigmine, suggesting that the drug improved behavior and cognition only to the extent that it had a specific central cholinomimetic effect. There was no significant association between response to physostigmine and results of a dexamethasone suppression test and physostigmine had no effect on growth hormone secretion.

Administration, Oral↗
PubMed1985

Oral physostigmine treatment of patients with Alzheimer's disease.

Twelve patients with Alzheimer's disease received 0.0, 0.5, 1.0, 1.5, and 2.0 mg of oral physostigmine every 2 hours for 3-5 days; symptoms after each dose were assessed with the Alzheimer's Disease Assessment Scale. Placebo and the dose associated with the least severe symptoms were then readministered for 3-5 days each. Of the 10 patients who completed the study, three showed clinically significant improvement on the highest physostigmine dose in both phases, four more were marginally improved in both phases, and three had inconsistent responses to physostigmine. Cortisol measures obtained during a sleep study suggest that patients whose symptoms improved on physostigmine were those in whom oral physostigmine enhanced central cholinergic activity.

Administration, Oral↗
PubMed1984

Apomorphine and schizophrenia. Treatment, CSF, and neuroendocrine responses.

Previous studies have variably reported the efficacy of apomorphine in treatment of schizophrenia and tardive dyskinesia. Stimulation of dopamine neuron autoreceptors is the presumed mode of action. Low-dose apomorphine (0.75 mg subcutaneously) and placebo were administered to 25 male schizophrenics to evaluate the drug's effect on psychotic and tardive dyskinetic symptoms. No significant improvement or deterioration was seen. Concomitant measurements of plasma prolactin and growth hormone levels and CSF homovanillic acid level indicated that the dose used was centrally active. These results indicate that an active though nonsedating dose of apomorphine does not ameliorate symptoms of schizophrenia or tardive dyskinesia.

Adult↗
PubMed1984

Age and the dexamethasone suppression test in depression.

The authors examined the effects of age on plasma cortisol concentrations of 81 depressed men after dexamethasone administration. Dexamethasone nonsuppression was significantly more frequent in patients older than age 55 than those younger. Similarly, older patients had significantly higher postdexamethasone cortisol concentrations than younger patients at all time points sampled. These differences could not be attributed to severity or to the prevalence of psychosis in older and younger depressed patients.

Adolescent↗
PubMed1983

Gamma-hydroxybutyrate in the treatment of schizophrenia.

Gamma-Hydroxybutyrate (GHB) inhibits firing of dopaminergic neurons and is thus potentially useful in the treatment of schizophrenia. GHB was administered to 10 schizophrenics concurrently with low-dose fluphenazine in a 6-week double-blind crossover study. No antipsychotic efficacy of GHB was noted. GHB had little if any effect on plasma prolactin levels after a single administration and caused few side effects. Trials with higher doses of GHB may be warranted.

Adult↗