@article{bast_cognitive_2017,
	title = {Cognitive deficits caused by prefrontal cortical and hippocampal neural disinhibition},
	volume = {174},
	issn = {0007-1188},
	url = {http://dx.doi.org/10.1111/bph.13850},
	doi = {10.1111/bph.13850},
	abstract = {We review recent evidence concerning the significance of inhibitory GABA
transmission and of neural disinhibition, that is, deficient GABA
transmission, within the prefrontal cortex and the hippocampus, for
clinically relevant cognitive functions. Both regions support important
cognitive functions, including attention and memory, and their dysfunction
has been implicated in cognitive deficits characterizing neuropsychiatric
disorders. GABAergic inhibition shapes cortico-hippocampal neural
activity, and, recently, prefrontal and hippocampal neural disinhibition
has emerged as a pathophysiological feature of major neuropsychiatric
disorders, especially schizophrenia and age-related cognitive decline.
Regional neural disinhibition, disrupting spatio-temporal control of
neural activity and causing aberrant drive of projections, may disrupt
processing within the disinhibited region and efferent regions. Recent
studies in rats showed that prefrontal and hippocampal neural
disinhibition (by local GABA antagonist microinfusion) dysregulates burst
firing, which has been associated with important aspects of neural
information processing. Using translational tests of clinically relevant
cognitive functions, these studies showed that prefrontal and hippocampal
neural disinhibition disrupts regional cognitive functions (including
prefrontal attention and hippocampal memory function). Moreover,
hippocampal neural disinhibition disrupted attentional performance, which
does not require the hippocampus but requires prefrontal-striatal circuits
modulated by the hippocampus. However, some prefrontal and hippocampal
functions (including inhibitory response control) are spared by regional
disinhibition. We consider conceptual implications of these findings,
regarding the distinct relationships of distinct cognitive functions to
prefrontal and hippocampal GABA tone and neural activity. Moreover, the
findings support the proposition that prefrontal and hippocampal neural
disinhibition contributes to clinically relevant cognitive deficits, and
we consider pharmacological strategies for ameliorating cognitive deficits
by rebalancing disinhibition-induced aberrant neural activity. Linked
Articles This article is part of a themed section on Pharmacology of
Cognition: a Panacea for Neuropsychiatric Disease? To view the other
articles in this section visit
http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.19/issuetoc.},
	number = {19},
	journal = {Br. J. Pharmacol.},
	author = {Bast, Tobias and Pezze, Marie and McGarrity, Stephanie},
	month = oct,
	year = {2017},
	note = {00000},
	keywords = {Sep 20 import, duplicate},
	pages = {3211--3225}
}

{"_id":"WFvjv2NoDAF5SuEAs","bibbaseid":"bast-pezze-mcgarrity-cognitivedeficitscausedbyprefrontalcorticalandhippocampalneuraldisinhibition-2017","downloads":0,"creationDate":"2018-04-27T04:04:44.347Z","title":"Cognitive deficits caused by prefrontal cortical and hippocampal neural disinhibition","author_short":["Bast, T.","Pezze, M.","McGarrity, S."],"year":2017,"bibtype":"article","biburl":"https://bibbase.org/zotero/davidlloyd33","bibdata":{"bibtype":"article","type":"article","title":"Cognitive deficits caused by prefrontal cortical and hippocampal neural disinhibition","volume":"174","issn":"0007-1188","url":"http://dx.doi.org/10.1111/bph.13850","doi":"10.1111/bph.13850","abstract":"We review recent evidence concerning the significance of inhibitory GABA transmission and of neural disinhibition, that is, deficient GABA transmission, within the prefrontal cortex and the hippocampus, for clinically relevant cognitive functions. Both regions support important cognitive functions, including attention and memory, and their dysfunction has been implicated in cognitive deficits characterizing neuropsychiatric disorders. GABAergic inhibition shapes cortico-hippocampal neural activity, and, recently, prefrontal and hippocampal neural disinhibition has emerged as a pathophysiological feature of major neuropsychiatric disorders, especially schizophrenia and age-related cognitive decline. Regional neural disinhibition, disrupting spatio-temporal control of neural activity and causing aberrant drive of projections, may disrupt processing within the disinhibited region and efferent regions. Recent studies in rats showed that prefrontal and hippocampal neural disinhibition (by local