In vivo release of somatostatin from rat hippocampus and striatum.

Rats were implanted with microdialysis probes in hippocampi and striata, and somatostatin-like immunoreactivity (SS-LI) was measured in outflows obtained from awake, freely moving animals 48 and 72 h post implantation. SS-LI was measurable in all dialysates under basal conditions; concentrations were stable and within a narrow range, about 3-6 fmol/ml. Cysteamine (300 mg/kg, s.

Electroconvulsive stimuli and brain peptides: effect of modification of seizure duration on neuropeptide Y, neurokinin A, substance P and neurotensin.

We studied the effects of modification of duration of seizures induced by electroconvulsive stimuli (ECS) on the changes in concentration of neuropeptide Y (NPY), neurokinin A (NKA), substance P (SP) and neurotensin (NT)-like immunoreactivity (-LI) in specific rat brain regions. Rats were divided into groups pretreated with saline, indomethacin, flurbiprofen or diazepam prior to either six sham ECSs or six ECSs. After sacrifice by focused microwave irradiation, brains were dissected into frontal cortex, occipital cortex, striatum, hippocampus, pituitary and hypothalamic sections.

Brain neuropeptides: changes by treatment with the convulsants pentylenetetrazole and bicuculline.

1. The effects of chemically induced convulsions, clinically similar to those elicited by electroconvulsive treatment (ECT), on brain regional distribution of neuropeptide Y-, neurokinin A-, substance P- and neurotensin-like immunoreactivities were studied in the rat. 2.

MK-801 prevents the enhanced behavioural response to apomorphine elicited by repeated electroconvulsive treatment in mice.

Repeated administration of electroconvulsive stimuli (ECS) to mice once daily for a period of 7 days results in an enhanced locomotor response induced by apomorphine (1.0 mg/kg, IP). Pretreatment (30 min) with the N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (0.

Microwave irradiation increases recovery of neuropeptides from brain tissues.

The effect of focused high energy microwave treatment (MW) on brain concentrations and molecular forms of substance P, neurokinin A, neuropeptide Y, neurotensin, galanin and calcitonin gene-related peptide was investigated. Groups of rats were treated as follows: 1) MW, storage for 60 min at 22 degrees C, 2) Decapitation, storage for 60 min at 22 degrees C. 3) Decapitation, storage for 60 min at 22 degrees C, MW treatment, 4) MW, decapitation, storage for 2 min at 22 degrees C and 5) Decapitation, storage for 2 min at 22 degrees C.

Effect of lithium on tachykinins, calcitonin gene-related peptide, and neuropeptide Y in rat brain.

The effects of lithium on brain regional concentrations of substance P (SP)-, neurokinin A (NKA)-, calcitonin gene-related peptide (CGRP)- and neuropeptide Y (NPY)-like immunoreactivities (-LI) were studied in rat. In the pilot study, rats were divided into three groups that were administered vehicle, or 1 or 4 mEq/kg lithium sulphate, respectively, intraperitoneally once/day for 9 days. In the second experiment, rats were divided into three groups receiving vehicle, or 1 or 2 mEq/kg lithium sulphate, respectively, intraperitoneally twice/day for 9 days.

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.

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.

Neuropeptides in brain: effects of microwave irradiation and decapitation.

Substance P (SP)-, neurokinin A (NKA)-, neurotensin (NT)-, neuropeptide Y (NPY)- and vasoactive intestinal polypeptide (VIP)-like immunoreactivity (Ll) were measured and characterized by specific radioimmunoassays (RIA) and reverse phase high performance liquid chromatography (HPLC) in extracts of rat brain. Concentrations of SP-Ll, NKA-Ll and NT-Ll in brains of decapitated animals were 59, 49 and 64 percent lower compared to those found in animals sacrificed by focused microwave irradiation (MW). In contrast, no difference in brain NPY-Ll and VIP-Ll levels was found between animals killed by MW and decapitation.

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.

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.

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).

Electroconvulsive therapy and plasma prostaglandin E2 metabolite in major depressive disorder.

1. Animal experiments show that PGE2 affects the release of ACTH and corticosteroids. In depressed subjects, plasma concentrations of the same hormones are increased immediately following ECT.

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.

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.

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.

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.

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.

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.

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.

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.