Progress in neuro-psychopharmacology最新文献

{"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":"Comments on the foundation and activities of the International Committee for Prevention and Treatment of Depression","authors":"P. Kielholz","doi":"10.1016/0364-7722(81)90072-2","DOIUrl":"10.1016/0364-7722(81)90072-2","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Experience thus far acquired by an International Committee for Prevention and Treatment of Depression which was founded in 1975, and whose aim is to improve treatment for depressive patients in everyday practice, would confirmed that the Committee's activities fulfil a genuine need. In this connection one of the major objective of the PTD Committee is to diseminate pertinent information about depression to general practitioner.</p></span></li><li><span>2.</span><span><p>2. It is gratifying to observe that practitioners who are not themselves psychiatrists are showing an increasing willingness to treat cases of depression on an ambulatory basis and that they are also grateful to receive practical information on diagnosis and treatment of depressive states.</p></span></li><li><span>3.</span><span><p>3. The Committee deliberately decided to concentrate its efforts initially on a selection of European countries, in order to accumulate the experience which would be required to develop a comprehensive system of post-graduate instruction.</p></span></li><li><span>4.</span><span><p>4. After this preliminary phase of its work was completed, the Committee expanded its activities to the United States and Japan.</p></span></li><li><span>5.</span><span><p>5. The main objective of the Committee is to obtain that the right patient will have the right diagnosis and get the right anti-depressant.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 2","pages":"Pages 205-208"},"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)90072-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17233592","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":"Acetylcholine turnover and aggression in related three strains of mice","authors":"Alexander G. Karczmar,&nbsp;Gisela H. Kindel","doi":"10.1016/0364-7722(81)90003-5","DOIUrl":"10.1016/0364-7722(81)90003-5","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. This study compares brain levels of acetylcholine (ACh) and choline, and ACh brain turnover in 3 inbred strains of mice, CF-1, C57B1/6 By and Balb-c-By; these parameters were measured in control (aggregated) mice as well as following two paradigms, mild footshock and isolation, applied alone or in combination.</p></span></li><li><span>2.</span><span><p>2. Enzymic radioassay method was used to measure brain ACh and choline; ACh turnover was evaluated by two computation methods.</p></span></li><li><span>3.</span><span><p>3. Aggregated Balb-c-By mice exhibited low ACh and choline levels as compared to those of the mice of the two other strains. ACh levels of C57B1/6 By and CF-1 mice did not differ significantly; choline levels of CF-1 mice were almost twofold higher than those of C57B1/6 By mice.</p></span></li><li><span>4.</span><span><p>4. ACh turnover of aggregated CF-1 mice was about twice as high as that of C57B1/6 By and more than twice higher than that of Balb-c-By mice.</p></span></li><li><span>5.</span><span><p>5. The effects of shock, isolation, or shock combined with isolation on the brain levels of ACh and choline of mice of the 3 strains were inconsistent and, frequently absent.</p></span></li><li><span>6.</span><span><p>6. ACh turnover was significantly decreased in the brains of CF-1 by the two paradigms, whether employed alone or in combination; there was no additive effect when footshock was combined with isolation.</p></span></li><li><span>7.</span><span><p>7. ACh turnover did not change consistently after the two paradigms, employed alone or in combination, in the case of C57B1/6 By and Balb-c-By mice; in some cases, ACh turnover was increased.</p></span></li><li><span>8.</span><span><p>8. Footshock proved to be a mild inducer of aggression as compared to isolation in the 3 mice strains; footshock combined with isolation proved to synergize with respect to aggression in the 3 strains. Whether exposed to footshock and isolation alone or to the combination of these procedures, CF-1 mice were significantly more aggressive than Balb-c-By and C57B1/6 By mice.</p></span></li><li><span>9.</span><span><p>9. It is emphasized that consistent facilitatory effect of the two paradigms on aggression as well as additive effect on aggression resulting from combining footshock and isolation should be contrasted with the inconsistent effects of the two paradigms, applied alone or in isolation, on ACh turnover; altogether, the data did not indicate that aggression is related to increased brain ACh turnover.