Journal of neural transmission. General section最新文献

{"title":"Evidence for prolonged recovery of dopaminergic transmission after detoxification in alcoholics with poor treatment outcome.","authors":"A Heinz,&nbsp;B Lichtenberg-Kraag,&nbsp;S S Baum,&nbsp;K Graf,&nbsp;F Kruger,&nbsp;M Dettling,&nbsp;H Rommelspacher","doi":"10.1007/BF01276510","DOIUrl":"https://doi.org/10.1007/BF01276510","url":null,"abstract":"<p><p>It has been hypothesized that dysfunction of dopaminergic neurotransmission is involved in the pathogenesis of alcohol addiction. Therefore, peripheral dopamine levels, sensitivity of central dopamine receptors (apomorphine-induced Growth Hormone (GH) secretion), and the inhibitory efficacy of G-proteins on adenylyl cyclase activity (as an indicator for dopamine D2-receptor coupled second messenger mechanisms) were measured in 45 alcohol-dependent patients before and after detoxification and in 10 healthy controls. The time needed to adjust to abstinence conditions differed between patients with good and poor treatment outcome. In subsequent abstainers, effects of alcohol withdrawal were already found during the first 24 hours of abstinence (normalisation of GH response, increases in dopamine levels and the inhibitory efficacy of G-proteins). During the next 7 days of abstinence, no more significant changes were observed in the assessed variables. In subsequent relapsers, no significant effect of acute ethanol withdrawal on the same measures was found. However, at day 8 of abstinence, increases in apomorphine-induced GH secretion (towards normalisation), in dopamine plasma levels, and in the inhibitory efficacy of G-proteins (towards above-normal levels) were observed. This retarded adjustment of dopaminergic signal transduction seems to reflect the relapse risk of treatment nonresponders.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 2","pages":"149-57"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276510","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19720930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The yohimbine-induced anticonflict effect in the rat, Part I. Involvement of noradrenergic, serotonergic and endozepinergic(?) mechanisms.","authors":"A Söderpalm,&nbsp;O Blomqvist,&nbsp;B Söderpalm","doi":"10.1007/BF01276457","DOIUrl":"https://doi.org/10.1007/BF01276457","url":null,"abstract":"<p><p>The alpha 2-adrenoceptor antagonist yohimbine has in several previous studies been found to produce anticonflict effects comparable to those produced by the benzodiazepines (BDZ) in rat punished conflict models. In this and a following paper we have tried to elucidate the neurochemical mechanisms underlying these effects in a modified Vogel's drinking conflict test. Since yohimbine previously has been demonstrated to interfere both with noradrenaline (NA) and serotonin (5-HT) neurochemistry, and, in addition, shows affinity for the BDZ binding site, we have focused on the putative involvement of these neuronal systems in the yohimbine-induced anticonflict effect. The alpha 2-adrenoceptor agonist clonidine (10 micrograms/kg, i.p.) completely antagonized the anticonflict effect of yohimbine (4.0 mg/kg, i.p.), whereas the alpha 1-adrenoceptor agonist ST 587 (1.0 mg/kg, i.p.) had no effect. The anticonflict effect of yohimbine was totally abolished also following lesioning of NA neurons with 6-hydroxy-dopamine. A high dose of the mixed beta 1 and beta 2 adrenoceptor antagonist propranolol (8.0 mg/kg, i.p.) caused a partial blockade of the yohimbine-induced effect in intact animals, whereas the selective beta 1-adrenoceptor antagonist metoprolol (4.0 mg/kg, i.p.) had no significant effect and the alpha 1-adrenoceptor antagonist prazosin instead potentiated the anticonflict action. The anticonflict effect of yohimbine was dose-dependently antagonized also by the 5-HT precursor L-5-hydroxytryptophan (25-100 mg/kg, i.p.). The BDZ receptor antagonist flumazenil (10 mg/kg, p.o.), as well as Ro 15-4513 (1.0 mg/kg, p.o.), a partial inverse agonist at BDZ receptors, partly, but significantly, counteracted the yohimbine-induced anticonflict effect, whereas low doses of both the chloride channel blocker picrotoxin and the GABAA antagonist bicuculline only tended to counteract the yohimbine effect. Taken together, the results in the present behavioral paper indicate that the anticonflict effect of yohimbine involves both increased NA and decreased 5-HT activity, and that direct or indirect activation of BDZ receptors may also be involved. Neurochemical findings related to these behavioral results are presented in a following paper.