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The Neurochemical Effects of Prazosin Treatment on Fear Circuitry in a Rat Traumatic Stress Model

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dc.contributor.authorAYDIN OMAY, BANU
dc.contributor.authorsKetenci, Sema; Acet, Nazife Gokce; Saridogan, Gokce Elif; Aydin, Banu; Cabadak, Hulya; Goren, Mehmet Zafer
dc.date.accessioned2022-03-14T10:12:22Z
dc.date.available2022-03-14T10:12:22Z
dc.date.issued2020-05-31
dc.description.abstractObjective: The timing of administration of pharmacologic agents is crucial in traumatic stress since they can either potentiate the original fear memory or may cause fear extinction depending on the phase of fear conditioning. Brain noradrenergic system has a role in fear conditioning. Data regarding the role of prazosin in traumatic stress are controversial. Methods: In this study, we examined the effects of prazosin and the noradrenergic system in fear conditioning in a predator stress rat model. We evaluated the direct or indirect effects of stress and prazosin on noradrenaline (NA), gamma-aminobuytyric acid (GABA), glutamate, glycine levels and choline esterase activity in the amygdaloid complex, the dorsal hippocampus, the prefrontal cortex and the rostral pons. Results: Our results demonstrated that prazosin might alleviate defensive behaviors and traumatic stress symptoms when given during the traumatic cue presentation in the stressed rats. However prazosin administration resulted in higher anxiety levels in non stressed rats when the neutral cue was presented. Conclusion: Prazosin should be used in PTSD with caution because prazosin might exacerbate anxiety in non-traumatized subjects. However prazosin might as well alleviate stress responses very effectively. Stress induced changes included increased NA and GABA levels in the amygdaloid complex in our study, attributing noradrenaline a possible inhibitory role on fear acquisition. Acetylcholine also has a role in memory modulation in the brain. We also demonstrated increased choline esterase acitivity. Cholinergic modulation might be another target for indirect prazosin action which needs to be further studied.
dc.identifier.doi10.9758/cpn.2020.18.2.219
dc.identifier.eissn2093-4327
dc.identifier.issn1738-1088
dc.identifier.pubmed32329303
dc.identifier.urihttps://hdl.handle.net/11424/244200
dc.identifier.wosWOS:000529831900007
dc.language.isoeng
dc.publisherKOREAN COLL NEUROPSYCHOPHARMACOLOGY
dc.relation.ispartofCLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNoradrenalline
dc.subjectRostral pons
dc.subjectCholinergic
dc.subjectGamma-aminobuytyric acid
dc.subjectGlutamic acid
dc.subjectGlycine
dc.subjectLOCUS-CERULEUS NEURONS
dc.subjectANIMAL-MODEL
dc.subjectALPHA-1-ADRENERGIC RECEPTORS
dc.subjectCARDIOVASCULAR-RESPONSES
dc.subjectAMYGDALA
dc.subjectEXTINCTION
dc.subjectANXIETY
dc.subjectCONSOLIDATION
dc.subjectPROPRANOLOL
dc.subjectANTAGONISTS
dc.titleThe Neurochemical Effects of Prazosin Treatment on Fear Circuitry in a Rat Traumatic Stress Model
dc.typearticle
dspace.entity.typePublication
local.avesis.idaaa8ec6e-1506-447b-94aa-1b026c7c67b9
local.import.packageSS16
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages12
local.journal.quartileQ3
oaire.citation.endPage230
oaire.citation.issue2
oaire.citation.startPage219
oaire.citation.titleCLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE
oaire.citation.volume18
relation.isAuthorOfPublicationaf9e48cc-cef6-4af2-bdb7-5b424aadfc2b
relation.isAuthorOfPublication.latestForDiscoveryaf9e48cc-cef6-4af2-bdb7-5b424aadfc2b

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