{"title":"Larger topographical variance and decreased duration of brain electric microstates in depression.","authors":"W K Strik, T Dierks, T Becker, D Lehmann","doi":"10.1007/BF01271480","DOIUrl":"https://doi.org/10.1007/BF01271480","url":null,"abstract":"<p><p>The topographical configuration of the spontaneous brain electric fields is considered to contain relevant information about the pattern of the generating cortical electrochemical activation and the associated cognitive processes. Space oriented segmentation allows to break down the stream of the spontaneous EEG into brain electric microstates with stable configuration of the fields. It has been shown that the mean duration of the microstates was consistent with the duration of elementary steps of cognitive processes, and that different topographies of the microstates are associated with different cognitive modalities. Space-oriented segmentation was applied to the resting EEG of 22 depressive patients and of 22 controls. The topographical variance was larger, and the most prominent brain electrical microstates of the EEG epochs were significantly shorter in the depressive group than in controls. No differences were found for the shortest microstates. This result cannot be explained by group differences in the frequency domain of the EEG. No topographical differences were found between the microstates of depressives and those of controls. Based on previous results in healthy volunteers during spontaneous cognition and in schizophrenic patients, the findings indicate that formal aspects rather than the modalities of the stream of cognition are altered in depression. Automatic and schematic processing, and attentional deficits as described in depressive patients might account for the finding of less sustained brain electrical microstates.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"213-22"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271480","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559364","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":"Detection of psychoactive drugs using 19F MR spectroscopy.","authors":"M Bartels, K Albert","doi":"10.1007/BF01271467","DOIUrl":"https://doi.org/10.1007/BF01271467","url":null,"abstract":"<p><p>In vivo 19F resonance spectroscopy measurements of trifluorinated neuroleptics (fluphenazine and trifluoperazine) and later trifluorinated antidepressants (fluoxetine and fluvoxamine) began with animal experiments in 1983. Using rats which have been treated with high oral doses of fluphenazine over a period of three weeks in the beginning of these experiments the measurement time was very long (up to 10 h). The application of better techniques using surface coils led to marked improvement of the signal noise ratio and measurement times in animal experiments could be reduced to minutes. These results encouraged us and other groups to perform experiments in humans to detect and try to estimate brain levels of trifluorinated neuroleptics and antidepressants. The present data of several research groups demonstrate that 19F MR spectroscopy has the potential of becoming a valuable tool for monitoring drug levels at the site of action. The extension of the animal studies to humans might facilitate a better treatment of schizophrenic and depressive patients.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271467","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559458","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":"Effects of ACTH and ACTH 4-10 on aversive memory retrieval in rats.","authors":"K B Kumar, K S Karanth","doi":"10.1007/BF01271559","DOIUrl":"https://doi.org/10.1007/BF01271559","url":null,"abstract":"<p><p>The aim of the study was to examine whether ACTH and ACTH-fragment 4-10, given before the test would produce a selectively enhanced retrieval of aversive memories, in the same way as preexposure to inescapable footshocks, in rats. For this purpose animals conditioned in a T-maze with appetitive (10% sucrose) and aversive (2.0 mA footshock) events were administered (s.c.) a single dose of 10, 20 or 40 ug/rat of ACTH or 5, 10 or 20 ug/rat of ACTH-fragment 4-10, 20-min before testing. The retention test conducted in the same training apparatus 72-hrs after conditioning showed a dose-dependent increase in latencies to enter the previously shocked goalarm with the absence of such a difference in responding to the nonshocked goalarm, in ACTH and ACTH 4-10 treated groups. This differential response was not observed in saline treated rats. This effect of peptides on memory retrieval was similar to that seen following inescapable footshock in rats. The results suggest the possible involvement of ACTH in the differential enhancement of memory of helplessness condition.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"223-9"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271559","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669636","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}