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 3","pages":"175-89"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunocytochemical localization of GTP cyclohydrolase I in the brain, adrenal gland, and liver of mice.","authors":"I Nagatsu,&nbsp;H Ichinose,&nbsp;M Sakai,&nbsp;K Titani,&nbsp;M Suzuki,&nbsp;T Nagatsu","doi":"10.1007/BF01281153","DOIUrl":"https://doi.org/10.1007/BF01281153","url":null,"abstract":"<p><p>GTP cyclohydrolase I (GCH) is the first and rate-limiting enzyme for the biosynthesis of tetrahydrobiopterin (BH4), the cofactor of phenylalanine, tyrosine, and tryptophan hydroxylases, the enzymes that synthesize tyrosine, catecholamines (dopamine, noradrenaline, and adrenaline), and serotonin, respectively. We produced for the first time polyclonal antibody with highly sensitive immunoreactivity against an oligopeptide of rat enzyme, GEPERELPRPGA, by immunization of rabbits with the peptide conjugated to hemocyanin by glutaraldehyde. The specificity of the antibody was confirmed by Western blot analysis. Using this antibody specific for GCH, we observed strong GCH immunostaining in the liver cells, in the dopamine-, noradrenaline-, adrenaline-, or serotonin-containing cells of the brain, and in the adrenal gland of mice. Immunocytochemical studies revealed GCH to be localized in monoamine-containing perikarya in the periglomerular cells of the olfactory bulb, zona incerta, arcuate nucleus, ventral tegmental area, substantia nigra pars compacta, locus ceruleus, nucleus tractus solitarius, area postrema, and ventrolateral area of the medulla oblongata. GCH immunostaining was particularly strong in serotoninergic nuclei, such as dorsal and median raphe nuclei, nucleus raphe pallidus, and nucleus raphe magnus. By immunoelectron microscopy, GCH-labeled cytoplasm and microtubules in the processes were observed ultrastructurally, but no staining was found in the mitochondria, and Golgi apparatus. Immunostaining was observed neither in the group D neurons that contain only aromatic amino acid decarboxylase without tyrosine hydroxylase, nor in glial cells and endothelial cells. These results indicate the abundant presence of GCH in catecholaminergic and serotoninergic neurons as well as in the adrenal medulla and liver, where BH4 is synthesized as the cofactor of tyrosine, tryptophan, and phenylalanine hydroxylases.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 3","pages":"175-188"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01281153","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Turning behavior in rats with unilateral lesions of the subthalamic nucleus: synergism between D1 and D2 receptors.","authors":"M G Murer,&nbsp;V Sinay,&nbsp;J H Pazo","doi":"10.1007/BF01271535","DOIUrl":"https://doi.org/10.1007/BF01271535","url":null,"abstract":"<p><p>Rats with unilateral kainic acid lesion of the subthalamic nucleus showed a dose dependent rotational response to the lesioned side (ipsilateral) after systemic administration of the non-selective dopaminergic agonist apomorphine. Both D2 and D1 selective antagonists ((-)sulpiride and SCH23390) inhibited the response to apomorphine in these rats. Selective D2 and D1 agonists (quinpirole and SKF38393) were unable to induce turning behavior. However, an ipsilateral circling response was obtained after the simultaneous application of both agonists. The interaction mechanism between dopaminergic receptor subtypes seems to be similar to that of other normosensitive models of turning previously studied (Barone et al., 1986; Robertson and Robertson, 1986; Arnt and Perregard, 1987; Asim et al., 1990; Pazo et al., 1993). It is proposed that the ipsilateral turning response to dopaminergic agonists in rats with subthalamic nucleus lesion results from an impaired behavioral expression of the action of dopaminergic agonists on one side, leading the rats to turn away from the intact hemisphere.