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Article ; Online: Ventral Hippocampal Input to Infralimbic Cortex Is Necessary for the Therapeutic-Like Effects of Extinction in Stressed Rats.

Paredes, Denisse / Morilak, David A

The international journal of neuropsychopharmacology

2023 Volume 26, Issue 8, Page(s) 529–536

Abstract: Background: Posttraumatic stress disorder is characterized by deficits in cognitive flexibility related to dysfunction of the medial prefrontal cortex (mPFC). Exposure therapy can effectively reverse these deficits. Fear extinction in rodents bears ... ...

Abstract	Background: Posttraumatic stress disorder is characterized by deficits in cognitive flexibility related to dysfunction of the medial prefrontal cortex (mPFC). Exposure therapy can effectively reverse these deficits. Fear extinction in rodents bears similarity to exposure therapy. Extinction reverses chronic stress-induced deficits in cognitive flexibility on the attentional set-shifting test (AST), an mPFC-mediated process. This therapeutic effect requires activity of pyramidal neurons and brain derived neurotrophic factor (BDNF) signaling in infralimbic cortex (IL). However, the circuit mechanisms governing BDNF-mediated plasticity initiated by extinction in IL are unknown. The ventral hippocampus (vHipp) plays a role in regulating IL activity during extinction, and plasticity in vHipp is necessary for extinction memory consolidation. Therefore, we investigated the role of vHipp input to IL in the effects of extinction in reversing stress-induced cognitive deficits. Methods: vHipp input to IL was silenced using a Gi-Designer Receptors Exclusively Activated by Designer Drugs (DREADD) via local infusion of clozapine-N-oxide (CNO) into IL before extinction. A day later, rats were tested on AST. In a separate experiment, we tested whether vHipp input to the IL induces BDNF signaling to exert therapeutic effects. We activated the vHipp using a Gq-DREADD, and injected an anti-BDNF neutralizing antibody into IL. Rats were tested on the AST 24 hours later. Results: Silencing the vHipp input to IL prevented the beneficial effects of extinction in reversing stress-induced cognitive deficits. Activating vHipp input to IL in the absence of extinction was sufficient to reverse stress-induced deficits in set-shifting. The beneficial effects were blocked by local infusion of a neutralizing anti-BDNF antibody into IL. Conclusions: vHipp-driven BDNF signaling in IL is critical for extinction to counteract the deleterious cognitive effects of chronic stress.
MeSH term(s)	Rats ; Animals ; Extinction, Psychological ; Fear ; Cerebral Cortex ; Hippocampus ; Pyramidal Cells
Language	English
Publishing date	2023-07-21
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1440129-0
ISSN	1469-5111 ; 1461-1457
ISSN (online)	1469-5111
ISSN	1461-1457
DOI	10.1093/ijnp/pyad043
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Zs.A 5187: Show issues

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Article ; Online: Vortioxetine Reverses Impairment of Visuospatial Memory and Cognitive Flexibility Induced by Degarelix as a Model of Androgen Deprivation Therapy in Rats.

Vaiana, Alexandra M / Asher, Amber M / Tapia, Karla / Morilak, David A

Neuroendocrinology

2023 Volume 114, Issue 3, Page(s) 279–290

Abstract: Introduction: Androgen deprivation therapy (ADT) is a mainstay treatment for prostate cancer, but many patients experience cognitive impairment in domains mediated by the medial prefrontal cortex (mPFC) and hippocampus. Prostate cancer typically occurs ... ...

