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Article ; Online: Prefrontal cortex circuits in depression and anxiety: contribution of discrete neuronal populations and target regions.

Hare, Brendan D / Duman, Ronald S

2020 Volume 25, Issue 11, Page(s) 2742–2758

Abstract: Our understanding of depression and its treatment has advanced with the advent of ketamine as a rapid-acting antidepressant and the development and refinement of tools capable of selectively altering the activity of populations of neuronal subtypes. This ...

Abstract	Our understanding of depression and its treatment has advanced with the advent of ketamine as a rapid-acting antidepressant and the development and refinement of tools capable of selectively altering the activity of populations of neuronal subtypes. This work has resulted in a paradigm shift away from dysregulation of single neurotransmitter systems in depression towards circuit level abnormalities impacting function across multiple brain regions and neurotransmitter systems. Studies on the features of circuit level abnormalities demonstrate structural changes within the prefrontal cortex (PFC) and functional changes in its communication with distal brain structures. Treatments that impact the activity of brain regions, such as transcranial magnetic stimulation or rapid-acting antidepressants like ketamine, appear to reverse depression associated circuit abnormalities though the mechanisms underlying the reversal, as well as development of these abnormalities remains unclear. Recently developed optogenetic and chemogenetic tools that allow high-fidelity control of neuronal activity in preclinical models have begun to elucidate the contributions of the PFC and its circuitry to depression- and anxiety-like behavior. These tools offer unprecedented access to specific circuits and neuronal subpopulations that promise to offer a refined view of the circuit mechanisms surrounding depression and potential mechanistic targets for development and reversal of depression associated circuit abnormalities.
MeSH term(s)	Antidepressive Agents/pharmacology ; Antidepressive Agents/therapeutic use ; Anxiety/drug therapy ; Anxiety/pathology ; Depression/drug therapy ; Depression/pathology ; Ketamine/pharmacology ; Ketamine/therapeutic use ; Neural Pathways/drug effects ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/pathology
Chemical Substances	Antidepressive Agents ; Ketamine (690G0D6V8H)
Language	English
Publishing date	2020-02-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-020-0685-9
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Article: A medial prefrontal cortex cell type necessary and sufficient for a rapid antidepressant response.

Hare, Brendan D / Duman, Ronald S

Chronic stress (Thousand Oaks, Calif.)

2019 Volume 3

Language	English
Publishing date	2019-04-15
Publishing country	United States
Document type	Journal Article
ISSN	2470-5470
ISSN	2470-5470
DOI	10.1177/2470547019841358
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Article ; Online: Bringing in the ACE(i): Angiotensin-Converting Enzyme Inhibitors as Antidepressants.

Hare, Brendan D / DiLeone, Ralph J

Biological psychiatry

2020 Volume 88, Issue 5, Page(s) 365–366

MeSH term(s)	Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Antidepressive Agents ; Bradykinin ; TOR Serine-Threonine Kinases
Chemical Substances	Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Antidepressive Agents ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Bradykinin (S8TIM42R2W)
Language	English
Publishing date	2020-08-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2020.05.025
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Article: Exercise reduces the anxiogenic effects of meta-chlorophenylpiperazine: The role of 5-HT2C receptors in the bed nucleus of the stria terminalis.

Fox, James H / Boucher, Melissa N / Abedrabbo, Khalil S / Hare, Brendan D / Grimmig, Bethany A / Falls, William A / Hammack, Sayamwong E

Frontiers in synaptic neuroscience

2023 Volume 14, Page(s) 1067420

Abstract: Introduction: Two weeks of voluntary exercise in group-housed mice produces a reduction in anxiety-like behaviors across a number of different measures, including a reduction in the anxiety levels typically produced by the anxiogenic serotonergic drug m- ...

Abstract	Introduction: Two weeks of voluntary exercise in group-housed mice produces a reduction in anxiety-like behaviors across a number of different measures, including a reduction in the anxiety levels typically produced by the anxiogenic serotonergic drug m-chlorophenylpiperazine (mCPP), an agonist at 5-HT2C/2b receptors. We have previously demonstrated that 2-weeks of voluntary exercise blunted the anxiogenic effects of systemic mCPP, and we have also shown that mCPP infused into the bed nucleus of the stria terminalis (BNST) is anxiogenic. Here we follow up on these reports. Methods: In Experiment 1 we infused several doses of mCPP into the BNST with or without the 5-HT2C antagonist SB242084. In Experiment 2, we administered mCPP into amygdala subregions and the dorsal hippocampus to investigate site specificity. In Experiment 4 we lesioned the BNST and subsequently infused mCPP systemically, and in Experiment 4 we used RNAscope Results: BNST mCPP infusion increased acoustic startle responding, which was by 5-HT2C antagonism, while neither mCPP infused into the amygdala nor hippocampus was anxiogenic. Lesions of the BNST prevented the anxiogenic effect of systemically administered mCPP. Lastly, exercise reduced 5-HT2C transcripts in the BNST. Discussion: These results suggest that the BNST is a critical site of action for the effects of exercise on mCPP. Together these data suggest that exercise may reduce 5-HT2C receptor function in the BNST, which may, in part, explain some of the anxiolytic effects associated with wheel running.
Language	English
Publishing date	2023-01-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592086-8
ISSN	1663-3563
ISSN	1663-3563
DOI	10.3389/fnsyn.2022.1067420
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Article ; Online: Rapastinel, an NMDAR positive modulator, produces distinct behavioral, sleep, and EEG profiles compared with ketamine.

Banerjee, Pradeep / Donello, John E / Hare, Brendan / Duman, Ronald S

Behavioural brain research

2020 Volume 391, Page(s) 112706

Abstract: Rapastinel, a positive NMDAR modulator, produces rapid-acting and long-lasting antidepressant-like effects; however, unlike ketamine, the abuse potential for rapastinel is minimal. Ketamine has also been shown to induce psychotomimetic/dissociative side ... ...