P Hartvig, K J Lindner, P Bjurling, B Laengstrom, J Tedroff
{"title":"Pyridoxine effect on synthesis rate of serotonin in the monkey brain measured with positron emission tomography.","authors":"P Hartvig, K J Lindner, P Bjurling, B Laengstrom, J Tedroff","doi":"10.1007/BF01276505","DOIUrl":"https://doi.org/10.1007/BF01276505","url":null,"abstract":"<p><p>The influence of the co-factor pyridoxine, vitamin B6, on the activity of aromatic amino acid decarboxylase enzyme was studied by positron emission tomography, PET in the brain of the Rhesus monkey using the precursor for serotonin synthesis 5-hydroxy-L-tryptophan (5-HTP) radiolabelled with 11C in the beta-position. The rate constant for the formation of serotonin in the corpus striatum was calculated using a two tissue compartment model with reference area in the brain. In baseline investigations, the mean rate constants (+/-S.D:) for selective utilization of [11C]5-HTP to form [11C]serotonin in the corpus striatum was 0.0080 +/- 0.0011 min(-1). Pretreatment with intravenous pyridoxine hydrochloride 10 mg/kg bodyweight before doing a second PET study resulted in an enhanced rate constant by a mean of 20%. The rate increase was statistically significant. The increase varied considerably in different monkeys from no effect to more than 60%. The effect of pyridoxine on aromatic amino acid decarboxylase activity supported a regulatory role of pyridoxine on the synthesis of neurotransmitter in vivo, and may be of importance in diseases with deficiencies in neurotransmitter function.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 2","pages":"91-7"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276505","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19720925","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}
S S Wolf, T M Hyde, R C Saunders, M M Herman, D R Weinberger, J E Kleinman
{"title":"Autoradiographic characterization of neurotensin receptors in the entorhinal cortex of schizophrenic patients and control subjects.","authors":"S S Wolf, T M Hyde, R C Saunders, M M Herman, D R Weinberger, J E Kleinman","doi":"10.1007/BF01276565","DOIUrl":"https://doi.org/10.1007/BF01276565","url":null,"abstract":"<p><p>Neurotensin, an endogenous peptide and putative neurotransmitter, exhibits a wide range of interactions with dopaminergic neurons and displays some actions akin to neuroleptics. Moreover, neurotensin receptors are abundant in specific layers of the entorhinal cortex where cytoarchitectural abnormalities have been reported in schizophrenia. We therefore examined the entorhinal cortex from postmortem specimens of five control patients and six schizophrenic patients for alterations in neurotensin receptor quantitation and distribution using receptor autoradiography. Specific 125I- neurotensin binding was concentrated in layer II cell clusters, with a 40% reduction in binding in the schizophrenic group (p < 0.05). Moderate binding was observed in both cohorts in deep layers V/VI, with negligible binding in the hippocampus. There was no statistical difference in quantitative neurotensin binding in other lamina of the entorhinal cortex of schizophrenics compared with controls. The characteristic laminar pattern of binding did not differ between cohorts. The reduction in neurotensin binding in schizophrenics is consistent with an increasing number of reports of structural abnormalities in the medial temporal lobe of schizophrenics in general and the entorhinal cortex in particular. Further studies are required to examine the evidence for neuroanatomic and neurochemical pathology in the entorhinal cortex.