Abstract	Introduction: Androgen deprivation therapy (ADT) is a mainstay treatment for prostate cancer, but many patients experience cognitive impairment in domains mediated by the medial prefrontal cortex (mPFC) and hippocampus. Prostate cancer typically occurs in older patients (>65 years). As age is often accompanied by cognitive decline, it may impact the efficacy of any treatment aimed at restoring cognitive impairment induced by ADT. Vortioxetine, a multimodal antidepressant that improves cognition in depression, has been shown to be efficacious in elderly patients. Therefore, vortioxetine may improve cognition in older patients who experience cognitive decline after ADT. Methods: Young (3 months) and middle-aged (13 months) rats were used to investigate the influence of age on treating ADT-induced cognitive decline. As our previous studies used surgical castration, we tested if vortioxetine would reverse cognitive deficits associated with more translationally relevant chemical castration using degarelix. Vortioxetine was given in the diet for 21 days. Animals underwent behavioral testing to assess visuospatial memory mediated by the hippocampus and cognitive flexibility mediated by the mPFC. We also investigated changes in afferent-evoked responses in these regions in middle-aged rats. Results: Degarelix induced impairments in both visuospatial memory and cognitive flexibility that were reversed by vortioxetine. Vortioxetine also rescued afferent-evoked responses in the mPFC and hippocampus. However, modest age-related reductions in baseline visuospatial memory limited our ability to detect further decreases induced by degarelix in middle-aged rats due to a floor effect. Conclusion: These results suggest that vortioxetine may be a treatment option for older prostate cancer patients who experience cognitive decline after ADT.
MeSH term(s)	Male ; Aged ; Middle Aged ; Humans ; Rats ; Animals ; Vortioxetine/pharmacology ; Androgen Antagonists/pharmacology ; Androgens ; Prostatic Neoplasms ; Cognition ; Oligopeptides
Chemical Substances	Vortioxetine (3O2K1S3WQV) ; acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide ; Androgen Antagonists ; Androgens ; Oligopeptides
Language	English
Publishing date	2023-12-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	123303-8
ISSN	1423-0194 ; 0028-3835
ISSN (online)	1423-0194
ISSN	0028-3835
DOI	10.1159/000535365
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Article ; Online: Role of Orbitofrontal Cortex and Differential Effects of Acute and Chronic Stress on Motor Impulsivity Measured With 1-Choice Serial Reaction Time Test in Male Rats.

Girotti, Milena / Carreno, Flavia R / Morilak, David A

The international journal of neuropsychopharmacology

2022 Volume 25, Issue 12, Page(s) 1026–1036

Abstract: Background: Deficits in motor impulsivity, that is, the inability to inhibit a prepotent response, are frequently observed in psychiatric conditions. Several studies suggest that stress often correlates with higher impulsivity. Among the brain areas ... ...

Abstract	Background: Deficits in motor impulsivity, that is, the inability to inhibit a prepotent response, are frequently observed in psychiatric conditions. Several studies suggest that stress often correlates with higher impulsivity. Among the brain areas affected by stress, the orbitofrontal cortex (OFC) is notable because of its role in impulse control. OFC subregions with unique afferent and efferent circuitry play distinct roles in impulse control, yet it is not clear what OFC subregions are engaged during motor impulsivity tasks. Methods: In this study we used a rodent test of motor impulsivity, the 1-choice serial reaction time test, to explore activation of OFC subregions either during a well-learned motor impulsivity task or in a challenge task with a longer wait time that increases premature responding. We also examined the effects of acute inescapable stress, chronic intermittent cold stress and chronic unpredictable stress on motor impulsivity. Results: Fos expression increased in the lateral OFC and agranular insular cortex during performance in both the mastered and challenge conditions. In the ventral OFC, Fos expression increased only during challenge, and within the medial OFC, Fos was not induced in either condition. Inescapable stress produced a transient effect on premature responses in the mastered task, whereas chronic intermittent cold stress and chronic unpredictable stress altered premature responses in both conditions in ways specific to each stressor. Conclusions: These results suggest that different OFC subregions have different roles in motor impulse control, and the effects of stress vary depending on the nature and duration of the stressor.
MeSH term(s)	Rats ; Male ; Animals ; Reaction Time ; Impulsive Behavior ; Prefrontal Cortex/metabolism ; Frontal Lobe ; Cerebral Cortex ; Choice Behavior
Language	English
Publishing date	2022-09-07
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	1440129-0
ISSN	1469-5111 ; 1461-1457
ISSN (online)	1469-5111
ISSN	1461-1457
DOI	10.1093/ijnp/pyac062
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Zs.A 5187: Show issues

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Article: A Rodent Model of Exposure Therapy: The Use of Fear Extinction as a Therapeutic Intervention for PTSD.

Paredes, Denisse / Morilak, David A

Frontiers in behavioral neuroscience

2019 Volume 13, Page(s) 46

Abstract: The symptoms of post-traumatic stress disorder (PTSD) include cognitive impairment related to medial prefrontal cortical dysfunction. Indeed, a deficit of cognitive flexibility, i.e., an inability to modify previously learned thoughts and behaviors based ...

