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The ultimate physicist", "creators": [], "abstractNote": "", "websiteTitle": "", "websiteType": "", "date": "", "publisher": "", "place": "", "DOI": "", "citationKey": "", "url": "http://www-scf.usc.edu/~kallos/feynman.htm", "accessDate": "2013-08-24T23:26:26Z", "shortTitle": "", "language": "", "rights": "", "extra": "", "tags": [], "collections": [ "T9V9URX9" ], "relations": {}, "dateAdded": "2013-08-24T23:26:26Z", "dateModified": "2013-08-24T23:26:26Z" } }, { "key": "3QGJGUJH", "version": 8, "library": { "type": "group", "id": 199781, "name": "FiN", "links": { "alternate": { "href": "https://www.zotero.org/groups/fin", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/199781/items/3QGJGUJH", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/fin/items/3QGJGUJH", "type": "text/html" } }, "meta": { "createdByUser": { "id": 1545721, "username": "sirrangan", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/sirrangan", "type": "text/html" } } }, "creatorSummary": "Guidotti et al.", "parsedDate": "2005-07-01", "numChildren": 0 }, "data": { "key": "3QGJGUJH", "version": 8, "itemType": "journalArticle", "title": "GABAergic dysfunction in schizophrenia: new treatment strategies on the horizon", "creators": [ { "creatorType": "author", "firstName": "Alessandro", "lastName": "Guidotti" }, { "creatorType": "author", "firstName": "James", "lastName": "Auta" }, { "creatorType": "author", "firstName": "John M.", "lastName": "Davis" }, { "creatorType": "author", "firstName": "Erbo", "lastName": "Dong" }, { "creatorType": "author", "firstName": "Dennis R.", "lastName": "Grayson" }, { "creatorType": "author", "firstName": "Marin", "lastName": "Veldic" }, { "creatorType": "author", "firstName": "Xianquan", "lastName": "Zhang" }, { "creatorType": "author", "firstName": "Erminio", "lastName": "Costa" } ], "abstractNote": "Rationale Cortical γ-aminobutyric acid (GABA)ergic neurons contribute to the orchestration of pyramidal neuron population firing as follows: (1) by releasing GABA on GABAA and GABAB receptors, (2) by releasing reelin in the proximity of integrin receptors located on cortical pyramidal neuron dendritic spines, and (3) through reelin contributing to the regulation of dendritic spine plasticity by modulating dendritic resident mRNA translation. In schizophrenia (SZ) and bipolar (BP) postmortem brains, the downregulation of mRNAs encoding glutamic acid decarboxylase 67 (GAD67) and reelin decreases the cognate proteins coexpressed in prefrontal cortex (PFC) GABAergic neurons. This finding has been replicated in several laboratories. Such downregulation suggests that the neuropil hypoplasticity found in the PFC of SZ and BP disorder patients may depend on a downregulation of GABAergic function, which is associated with a decrease in reelin secretion from GABAergic neuron axon terminals on dendrites, somata, or axon initial segments of pyramidal neurons. Indirectly, this GABAergic neuron downregulation may play a key role in the expression of positive and negative symptoms of SZ and BP disorders. Objectives The above described GABAergic dysfunction may be addressed by pharmacological interventions to treat SZ and BP disorders using specific benzodiazepines (BZs), which are devoid of intrinsic activity at GABAA receptors including α1 subunits but that act as full positive allosteric modulators of GABA action at GABAA receptors containing α2, α3, or α5 subunits. These drugs are expected to enhance GABAergic signal transduction without eliciting sedation, amnesia, and tolerance or dependence liabilities. Results and conclusions BZs, such as diazepam, although they are efficient in equilibrating GABAA receptor signal transduction in a manner beneficial in the treatment of positive and negative symptoms of SZ, may not be ideal drugs, because by mediating a full positive allosteric modulation of GABAA receptors containing the α1 subunit, they contribute to sedation and to the development of tolerance after even a brief period of treatment. In contrast, other BZ-binding site ligands, such as 6-(2bromophenyl)-8-fluoro-4H-imidazo [1,5-a][1,4] benzodiazepine-3-carboxamide (imidazenil), which fail to allosterically and positively modulate the action of GABA at GABAA receptors with α1 subunits but that selectively allosterically modulate cortical GABAA receptors containing α5 subunits, contribute to the anxiolytic, antipanic, and anticonvulsant actions of these ligands without producing sedation, amnesia, or tolerance. Strong support for the use of imidazenil in psychosis emerges from experiments with reeler mice or with methionine-treated mice, which express a pronounced reelin and GAD67 downregulation that is also operative in SZ and BP disorders. In mice that model SZ symptoms, imidazenil increases signal transduction at GABAA receptors containing α5 subunits and contributes to the reduction of behavioral deficits without producing sedation or tolerance liability. Hence, we suggest that imidazenil may be considered a prototype for a new generation of positive allosteric modulators of GABAA receptors, which, either alone or in combination with neuroleptics, should be evaluated in GABAergic dysfunction operative in the treatment of SZ and BP disorders with psychosis.", "publicationTitle": "Psychopharmacology", "publisher": "", "place": "", "date": "2005/07/01", "volume": "180", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "191-205", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Psychopharmacology", "DOI": "10.1007/s00213-005-2212-8", "citationKey": "", "url": "http://link.springer.com/article/10.1007/s00213-005-2212-8", "accessDate": "2013-08-18T03:55:30Z", "PMID": "", "PMCID": "", "ISSN": "0033-3158, 