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"55-65"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276565","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756681","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":"Prevention of nimodipine-induced impairment of learning by the selective sigma ligand PRE-084.","authors":"T Maurice, T P Su, D W Parish, A Privat","doi":"10.1007/BF01276561","DOIUrl":"https://doi.org/10.1007/BF01276561","url":null,"abstract":"<p><p>The high selectivity of the phencyclidine derivative PRE-084 for sigma (sigma) sites is demonstrated. We previously reported that this compound is able to markedly attenuate the impairment of learning induced in mice by the non-competitive NMDA antagonist MK-801, and the cholinergic nicotinic antagonist mecamylamine. In this study, we examined the effect of PRE-084 on the impairment of learning induced by acute administration of the calcium channel antagonist nimodipine. Nimodipine (0.3 mg/kg i.p.) impaired the spontaneous alternation behaviour in a Y-maze, decreased the step-down latency (SDL) in a passive avoidance task, and altered place learning and retention in a water-maze paradigm, with no marked effect on the motility observed using an open-field test. Preadministration of PRE-084 resulted in an attenuation of the impairment of alternation, in the 0.3-1 mg/kg s.c. range, in a marked increase in SDL, at 1-3 mg/kg, and improved place learning and retention in the water-maze, at 1 mg/kg. The effects on alternation behaviour and passive avoidance were completely prevented by co-administration of the purported sigma antagonist BMY-14802 (10 mg/kg i.p.), implicating the sigma sites. These results confirm the beneficial effect of the sigma ligand PRE-084 on pharmacological models of learning impairments, and indicate that sigma sites may modulate Ca2+ fluxes through VDCC, which may in turn bear some as yet unknown relationship to the previously described interaction with neurotransmitter systems.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"1-18"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276561","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19757408","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":"Synergistic interactions between COMT-/MAO-inhibitors and L-Dopa in MPTP-treated mice.","authors":"A Fredriksson, T Archer","doi":"10.1007/BF01276562","DOIUrl":"https://doi.org/10.1007/BF01276562","url":null,"abstract":"<p><p>Four experiments were performed to investigate the anti-akinesia effects of combining a sub-threshold dose (5 mg/kg, s.c.) of L-Dopa with different doses and combinations of COMT and MAO inhibitors upon the hypokinesia observed in MPTP-treated mice. Ro 40-7592 (1 and 3 mg/kg, s.c.), a novel COMT inhibitor, 60 min before L-Dopa reinstated both locomotion and rearing during a 2-hr interval after L-Dopa in MPTP mice; control mice were unaffected. The combination of Ro 40-7592 (3 mg/kg, s.c.) and pargyline (5 mg/kg, s.c.), a MAO inhibitor, with L-Dopa produced increases in both the peak effect and duration of action indicating a distinct potentiation of the effects of Ro 40-7592 by pargyline. L-Deprenyl, a MAOB inhibitor, together with L-Dopa, restored locomotion and rearing behaviour at all three doses applied (1, 3 and 10 mg/kg, s.c.); in control mice, motor activity was stimulated at the higher doses (3 and 10 mg/kg, s.c.), independent of L-Dopa administration. Combining L-Deprenyl (3 mg/kg, s.c.) with Ro 40-7592 (3 mg/kg, s.c.) one hr before L-Dopa to MPTP mice potentiated the restorative effects of each compound by itself, although no increase in peak effect was obtained. In the control mice, L-Deprenyl plus Ro 40-7592 or L-Deprenyl, by itself, stimulated motor activity following injection of L-Dopa. Marked dopamine (DA) depletions in the striatum of MPTP-treated mice were evident. The present results demonstrate that the effects of the COMT/MAO inhibitors in combination, and in conjunction with L-Dopa (at a dose that was without effect by itself), were well in excess of a summation of their individual effects. It was concluded therefore that a synergism of the restorative, anti-akinesic action of these compounds in MPTP-treated mice could offer a broader therapeutic spectrum in the treatment of Parkinson's disorder.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"19-34"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276562","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19757409","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}
P Riederer, W Gsell, L Calza, E Franzek, G Jungkunz, K Jellinger, G P Reynolds, T Crow, F F Cruz-Sánchez, H Beckmann