Abstract	The symptoms of post-traumatic stress disorder (PTSD) include cognitive impairment related to medial prefrontal cortical dysfunction. Indeed, a deficit of cognitive flexibility, i.e., an inability to modify previously learned thoughts and behaviors based on changes in the environment, may underlie many of the other symptoms of PTSD, such as changes in mood, hyper-arousal, intrusive thoughts, exaggerated and over-generalized fear, and avoidance behavior. Cognitive-behavioral therapies target the cognitive dysfunction observed in PTSD patients, training them to recalibrate stress-related perceptions, interpretations and responses. Preclinically, the extinction of conditioned fear bears resemblance to one form of cognitive therapy, exposure therapy, whereby an individual learns, through repeated exposure to a fear-provoking stimulus in a safe environment, that the stimulus no longer signals imminent threat, and their fear response is suppressed. In this review article, we highlight recent findings from our lab using fear extinction as a preclinical model of exposure therapy in rodents exposed to chronic unpredictable stress (CUS). We specifically focus on the therapeutic effects of extinction on stress-compromised set-shifting as a measure of cognitive flexibility, and active vs. passive coping behavior as a measure of avoidance. Finally, we discuss mechanisms involving activity and plasticity in the medial prefrontal cortex (mPFC) necessary for the therapeutic effects of extinction on cognitive flexibility and active coping.
Language	English
Publishing date	2019-03-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452960-6
ISSN	1662-5153
ISSN	1662-5153
DOI	10.3389/fnbeh.2019.00046
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Article ; Online: Infralimbic BDNF signaling is necessary for the beneficial effects of extinction on set shifting in stressed rats.

Paredes, Denisse / Knippenberg, Anna R / Morilak, David A

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2021 Volume 47, Issue 2, Page(s) 507–515

Abstract: Current pharmacotherapies for posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) are ineffective for many patients, and often do not restore cognitive dysfunction associated with these disorders. Behavioral therapies, such as ... ...

Abstract	Current pharmacotherapies for posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) are ineffective for many patients, and often do not restore cognitive dysfunction associated with these disorders. Behavioral therapies, such as exposure therapy, can be effective for treatment-resistant patients. The mechanisms underlying exposure therapy are not well-understood. Fear extinction as an intervention after chronic stress can model the beneficial effects of exposure therapy in rats. Extinction requires neuronal activity and protein synthesis in the infralimbic (IL) cortex for its beneficial effects. We hypothesized that extinction requires Brain-Derived Neurotrophic Factor (BDNF) activity in the IL cortex to reverse stress-induced cognitive flexibility impairments. Extinction learning reversed set-shifting deficits induced by Chronic Unpredictable Stress (CUS), tested 24 h after extinction. Blocking BDNF signaling in the IL cortex during extinction by local administration of a neutralizing antibody prevented the beneficial effects of extinction on set shifting after stress. Extinction induced activation of the BDNF TrkB receptor, and signaling pathways associated with BDNF (Akt and Erk). Administration of exogenous BDNF into IL cortex in the absence of extinction was sufficient to reverse the effects of stress on set shifting. The effects of extinction were prevented by blocking either Erk or Akt signaling in the IL cortex, whereas the effects of exogenous BDNF were dependent on Erk, but not Akt, signaling. Our observations suggest that BDNF-Erk signaling induced by extinction underlies plastic changes that can reverse or counteract the effects of chronic stress in the IL cortex.
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Depressive Disorder, Major ; Extinction, Psychological ; Fear/physiology ; Implosive Therapy ; Rats
Chemical Substances	Bdnf protein, rat ; Brain-Derived Neurotrophic Factor
Language	English
Publishing date	2021-09-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-021-01171-7
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Zs.A 2379: Show issues

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Article: Shock-probe Defensive Burying Test to Measure Active versus Passive Coping Style in Response to an Aversive Stimulus in Rats.

Fucich, Elizabeth A / Morilak, David A

Bio-protocol

2018 Volume 8, Issue 17

Abstract: Maladaptive avoidance behaviors are seen in many stress-related psychiatric illnesses. Patients with these illnesses favor passive, avoidant coping strategies rather than adaptive, active coping strategies. Preclinically, coping strategy can be measured ... ...