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 2","pages":"123-35"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271535","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19924823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disturbances of cerebrospinal fluid (CSF) circulation--neuropsychiatric symptoms and neuroradiological contribution.","authors":"E Hofmann,&nbsp;T Becker,&nbsp;J Meixensberger,&nbsp;M Jackel,&nbsp;M Schneider,&nbsp;H Reichmann","doi":"10.1007/BF01271471","DOIUrl":"https://doi.org/10.1007/BF01271471","url":null,"abstract":"<p><p>The present study aimed at relating dementia, pseudo-neurasthenic and affective organic brain syndromes to underlying type of CSF flow disorder and to subsequent alteration of anatomy. T2*-weighted magnetic resonance imaging (MRI) in the midsagittal plane permitted an analysis of aqueductal CSF flow phenomena and hydrocephalus-induced elevation, thinning and dorsal impingement of the corpus callosum. Furthermore, the width of the third ventricle was measured on the transverse scout images. 72 patients with communicating hydrocephalus (increased aqueductal CSF pulsations) and 26 patients with aqueductal stenosis (absence of aqueductal flow phenomena) were compared with 22 controls. Dementia and affective disorders were distributed equally among both CSF flow subgroups whereas pseudo-neurasthenic syndromes were observed more frequently in non-communicating hydrocephalus (p < 0.03). Alzheimer-type and multiinfarct dementia syndromes were found more frequently in communicating hydrocephalus whereas non-classifiable dementia showed some predilection for non-communicating hydrocephalus. Callosal height, area and third ventricular width did not predict affective or pseudoneurasthenic disorder whereas third ventricular width (p < 0.01) and callosal area (p < 0.05) discriminated between demented and non-demented patients. Dorsal impingement of the corpus callosum by the falx was a non-specific finding.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"79-88"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271471","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EEG reactivity and EEG activity in never-treated acute schizophrenics, measured with spectral parameters and dimensional complexity.","authors":"M Koukkou,&nbsp;D Lehmann,&nbsp;A Federspiel,&nbsp;M C Merlo","doi":"10.1007/BF01271472","DOIUrl":"https://doi.org/10.1007/BF01271472","url":null,"abstract":"<p><p>Our approaches to the use of EEG studies for the understanding of the pathogenesis of schizophrenic symptoms are presented. The basic assumptions of a heuristic and multifactorial model of the psychobiological brain mechanisms underlying the organization of normal behavior is described and used in order to formulate and test hypotheses about the pathogenesis of schizophrenic behavior using EEG measures. Results from our studies on EEG activity and EEG reactivity (= EEG components of a memory-driven, adaptive, non-unitary orienting response) as analyzed with spectral parameters and \"chaotic\" dimensionality (correlation dimension) are summarized. Both analysis procedures showed a deviant brain functional organization in never-treated first-episode schizophrenia which, within the framework of the model, suggests as common denominator for the pathogenesis of the symptoms a deviation of working memory, the nature of which is functional and not structural.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"89-102"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271472","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological problems and clinical relevance of structural neuroimaging in dementia research.","authors":"C J Lang","doi":"10.1007/BF01271474","DOIUrl":"https://doi.org/10.1007/BF01271474","url":null,"abstract":"<p><p>Structural neuroimaging and dementia are conceptually different being only loosely correlated. Computed tomography or magnetic resonance imaging can never \"prove\" a clinical syndrome such as dementia, but yield clues as to its cause and the site and extent of pathological changes. Conversely, the type and degree of intellectual deterioration can hardly predict neuroradiological findings. The value of structural neuroimaging lies in detecting or excluding possible causes of dementia and quantifying linear or volumetric parameters of tissue and fluid volume. If based on a presumed or established etiology, however, specific neuropsychological and dementia syndromes may correspond to focal pathological changes seen in well-defined cerebral areas as recent investigations have shown with hippocampal atrophy in Alzheimer's dementia.