1432-2072", "archive": "", "archiveLocation": "", "shortTitle": "GABAergic dysfunction in schizophrenia", "language": "en", "libraryCatalog": "link.springer.com", "callNumber": "", "rights": "", "extra": "", "tags": [ { "tag": "Benzodiazepines", "type": 1 }, { "tag": "Bipolar disorder", "type": 1 }, { "tag": "Diazepam", "type": 1 }, { "tag": "GABA-mimetics", "type": 1 }, { "tag": "GABAA receptors", "type": 1 }, { "tag": "Glutamic acid decarboxylase", "type": 1 }, { "tag": "Imidazenil", "type": 1 }, { "tag": "Psychoses", "type": 1 }, { "tag": "Reelin", "type": 1 }, { "tag": "Schizophrenia", "type": 1 } ], "collections": [ "T9V9URX9" ], "relations": {}, "dateAdded": "2013-08-24T07:32:15Z", "dateModified": "2013-08-24T07:32:15Z" } }, { "key": "K2CAXCVE", "version": 8, "library": { "type": "group", "id": 199781, "name": "FiN", "links": { "alternate": { "href": "https://www.zotero.org/groups/fin", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/199781/items/K2CAXCVE", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/fin/items/K2CAXCVE", "type": "text/html" } }, "meta": { "createdByUser": { "id": 1545721, "username": "sirrangan", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/sirrangan", "type": "text/html" } } }, "creatorSummary": "Guidotti A et al.", "parsedDate": "2000-11-01", "numChildren": 0 }, "data": { "key": "K2CAXCVE", "version": 8, "itemType": "journalArticle", "title": "Decrease in reelin and glutamic acid decarboxylase67 (gad67) expression in schizophrenia and bipolar disorder: A postmortem brain study", "creators": [ { "creatorType": "author", "name": "Guidotti A" }, { "creatorType": "author", "name": "Auta J" }, { "creatorType": "author", "name": "Davis JM" }, { "creatorType": "author", "name": "et al" } ], "abstractNote": "Background \nReelin (RELN) is a glycoprotein secreted preferentially by cortical γ-aminobutyric acid-ergic (GABAergic) interneurons (layers I and II) that binds to integrin receptors located on dendritic spines of pyramidal neurons or on GABAergic interneurons of layers III through V expressing the disabled-1 gene product (DAB1), a cytosolic adaptor protein that mediates RELN action. To replicate earlier findings that RELN and glutamic acid decarboxylase (GAD)67, but not DAB1 expression, are down-regulated in schizophrenic brains, and to verify whether other psychiatric disorders express similar deficits, we analyzed, blind, an entirely new cohort of 60 postmortem brains, including equal numbers of patients matched for schizophrenia, unipolar depression, and bipolar disorder with nonpsychiatric subjects.Methods Reelin, GAD65, GAD67, DAB1, and neuron-specific–enolase messenger RNAs (mRNAs) and respective proteins were measured with quantitative reverse transcriptase–polymerase chain reaction (RT-PCR) or Western blot analyses. Reelin-positive neurons were identified by immunohistochemistry using a monoclonal antibody.Results Prefrontal cortex and cerebellar expression of RELN mRNA, GAD67 protein and mRNA, and prefrontal cortex RELN-positive cells was significantly decreased by 30% to 50% in patients with schizophrenia or bipolar disorder with psychosis, but not in those with unipolar depression without psychosis when compared with nonpsychiatric subjects. Group differences were absent for DAB1,GAD65 and neuron-specific–enolase expression implying that RELN and GAD67 down-regulations were unrelated to neuronal damage. Reelin and GAD67 were also unrelated to postmortem intervals, dose, duration, or presence of antipsychotic medication.Conclusions The selective down-regulation of RELN and GAD67 in prefrontal cortex of patients with schizophrenia and bipolar disorder who have psychosis is consistent with the hypothesis that these parameters are vulnerability factors in psychosis; this plus the loss of the correlation between these 2 parameters that exists in nonpsychotic subjects support the hypothesis that these changes may be liability factors underlying psychosis.", "publicationTitle": "Archives of General Psychiatry", "publisher": "", "place": "", "date": "November 1, 2000", "volume": "57", "issue": "11", "section": "", "partNumber": "", "partTitle": "", "pages": "1061-1069", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Arch Gen Psychiatry", "DOI": "10.1001/archpsyc.57.11.1061", "citationKey": "", "url": "http://dx.doi.org/10.1001/archpsyc.57.11.1061", "accessDate": "2013-08-18T03:54:32Z", "PMID": "", "PMCID": "", "ISSN": "0003-990X", "archive": "", "archiveLocation": "", "shortTitle": "Decrease in reelin and glutamic acid decarboxylase67 (gad67) expression in schizophrenia and bipolar disorder", "language": "", "libraryCatalog": "Silverchair", "callNumber": "", "rights": "", "extra": "", "tags": [], "collections": [ "T9V9URX9" ], "relations": {}, "dateAdded": "2013-08-24T07:32:15Z", "dateModified": "2013-08-24T07:32:15Z" } }, { "key": "R7GG2XSR", "version": 7, "library": { "type": "group", "id": 199781, "name": "FiN", "links": { "alternate": { "href": "https://www.zotero.org/groups/fin", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/199781/items/R7GG2XSR", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/fin/items/R7GG2XSR", "type": "text/html" } }, "meta": { "createdByUser": { "id": 1542384, "username": "ashleigh.sercombe", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/ashleigh.sercombe", "type": "text/html" } } }, "numChildren": 0 }, "data": { "key": "R7GG2XSR", "version": 7, "itemType": "webpage", "title": "Catalyst: Quantum Computing - 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