GABA antagonist microinfusion) dysregulates burst firing, which has been associated with important aspects of neural information processing. Using translational tests of clinically relevant cognitive functions, these studies showed that prefrontal and hippocampal neural disinhibition disrupts regional cognitive functions (including prefrontal attention and hippocampal memory function). Moreover, hippocampal neural disinhibition disrupted attentional performance, which does not require the hippocampus but requires prefrontal-striatal circuits modulated by the hippocampus. However, some prefrontal and hippocampal functions (including inhibitory response control) are spared by regional disinhibition. We consider conceptual implications of these findings, regarding the distinct relationships of distinct cognitive functions to prefrontal and hippocampal GABA tone and neural activity. Moreover, the findings support the proposition that prefrontal and hippocampal neural disinhibition contributes to clinically relevant cognitive deficits, and we consider pharmacological strategies for ameliorating cognitive deficits by rebalancing disinhibition-induced aberrant neural activity. Linked Articles This article is part of a themed section on Pharmacology of Cognition: a Panacea for Neuropsychiatric Disease? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.19/issuetoc.","number":"19","journal":"Br. J. Pharmacol.","author":[{"propositions":[],"lastnames":["Bast"],"firstnames":["Tobias"],"suffixes":[]},{"propositions":[],"lastnames":["Pezze"],"firstnames":["Marie"],"suffixes":[]},{"propositions":[],"lastnames":["McGarrity"],"firstnames":["Stephanie"],"suffixes":[]}],"month":"October","year":"2017","note":"00000","keywords":"Sep 20 import, duplicate","pages":"3211--3225","bibtex":"@article{bast_cognitive_2017,\n\ttitle = {Cognitive deficits caused by prefrontal cortical and hippocampal neural disinhibition},\n\tvolume = {174},\n\tissn = {0007-1188},\n\turl = {http://dx.doi.org/10.1111/bph.13850},\n\tdoi = {10.1111/bph.13850},\n\tabstract = {We review recent evidence concerning the significance of inhibitory GABA\ntransmission and of neural disinhibition, that is, deficient GABA\ntransmission, within the prefrontal cortex and the hippocampus, for\nclinically relevant cognitive functions. Both regions support important\ncognitive functions, including attention and memory, and their dysfunction\nhas been implicated in cognitive deficits characterizing neuropsychiatric\ndisorders. GABAergic inhibition shapes cortico-hippocampal neural\nactivity, and, recently, prefrontal and hippocampal neural disinhibition\nhas emerged as a pathophysiological feature of major neuropsychiatric\ndisorders, especially schizophrenia and age-related cognitive decline.\nRegional neural disinhibition, disrupting spatio-temporal control of\nneural activity and causing aberrant drive of projections, may disrupt\nprocessing within the disinhibited region and efferent regions. Recent\nstudies in rats showed that prefrontal and hippocampal neural\ndisinhibition (by local GABA antagonist microinfusion) dysregulates burst\nfiring, which has been associated with important aspects of neural\ninformation processing. Using translational tests of clinically relevant\ncognitive functions, these studies showed that prefrontal and hippocampal\nneural disinhibition disrupts regional cognitive functions (including\nprefrontal attention and hippocampal memory function). Moreover,\nhippocampal neural disinhibition disrupted attentional performance, which\ndoes not require the hippocampus but requires prefrontal-striatal circuits\nmodulated by the hippocampus. However, some prefrontal and hippocampal\nfunctions (including inhibitory response control) are spared by regional\ndisinhibition. We consider conceptual implications of these findings,\nregarding the distinct relationships of distinct cognitive functions to\nprefrontal and hippocampal GABA tone and neural activity. Moreover, the\nfindings support the proposition that prefrontal and hippocampal neural\ndisinhibition contributes to clinically relevant cognitive deficits, and\nwe consider pharmacological strategies for ameliorating cognitive deficits\nby rebalancing disinhibition-induced aberrant neural activity. Linked\nArticles This article is part of a themed section on Pharmacology of\nCognition: a Panacea for Neuropsychiatric Disease? To view the other\narticles in this section visit\nhttp://onlinelibrary.wiley.com/doi/10.1111/bph.v174.19/issuetoc.},\n\tnumber = {19},\n\tjournal = {Br. J. 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