Abstract	Maladaptive avoidance behaviors are seen in many stress-related psychiatric illnesses. Patients with these illnesses favor passive, avoidant coping strategies rather than adaptive, active coping strategies. Preclinically, coping strategy can be measured in rats using the shock-probe defensive burying test, wherein rats receive a shock from an electrified probe inserted into a test cage that mimics their home cage environment, and behavioral output (immobility or burying) is recorded for 15 min following the shock. Immobility in response to the perceived threat of the shock-probe, associated with elevated stress hormone levels, is regarded as a passive, maladaptive coping strategy. In opposition, burying the probe is associated with lower stress hormone levels and is considered an active, adaptive coping style. In rats, chronic stress induces a shift from active to passive coping in this test (
Language	English
Publishing date	2018-09-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.2998
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Article: Optogenetically-induced long term depression in the rat orbitofrontal cortex ameliorates stress-induced reversal learning impairment.

Adler, Samantha M / Girotti, Milena / Morilak, David A

Neurobiology of stress

2020 Volume 13, Page(s) 100258

Abstract: Cognitive flexibility is a higher-order executive function that requires plasticity in neuronal circuits of the prefrontal cortex. Deficits in cognitive flexibility are prominent in a variety of psychiatric disorders, such as major depression, obsessive- ... ...

Abstract	Cognitive flexibility is a higher-order executive function that requires plasticity in neuronal circuits of the prefrontal cortex. Deficits in cognitive flexibility are prominent in a variety of psychiatric disorders, such as major depression, obsessive-compulsive disorder, and posttraumatic stress disorder. Chronic stress induces deficits in cognitive flexibility, perhaps through effects on plasticity, but the mechanism is not well understood. Previous work has demonstrated that stress reduces activity and dendritic elaboration in the medial prefrontal cortex (mPFC). In contrast, stress appears to increase dendritic elaboration in the orbitofrontal cortex (OFC). This suggests that there may be a differential effect of stress on plasticity in different prefrontal cortical areas. To test this hypothesis, we examined the effects of inducing plasticity optogenetically in the OFC on reversal learning, an OFC-mediated form of cognitive flexibility, in stressed and non-stressed rats. Inducing opto-LTD in the projection from mediodorsal thalamus to OFC ameliorated reversal learning deficits in rats exposed to chronic intermittent cold (CIC) stress. Additionally, we found that inducing opto-LTP in non-stressed rats produced deficits in reversal learning similar to those seen in rats after CIC stress. Finally, CIC stress produced complex subregion-specific changes in dendritic material and spine subtype composition in the OFC. These results indicate that the effects of stress on plasticity in the OFC are distinct from those in the mPFC, and that the PFC should therefore not be treated as a homogenous region in studying either stress effects or potential treatments for stress-related psychiatric disorders.
Language	English
Publishing date	2020-10-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2816500-7
ISSN	2352-2895
ISSN	2352-2895
DOI	10.1016/j.ynstr.2020.100258
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Article: Adjunct treatment with ketamine enhances the therapeutic effects of extinction learning after chronic unpredictable stress.

Paredes, Denisse / Knippenberg, Anna R / Bulin, Sarah E / Keppler, Lydia J / Morilak, David A

Neurobiology of stress

2022 Volume 19, Page(s) 100468

Abstract: Post-traumatic stress disorder (PTSD) is a debilitating illness characterized by dysfunction in the medial prefrontal cortex (mPFC). Although both pharmacological and cognitive behavioral interventions have shown some promise at alleviating symptoms, ... ...

