Progress in neuro-psychopharmacology最新文献

{"title":"Localization of N-acetylserotonin (NAS) in the rat hindbrain by immunohistology","authors":"Olga M. Pulido ,&nbsp;Gregory M. Brown ,&nbsp;Lee J. Grota","doi":"10.1016/0364-7722(81)90049-7","DOIUrl":"10.1016/0364-7722(81)90049-7","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. A specific anti-NAS antibody and fluorescein-labelled second antibody were employed to investigate the topographic distribution of immunoreactive NAS (INAS) in the hindbrain of the rat.</p></span></li><li><span>2.</span><span><p>2. Positive identification of INAS was confirmed in the granular layer of the cerebellum, the spinal tract of the fifth cranial nerve and the pontine reticular formation.</p></span></li><li><span>3.</span><span><p>3. INAS was also identified in neuronal cell bodies and processes of Purkinje cells, all cerebellar nuclei, the locus coeruleus and other brain stem regions.</p></span></li><li><span>4.</span><span><p>4. The pattern of INAS distribution was found to be different from that of serotonin and melatonin.</p></span></li><li><span>5.</span><span><p>5. Overlap of INAS- and NE- containing structures was identified in areas such as cerebellum and locus coeruleus, suggesting the possibility of a functional connection between these substances in some regions.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 573-576"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90049-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18088396","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":"Dopaminergic involvement in attention a novel animal model","authors":"R.J Katz,&nbsp;K Schmaltz","doi":"10.1016/0364-7722(81)90099-0","DOIUrl":"10.1016/0364-7722(81)90099-0","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Adult male outbred albino mice were acutely injected with either of two dopamine (DA) agonists; Apomorphine, a receptor agonist, or Amantadine, a DA releasing agent.</p></span></li><li><span>2.</span><span><p>2. Both drugs produced dose-related alterations in initial Y-maze behavior, consisting of significantly increased proportions of 2-arm entries.</p></span></li><li><span>3.</span><span><p>3. This behavior has previously been shown to reflect an abnormal attentional process.</p></span></li><li><span>4.</span><span><p>4. Thus DA activation may cause sensory perseveration.</p></span></li><li><span>5.</span><span><p>5. The implications of this finding for DA theories of psychopathology is discussed.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"4 6","pages":"Pages 585-590"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90099-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18234192","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":"Clinical response, plasma levels and pharmacokinetics of desiramine in depressed in-patients","authors":"Pavel D Hrdina ,&nbsp;Yvon D Lapierre","doi":"10.1016/0364-7722(81)90100-4","DOIUrl":"10.1016/0364-7722(81)90100-4","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Correlation between clinical response and plasma levels was investigated in seven patients with endogenous depression treated with 2×1 mg/kg/day of desipramine (DMI) for 21 days. Clinical response was measured by reduction in Hamilton Depression Rating Scale (HDRS) scores.</p></span></li><li><span>2.</span><span><p>2. A beneficial effect of DMI was seen in five out of seven patients studied and was fully evident already one week after the beginning of treatment.</p></span></li><li><span>3.</span><span><p>3. Great inter-individual differences were observed in DMI plasma levels both after a single dose and at ‘steady state’. The maximum plasma concentration after a single dose (C_max) ranged between 19 and 179 ng/ml and the mean ‘steady state’ concentration between 65 and 240 ng/ml.</p></span></li><li><span>4.</span><span><p>4. No significant correlation was found between HDRS scores and plasma levels of DMI; however, a plot of plasma levels and amelioration scores at the end (22nd day) of treatment was suggestive of a curvilinear relationship.</p></span></li><li><span>5.</span><span><p>5. Post ‘steady state’ plasma disappearance half-lives of DMI calculation in four patients ranged from 11.5 to 34.3 hr (mean ± S.E.M. = 26.2 ± 5.0).</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"4 6","pages":"Pages 591-600"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90100-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18234193","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":"Methods of multicenter trials in psychiatry part I: Review","authors":"Kurt A Fischer-Cornelssen","doi":"10.1016/0364-7722(81)90096-5","DOIUrl":"10.1016/0364-7722(81)90096-5","url":null,"abstract":"<div><p>General</p><p>Fifty out of 100 publications on multicenter trials and 21 on methods are listed and partly discussed. Our discussions concentrate only on double blind, therapeutic trials. Multicenter trials are the only way, to keep sources of heterogeneity or error under control. Making high demands, the advantages of well-done multicenter trials surpass by far the disadvantages. </p><ul><li><span>1.</span><span><p>1. How to conduct a multicenter trial. </p><ul><li><span>1.1.