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"131-43"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"99mTc-HMPAO-SPECT in the diagnosis of senile dementia of Alzheimer's type--a study under clinical routine conditions.","authors":"G Stoppe,&nbsp;J Staedt,&nbsp;A Kögler,&nbsp;R Schütze,&nbsp;H J Kunert,&nbsp;D Sandrock,&nbsp;D L Munz,&nbsp;D Emrich,&nbsp;E Rüther","doi":"10.1007/BF01271479","DOIUrl":"https://doi.org/10.1007/BF01271479","url":null,"abstract":"<p><p>This study was designed to evaluate, whether investigations of cerebral blood flow can be a helpful diagnostic tool in the differential diagnosis between (senile) dementia of Alzheimer's type [(S)DAT] and geriatric depression with cognitive impairment. Under clinical routine conditions we performed Single Photon Emission Computed Tomography (SPECT) using 99mTc-Hexamethylpropyleneamine Oxime (HMPAO) in 23 patients with (S)DAT (14f, 9m; mean age 68.9 y), 17 patients with geriatric depression (9 f, 8 m; mean age 66.4 y) and 12 age-matched controls (9 f, 3 m; mean age 69.2 y). Semiquantitative analysis (corticocerebellar ratios) of eight different regions of interest (ROI) revealed a significantly (p < 0.05) reduced perfusion in the (S)DAT patients compared to the control group. The depression group exhibited perfusion values between the (S)DAT and control group. The difference between the depression and (S)DAT group was most prominent in the left parieto-occipital ROI (p = 0.008). We discuss the data with extensive regard to the literature and conclude that 99mTc-HMPAO SPECT is a valuable additional tool in the differential diagnosis of depression and dementia in the elderly.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"195-211"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271479","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MK801 induces late regional increases in NMDA and kainate receptor binding in rat brain.","authors":"X M Gao,&nbsp;C A Tamminga","doi":"10.1007/BF01271549","DOIUrl":"https://doi.org/10.1007/BF01271549","url":null,"abstract":"<p><p>We have previously shown that a single dose of PCP produces a dose-related increase in NMDA-sensitive 3H-glutamate binding in CA1 of hippocampus 24 hours later, and some regional changes in kainate binding. Here we report that dizocilpine (MK 801) (0.1 mg/kg and 1 mg/kg), a selective agonist at the PCP receptor and a noncompetitive antagonist of NMDA, produces a similar increase in NMDA-sensitive glutamate and kainate receptor binding in hippocampus 24 hours after a dose. These observations support the conclusion that blockade of glutamate-mediated transmission at the NMDA receptor selectively increases NMDA-sensitive glutamate receptor binding in CA1 of hippocampus and kainate binding in CA3 and dentate gyrus at putatively delayed time points. Several additional areas outside of hippocampus also showed receptor changes at 24 hours after MK801.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"105-13"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271549","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo formation of diazepam-like 1,4-benzodiazepines by Penicillium verrucosum var. verrucosum after administration of 2-aminobenzophenones and glycine.","authors":"G Bringmann,&nbsp;T Mader","doi":"10.1007/BF01271554","DOIUrl":"https://doi.org/10.1007/BF01271554","url":null,"abstract":"<p><p>The in vivo formation of the diazepam-like 1,4-benzodiazepine deschloronordiazepam from its assumed biogenetic precursors, 2-amino-benzophenone and glycine, by the mould strain Penicillium verrucosum var. verrucosum, is described. Deschloronordiazepam formation was established by GC/MSD analysis monitoring characteristic fragment patterns of the benzodiazepine moiety. The identification of deschloronordiazepam was confirmed by feeding experiments of D5-2-aminobenzophenone, as well as its brominated and chlorinated derivatives to the mould. The formation of the 1,4-benzodiazepine was observed to depend on various factors, e.g. the time of application of the precursors, duration of the incubation and kind of cultivation. The results represent the first actual de novo synthesis of such diazepam-like 1,4-benzodiazepines from plausible biosynthetic precursors in a living organism, in agreement with a biosynthetic concept recently established in our group. Such pharmacologically active 1,4-benzodiazepines had been detected in trace amounts in mammalian and plant tissues. Because of their unusual molecular framework, they had previously been considered not to fit into any conventional biosynthetic route.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"169-81"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271554","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}