{"title":"Consensus on minimal criteria of clinical and neuropathological diagnosis of schizophrenia and affective disorders for post mortem research. Report from the European Dementia and Schizophrenia Network (BIOMED I).","authors":"P Riederer, W Gsell, L Calza, E Franzek, G Jungkunz, K Jellinger, G P Reynolds, T Crow, F F Cruz-Sánchez, H Beckmann","doi":"10.1007/BF01281160","DOIUrl":"https://doi.org/10.1007/BF01281160","url":null,"abstract":"<p><p>The sophisticated analysis of and growing information on the human brain requires that acquisition, dissection, storage and distribution of rare material are managed in a professional way. In this publication we present the consensus of the European work group \"European Dementia and Schizophrenia Network\", granted by the BIOMED I project of the EU, on minimal neuropathological and clinical requirements to include brains of patients with schizophrenia and affective disorders in post mortem studies. The description of clinical prerequisites in different EU countries and institutions is followed by a consensus on tissue handling, a consensus on minimal neuropathological criteria and a consensus on minimal clinical diagnostic criteria including clinical vignette, family, social, education/professional and general medical histories, general physical history including neurostatus, neurological, psychiatric, medication and general pathological histories, psychostatus, laboratory tests and a history provided by family/health care giver questionnaire. This publication should give help to interconnect different European brain bank centers on a basis of standardized protocols.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 3","pages":"255-64"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01281160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758884","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 effect of prolonged treatment with imipramine and electroconvulsive shock on the levels of endogenous enkephalins in the nucleus accumbens and the ventral tegmentum of the rat.","authors":"M Dziedzicka-Wasylewska, R Rogoz","doi":"10.1007/BF01281156","DOIUrl":"https://doi.org/10.1007/BF01281156","url":null,"abstract":"<p><p>The present study was designed to find out whether the prolonged administration of imipramine (IMI) or electroconvulsive shock (ECS) influences levels of endogenous enkephalins in the nucleus accumbens (NAS) and the ventral tegmentum (VTA) of the rat. Ressults indicate that treatment with IMI as well as with ECS has a profound effect on the levels of enkephalins in both structures. In the NAS both treatments lead to an increase in the levels of endogenous enkephalins and this effect is accompanied by an increase in mRNA coding for proenkephalin (measured by in situ hybridization) in this structure, indicating the enhancement of biosynthesis of endogenous enkephalinergic peptides following antidepressant treatment. The results are discussed in the light of the hypothesis concerning the influence of endogenous enkephalins on mesolimbic dopamine neurons, the activity of which plays a crucial role in the etiology of depression.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 3","pages":"221-28"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01281156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758956","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":"Glucocorticoids attenuate haloperidol-induced catalepsy through adrenal catecholamines.","authors":"C T Chopde, M S Hote, S N Mandhane, A V Muthal","doi":"10.1007/BF01276564","DOIUrl":"https://doi.org/10.1007/BF01276564","url":null,"abstract":"<p><p>To examine the influence of adrenal secretions on neuroleptic induced catalepsy, we studied the effect of adrenocorticoids, noradrenaline (NA) or adrenaline (AD) on haloperidol (HAL) induced catalepsy in adrenalectomised (ADX) and sham-adrenalectomised (sham-ADX) rats. HAL (1 mg/kg, i.p.) induced a greater degree of catalepsy in ADX rats as compared to sham-ADX rats. Corticosterone (CORT, 1-2 mg/kg, s.c.) or dexamethasone (1-2 mg/kg, s.c.) attenuated the HAL catalepsy in sham-ADX but not in ADX rats. Further, when the HAL (1 mg/kg) catalepsy score was maximal (at 120 min), the rats were subjected to cold stress (3 degrees C for 10 min) or treated with NA, AD (2 micrograms/kg, i.v.) or CORT (2 mg/kg, s.c.). After cold stress procedure or CORT treatment, the catalepsy was significantly reduced in sham-ADX but not in ADX rats, whereas NA or AD infusion caused an immediate but short lasting significant decrease in HAL catalepsy in both sham-ADX and ADX rats. The anticataleptic effect of NA or glucocorticoids was blocked by an alpha 1 adrenoceptor blocker, prazosin. These findings suggest that peripheral noradrenergic and adrenergic mechanisms play an important role in the neuroleptic induced catalepsy. Such mechanisms may mediate the anticataleptic action of glucocorticoids.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"47-54"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276564","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756680","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}