</span><span><p>1.1 Introduction: In a trial the variabilities of interest are the efficacy and tolerance of drugs. Therefore all efforts have to be made to minimize all other non-treatment variances or to keep them constant. A multicenter trial has to be a logical, feasable, carefully planned and standardized sequence of events, carried out exactly as planned.</p></span></li><li><span>1.2.</span><span><p>1.2 Sample consideration: Heterogeneity of patients' diagnoses is an additional variance. Every variability beside the drug-effect will lower the success of the trial, the reliability and validity of the results. To prove or reject a hypothesis, the only target patients for an efficient proof are endogenous depressions (antidepressant), exacerbated paranoid schizophrenia (neuroleptic) and chronic anxiety states (minor tranquilizer) of medium to severe degree. Despite difficulties diagnostic labeling of patients (WHO-ICD 9) is an absolute necessity: symptoms are only meaningful in the context of the diagnosis concerned. Also the course of illness, past and present, is of importance (spontaneous remission during study). Statistical reasons require much higher sample sizes than are usually considered: with an <span><math><mtext>α</mtext></math></span>-risk of 5 %, a <span><math><mtext>β</mtext></math></span>-risk of 10 %, a 50 % expected improvement of a standard and a 60% improvement of a new drug, two times 422 patients are necessary to demonstrate a difference.</p></span></li><li><span>1.3.</span><span><p>1.3 Settings and investigators: Cross-study variabilities of numerous sources should be minimized as much as possible, concentrating on efficacy and tolerance of drugs: “prevention is better than cure”. The higher the qualification, experience and capability of investigators and nurses, the better will be the results and reliability.</p></span></li><li><span>1.4.</span><span><p>1.4. Experimental design: Clinical multicenter trials should be organized and conducted in a way which resembles ordinary clinical practice and being in the best interest of the (future) patients (Declaration of Helsinki/Tokyo). The design, the protocol, patient forms, execution and evaluation should be a master-piece of clarity. There is only one way to minimize undesired variability and deviations: standardization of every detail from the beginning to the end, considering logical thinking, reality, feasibility and practicability. One kind of standardization should never be attempted, a fixe","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"4 6","pages":"Pages 545-560"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90096-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18235586","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":"Effect of acute or chronic pentobarbital administration on the steady state levels and the turnover rates of catecholamines in discrete brain areas of mice","authors":"Toshitaka Nabeshima,&nbsp;Kannosuke Fujimori,&nbsp;Ing K. Ho","doi":"10.1016/0364-7722(81)90060-6","DOIUrl":"10.1016/0364-7722(81)90060-6","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. In mice receiving a single injection of sodium pentobarbital, 75 mg/kg, i.p., the whole brain catecholamine contents did not change. However, norepinephrine levels of the diencephalon and mesencephalon and dopamine contents of the cortex and the striatum were increased by acute pentobarbital treatment. The depletion of norepinephrine after the treatment of <span><math><mtext>α-</mtext><mtext>methyl-</mtext><mtext>p</mtext><mtext>̄</mtext><mtext>tyrosine</mtext></math></span>, 250 mg/kg, 4 hr before sacrifice, was significantly smaller in the cortex, the pons plus medulla oblongata and the cerebellum in acute pentobarbital-treated animals. The rate of dopamine depletion after <span><math><mtext>α-</mtext><mtext>methyl-</mtext><mtext>p</mtext><mtext>̄</mtext><mtext>-tyrosine</mtext></math></span> treatment in the striatum was also slower than that of the control group.</p></span></li><li><span>2.</span><span><p>2. In pentobarbital tolerant animals, decreases in norepinephrine level of the pons plus medulla oblongata and in dopamine content of the striatum were observed. The depletion of dopamine after <span><math><mtext>α-</mtext><mtext>methyl-</mtext><mtext>p</mtext><mtext>̄</mtext><mtext>-tyrosine</mtext></math></span> treatment was significantly smaller than that of the control group.</p></span></li><li><span>3.</span><span><p>3. In pentobarbital dependent animals, changes of catecholamine steady state levels in discrete areas of the brain were returned to normal. The rates of norepinephrine depletion observed after <span><math><mtext>α-</mtext><mtext>methyl-</mtext><mtext>p</mtext><mtext>̄</mtext><mtext>-tyrosine</mtext></math></span> treatment in the cortex and the pons plus medulla oblongata were significantly greater than that of the control groups.</p></span></li><li><span>4.</span><span><p>4. The present results suggest that acute pentobarbital causes a depression of catecholaminergic neuronal activity by a decrease of catecholamine turnover (degradation) and the development of tolerance to pentobarbital accompanies with the suppression of catecholamine synthesis. In contrast, the norepinephrine turnover increases after the occurrence of abrupt withdrawal.