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 1","pages":"Pages 35-48"},"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)90003-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18212453","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":"Possible muscarinic-cholinergic mediation of patterned aggressive reflexes in the cat","authors":"R.J. Katz","doi":"10.1016/0364-7722(81)90004-7","DOIUrl":"10.1016/0364-7722(81)90004-7","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Adult female outbred cats were prepared with chronic hypothalamic stimulating electrodes and ventricular cannulae.</p></span></li><li><span>2.</span><span><p>2. Cats were restrained, and patterned aggressive reflexes of elicited head turning, biting, and paw striking to proximate stimulation were assessed under a variety of stimulation conditions.</p></span></li><li><span>3.</span><span><p>3. In comparison with vehicle injection cholinergic stimulation by arecoline facilitated the three reflexes and cholinergic blockade by scopolamine inhibited them.</p></span></li><li><span>4.</span><span><p>4. Cholinergic-muscarinic receptors may be involved as mediators of terminal (consummatory) behaviors in aggressive syndromes.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 1","pages":"Pages 49-56"},"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)90004-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18212454","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}

{"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":"Clinical detection and assessment of drug induced neurotoxicity","authors":"Claudio A. Naranjo ,&nbsp;Luis Fornazzari ,&nbsp;Edward M. Sellers","doi":"10.1016/0364-7722(81)90024-2","DOIUrl":"10.1016/0364-7722(81)90024-2","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Drug-induced neurological disease is a relatively common problem. For example, the Boston Collaborative Drug Surveillance Program reported that in 11,526 hospitalized patients, 14.2% of adverse drug reactions (ADRs) were neurological.</p></span></li><li><span>2.</span><span><p>2. Drugs can induce various syndromes such as: disturbances of consciousness, psychiatric disorders, headache, cranial nerve disorders, movement disorders, psychosis, peripheral neuropathy, myopathy and autonomic dysfunction.</p></span></li><li><span>3.</span><span><p>3. The vast majority of ADRs are dose-related (e.g. CNS depression by sedative-hypnotics). In these cases the frequency and severity of the ADRs is proportional to the administered dose, therefore, they can be prevented and/or treated by adjusting the dosage to patient's needs. Dose-unrelated ADRs (e.g. malignant hyperthermia by various anaesthetic agents) are uncommon and the development of the reaction is mainly dependent on increased patient's susceptibility. Accordingly, the ADR can only be prevented by not readministering the drug.</p></span></li><li><span>4.</span><span><p>4. Most of the evidence associating specific drugs with neurological adverse events comes from single case reports in which no systematic assessment of causality has been made. Recently, valid and reliable definitions of ADRs have been reported (e.g. <span>Kramer et al, 1979</span>; <span>Naranjo et al, 1981</span>). The systematic application of these methods greatly reduce the ambiguity for analyzing alleged cases of ADRs. These methods can be easily applied by practising physicians in the assessment and reporting of suspected drug-induced neurological diseases.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 427-434"},"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)90024-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17342640","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 methylphenidate on tardive dyskinesia","authors":"Dragoljub Radonjic,&nbsp;Yvon D. Lapierre,&nbsp;Verner Knott","doi":"10.1016/0364-7722(81)90031-X","DOIUrl":"10.1016/0364-7722(81)90031-X","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. The effect of methylphenidate on motor activity was studied on chronic schizophrenics with a history of two or more years of neuroleptic treatment.</p></span></li><li><span>2.</span><span><p>2. Clinical examination and polygraphic recording - (EEG, EOG and multichannel EMG) were carried out on 41 patients. Of these, 15 had tardive dyskinesia, 11 had minor dyskinetic phenomena and 15 had no clinical signs of hyperkinetic motor disorder.</p></span></li><li><span>3.