Abstract	Post-traumatic stress disorder (PTSD) is a debilitating illness characterized by dysfunction in the medial prefrontal cortex (mPFC). Although both pharmacological and cognitive behavioral interventions have shown some promise at alleviating symptoms, high attrition and persistence of treatment-resistant symptoms pose significant challenges that remain unresolved. Specifically, prolonged exposure therapy, a gold standard intervention to treat PTSD, has high dropout rates resulting in many patients receiving less than a fully effective course of treatment. Administering pharmacological treatments together with behavioral psychotherapies like prolonged exposure may offer an important avenue for enhancing therapeutic efficacy sooner, thus reducing the duration of treatment and mitigating the impact of attrition. In this study, using extinction learning as a rat model of exposure therapy, we hypothesized that administering ketamine as an adjunct treatment together with extinction will enhance the efficacy of extinction in reversing stress-induced deficits in set shifting, a measure of cognitive flexibility. Results showed that combining a sub-effective dose of ketamine with a shortened, sub-effective extinction protocol fully reversed stress-induced cognitive set-shifting deficits in both male and female rats. These effects may be due to shared molecular mechanisms between extinction and ketamine, such as increased neuronal plasticity in common circuitry (e.g., hippocampus-mPFC), or increased BDNF signaling. This work suggests that fast-acting drugs, such as ketamine, can be effectively used in combination with behavioral interventions to reduce treatment duration and potentially mitigate the impact of attrition. Future work is needed to delineate other pharmacotherapies that may complement the effects of extinction via shared or independent mechanisms.
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2816500-7
ISSN	2352-2895
ISSN	2352-2895
DOI	10.1016/j.ynstr.2022.100468
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Article ; Online: Effects of vortioxetine on hippocampal-related cognitive impairment induced in rats by androgen deprivation as a model of prostate cancer treatment.

Vaiana, Alexandra M / Chen, Yidong / Gelfond, Jonathan / Johnson-Pais, Teresa L / Leach, Robin J / Ramamurthy, Chethan / Thompson, Ian M / Morilak, David A

Translational psychiatry

2023 Volume 13, Issue 1, Page(s) 307

Abstract: Advances in prostate cancer treatment have significantly improved survival, but quality of life for survivors remains an under-studied area of research. Androgen deprivation therapy (ADT) is a foundational treatment for advanced prostate cancer and is ... ...

Abstract	Advances in prostate cancer treatment have significantly improved survival, but quality of life for survivors remains an under-studied area of research. Androgen deprivation therapy (ADT) is a foundational treatment for advanced prostate cancer and is used as an adjuvant for prolonged periods in many high-risk, localized tumors. More than half of patients treated with ADT experience debilitating cognitive impairments in domains such as spatial learning and working memory. In this study, we investigated the effects of androgen deprivation on hippocampal-mediated cognition in rats. Vortioxetine, a multimodal antidepressant, has been shown to improve cognition in depressed patients. Thus, we also tested the potential efficacy of vortioxetine in restoring impaired cognition after ADT. We further investigated mechanisms that might contribute to these effects, measuring changes in the circuitry and gene expression within the dorsal hippocampus. ADT via surgical castration induced impairments in visuospatial cognition on the novel object location test and attenuated afferent-evoked local field potentials recorded in the CA1 region of the dorsal hippocampus. Chronic dietary administration of vortioxetine effectively reversed these deficits. Castration significantly altered gene expression in the hippocampus, whereas vortioxetine had little effect. Pathway analysis revealed that androgen depletion altered pathways related to synaptic plasticity. These results suggest that the hippocampus may be vulnerable to ADT, contributing to cognitive impairment in prostate cancer patients. Further, vortioxetine may be a candidate to improve cognition in patients who experience cognitive decline after androgen deprivation therapy for prostate cancer and may do so by restoring molecular and circuit-level plasticity-related mechanisms compromised by ADT.
MeSH term(s)	Humans ; Male ; Rats ; Animals ; Vortioxetine/metabolism ; Vortioxetine/pharmacology ; Androgen Antagonists/adverse effects ; Androgen Antagonists/metabolism ; Prostatic Neoplasms/drug therapy ; Androgens/metabolism ; Androgens/pharmacology ; Quality of Life ; Cognitive Dysfunction/metabolism ; Hippocampus/metabolism
Chemical Substances	Vortioxetine (3O2K1S3WQV) ; Androgen Antagonists ; Androgens
Language	English
Publishing date	2023-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-023-02600-5
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Article ; Online: Modulating the modulators: interaction of brain norepinephrine and cannabinoids in stress.

Morilak, David A

Experimental neurology

2012 Volume 238, Issue 2, Page(s) 145–148

MeSH term(s)	Animals ; Benzoxazines/administration & dosage ; Cannabinoids/administration & dosage ; Male ; Morpholines/administration & dosage ; Naphthalenes/administration & dosage ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/physiology ; Receptors, Adrenergic, alpha-2/physiology ; Stress, Psychological/physiopathology
Chemical Substances	Benzoxazines ; Cannabinoids ; Morpholines ; Naphthalenes ; Receptors, Adrenergic, alpha-2
Language	English
Publishing date	2012-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2012.08.016
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