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 2","pages":"Pages 121-128"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90060-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18280699","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":"Stress induced facilitation of opiate catalepsy in the rat: A reply to R.J. Katz","authors":"Dr. K. Ornstein","doi":"10.1016/0364-7722(81)90081-3","DOIUrl":"10.1016/0364-7722(81)90081-3","url":null,"abstract":"","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 3","pages":"Pages 281-282"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90081-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18280707","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":"Synthesis and conclusion","authors":"Malcolm Lader D.Sc., Ph.D., M.D., F.R.C.Psych.","doi":"10.1016/0364-7722(81)90069-2","DOIUrl":"10.1016/0364-7722(81)90069-2","url":null,"abstract":"","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 2","pages":"Pages 193-195"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90069-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115837249","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":"Anxiety as a state of diminished gabaergic neurotransmission resulting from too frequent recruitment of gabaergic neurons: A neurophysiological model","authors":"Joannis N. Nestoros","doi":"10.1016/0364-7722(81)90053-9","DOIUrl":"10.1016/0364-7722(81)90053-9","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. All of the most commonly used antianxiety drugs (benzodiazepines, barbiturates, ethanol) selectively enhance GABA-mediated neurotransmission.</p></span></li><li><span>2.</span><span><p>2. The degree of GABA-potentiation produced by benzodiazepines correlates well with their relative affinities for the benzodiazepine receptor.</p></span></li><li><span>3.</span><span><p>3. Repetitive stimulation of the recurrent inhibitory GABAergic pathway in rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this “disinhibition” is counteracted by antianxiety drugs.</p></span></li><li><span>4.</span><span><p>4. A neurophysiological model is proposed, conceptualizing anxiety as the by-product of hypervigilance occurring in frequencies higher than those that the GABAergic system can accommodate, before “fading” or “desensitization” occurs.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 591-594"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90053-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17342642","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":"NAD+-dependent acetaldehyde oxidation in Drosophila","authors":"Francoise Garcin,&nbsp;Denis Kasiencsuk,&nbsp;Simone Radouco-Thomas,&nbsp;Johanne Cote,&nbsp;Corneille Radouco-Thomas","doi":"10.1016/0364-7722(81)90059-X","DOIUrl":"10.1016/0364-7722(81)90059-X","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. NAD⁺-dependent acetaldehyde oxidation was measured spectrophotometrically in homogenates of flies Drosophila melanogaster.</p></span></li><li><span>2.</span><span><p>2. The reaction was specifically triggered by addition of acetaldehyde and proceeded linearily over five minutes.</p></span></li><li><span>3.</span><span><p>3. At low acetaldehyde concentrations the reaction rate was rapidly maximal whereas higher acetaldehyde concentrations proved to be inhibitary.</p></span></li><li><span>4.</span><span><p>4. Enzyme activity in regard to NAD⁺ concentration followed classical Michaelis kinetics. The apparent Km for NAD⁺ was 0.05 mM.</p></span></li><li><span>5.</span><span><p>5. These data provide evidence for the presence of a NAD⁺-dependent aldehyde dehydrogenase. It is suggested that this enzyme is involved in the oxidation of acetaldehyde in Drosophila.</p></span></li><li><span>6.</span><span><p>6. The biochemical and biological significance of this enzyme in regard to ethanol metabolism and ethanol tolerance is discussed.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 619-627"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90059-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17854772","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":"Effect of parachlorophenylalanine on the incidence of abnormal behaviors observed following diazepam withdrawal","authors":"Tsutomu Suzuki ,&nbsp;Toshio Yoshii ,&nbsp;Saizo Yanaura ,&nbsp;Ryuji Fukumori ,&nbsp;Tetsuo Satoh ,&nbsp;Haruo Kitagawa","doi":"10.1016/0364-7722(81)90094-1","DOIUrl":"10.1016/0364-7722(81)90094-1","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Rats were rendered dependent on diazepam by administrating escalating dosages of diazepam in diet.</p></span></li><li><span>2.</span><span><p>2. At the time of diazepam withdrawal, the animals were treated with parachlorophenylalanine (PCPA), a potent serotonin (5-HT) depleter, or the corresponding vehicle.</p></span></li><li><span>3.</span><span><p>3. After diazepam withdrawal, PCPA-treated animals showed abnormal behaviors, such as aggression, irritability, vocalization and muscular rigidity.</p></span></li><li><span>4.</span><span><p>4. In contrast, little or no changes in behavior were observed in control animals.</p></span></li><li><span>5.</span><span><p>5. These results suggest that depletion of brain 5-HT by PCPA potentiates diazepam withdrawal signs.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 4","pages":"Pages 415-417"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0364-7722(81)90094-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17516481","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}