</span><span><p>3. A distinct qualitative pattern of motor activity was observed in TD patients as pseudorhythmic bursts of muscle action potentials which appeared in varying muscle groups at the rate of 0.6 - 1.2/second. These bursts of muscle activity were not found in the non-TD group of patients.</p></span></li><li><span>4.</span><span><p>4. Ritalin administration had a marked effect on TD patients as observed by the increased amplitude, duration and distribution of pseudorhythmic bursts. Eight out of 11 patients, with minor dyskinetic manifestations responded to methylphenidate with the same pattern as TD.</p></span></li><li><span>5.</span><span><p>5. Methylphenidate was found to evoke and enhance abnormal muscle activity in patients whose extrapyramidal motor system is already affected by neuroleptics. These findings suggest that methylphenidate administration, in combination with polygraphic recordings, may be a useful tool in the early diagnosis of TD.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 491-494"},"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)90031-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18351883","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":"Seasonal variation in plasma tryptophan in parturient women","authors":"Judith M. Baker ,&nbsp;Sheila L. Handley ,&nbsp;Gill Waldron ,&nbsp;T.Leslie Dunn","doi":"10.1016/0364-7722(81)90037-0","DOIUrl":"10.1016/0364-7722(81)90037-0","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. Blood samples were collected from 71 subjects between thirty-six weeks gestation and six weeks postpartum. Sample collection was carried out over a ten-month period. Subjects entered the study in three phases, month of parturition being July-September, October-December, or January-April. Data from each group and each sampling point relative to parturition were analysed separately.</p></span></li><li><span>2.</span><span><p>2. Seasonal variation in total tryptophan concentration was noted at six weeks postpartum, when women giving birth between January and April exhibited higher plasma levels than those in the other two groups.</p></span></li><li><span>3.</span><span><p>3. Percent unbound tryptophan was highest in women giving birth between July and September, and lowest for the January to April group. This seasonal effect was highly significant from thirty-six weeks gestation to day two postpartum, had disappeared by day five postpartum and reappeared at six weeks postpartum. Plasma concentrations of unbound tryptophan changed in parallel with percent unbound tryptophan. There is some evidence for a partial dependence of plasma unbound tryptophan on environmental temperature.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 515-518"},"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)90037-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18351889","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":"Pharmacological characterization of [3H] desipramine binding in rat cerebral cortex","authors":"Pavel D. Hrdina","doi":"10.1016/0364-7722(81)90045-X","DOIUrl":"10.1016/0364-7722(81)90045-X","url":null,"abstract":"<div><p></p><ul><li><span>1.</span><span><p>1. The specific binding of [³H]desipramine to membranes from rat brain cortex is biphasic and the Scatchard analysis of data shows two distinct components: the high affinity component, with a dissociation constant (K_D) of 4.5 nM and the low affinity component (K_D = 80 nM).</p></span></li><li><span>2.</span><span><p>2. Different order of potency in displacing the high affinity [³H]desipramine and [³H]imipramine binding was shown by various compounds tested. Nortriptyline and nisoxetine were the most potent displacers of [³H]desipramine specific binding while chlorimipramine and fluoxetine showed highest potency in competing for [³H]imipramine binding sites.</p></span></li><li><span>3.</span><span><p>3. Significant correlation was found between the ability of various drugs to inhibit [³H]desipramine binding and their potency to block the neuronal uptake of noradrenaline in brain.</p></span></li><li><span>4.</span><span><p>4. The results suggest that the high affinity binding of [³H]desipramine is distinct from that of [³H]imipramine and is most likely associated with sites involved in neuronal uptake of noradrenaline.</p></span></li></ul></div>","PeriodicalId":20801,"journal":{"name":"Progress in neuro-psychopharmacology","volume":"5 5","pages":"Pages 553-557"},"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)90045-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18351894","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}