Abstract	Rapastinel, a positive NMDAR modulator, produces rapid-acting and long-lasting antidepressant-like effects; however, unlike ketamine, the abuse potential for rapastinel is minimal. Ketamine has also been shown to induce psychotomimetic/dissociative side effects, aberrant gamma oscillations, and effects similar to sleep deprivation, which may potentially limit its clinical use. In this study, we compared the side effect profile and potential sleep-altering properties of rapastinel (3, 10, and 30 mg/kg) to ketamine (30 mg/kg) in rodents. In addition, we investigated corresponding changes in transcriptomics and proteomics. Rapastinel exhibited no effect on locomotor activity and prepulse inhibition in mice, while ketamine induced a significant increase in locomotor activity and a significant decrease in prepulse inhibition, which are indications of a psychosis-like state. The effects of rapastinel on sleep architecture were minimal, and rapastinel did not alter gamma frequency oscillations. In contrast, ketamine administration resulted in a greater latency to slow wave and REM sleep, disrupted duration of sleep, and affected duration of wakefulness during sleep. Further, ketamine increased cortical oscillations in the gamma frequency range, which is a property associated with psychosis. Rapastinel induced similar plasticity-related changes in transcriptomics to ketamine in rats but differed in several gene ontology classes, some of which may be involved in the regulation of sleep. In conclusion, rapastinel demonstrated a lower propensity than ketamine to induce CNS-related adverse side effects and sleep disturbances.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Depression/drug therapy ; Electroencephalography/drug effects ; Electroencephalography/methods ; Excitatory Amino Acid Antagonists/pharmacology ; Ketamine/metabolism ; Ketamine/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Oligopeptides/metabolism ; Oligopeptides/pharmacology ; Prepulse Inhibition/drug effects ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, N-Methyl-D-Aspartate/metabolism ; Sleep/drug effects ; Sleep/physiology ; Wakefulness/drug effects ; Wakefulness/physiology
Chemical Substances	Antidepressive Agents ; Excitatory Amino Acid Antagonists ; Oligopeptides ; Receptors, N-Methyl-D-Aspartate ; Ketamine (690G0D6V8H) ; GLYX-13 peptide (6A1X56B95E)
Language	English
Publishing date	2020-05-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2020.112706
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Article ; Online: Evaluation of real-world outcomes associated with use of a prescription digital therapeutic to treat substance use disorders.

Xiong, Xiaorui / Braun, Stephen / Stitzer, Maxine / Luderer, Hilary / Shafai, Gigi / Hare, Brendan / Stevenson, Michael / Maricich, Yuri

The American journal on addictions

2022 Volume 32, Issue 1, Page(s) 24–31

Abstract: Background and objectives: Digital therapeutics can expand the reach and fidelity of behavioral treatment for substance use disorders (SUDs). This analysis evaluated real-world engagement and clinical outcomes in patients diagnosed with SUD who were ... ...

Abstract	Background and objectives: Digital therapeutics can expand the reach and fidelity of behavioral treatment for substance use disorders (SUDs). This analysis evaluated real-world engagement and clinical outcomes in patients diagnosed with SUD who were prescribed reSET®, an FDA-authorized prescription digital therapeutic (PDT). Methods: Patients were prescribed a 12-week PDT comprising 61 therapy lessons (31 "core" and 30 "keep learning" lessons) and contingency management rewards (positive reinforcement message or monetary gift cards) based on lesson completion and negative urine drug screens. Engagement (defined as any activity in the PDT), retention (any activity in Weeks 9-12), and substance use data were collected automatically by the PDT and analyzed descriptively. Associations between early lesson completion and end-of-treatment outcomes were assessed. Results: Six hundred and fifty-eight patients filled their prescription. Evaluated were 602 patients who were exposed to therapeutic content by completing at least one lesson (median age 37 years, 33% female, 41% male, 26% unreported sex). Median lessons completed was 33 (out of 61 possible), and 52% of patients completed all core modules. Retention in treatment during the last 4 weeks of treatment was 74%, and 62% were abstinent (missing data considered positive). [Correction added on 13 December 2022, after first online publication: In the preceding sentence, the treatment percentage values were revised from 74.6% to 74%.] DISCUSSION AND CONCLUSIONS: Patients with SUD exhibited robust engagement with a PDT, high rates of retention through 12 weeks, and substantial rates of abstinence at end of treatment when the therapeutic was used in a real-world setting. PDT's hold promise as a new way to access effective SUD treatment. Scientific significance: This study is the first to report real-world PDT engagement and clinical outcomes data from a large, geographically diverse population of patients with SUDs.
MeSH term(s)	Humans ; Male ; Female ; Adult ; Substance-Related Disorders/drug therapy ; Substance-Related Disorders/epidemiology ; Behavior Therapy ; Treatment Outcome ; Prescriptions
Language	English
Publishing date	2022-10-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141440-6
ISSN	1521-0391 ; 1055-0496
ISSN (online)	1521-0391
ISSN	1055-0496
DOI	10.1111/ajad.13346
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Article ; Online: Neurobiology of rapid-acting antidepressants: convergent effects on GluA1-synaptic function.

Duman, Ronald S / Shinohara, Ryota / Fogaça, Manoela V / Hare, Brendan

Molecular psychiatry

2019 Volume 24, Issue 12, Page(s) 1816–1832

Abstract: Efforts to develop efficacious antidepressant agents with novel mechanisms have been largely unsuccessful since the 1950's until the discovery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that produces rapid and sustained ... ...

Abstract	Efforts to develop efficacious antidepressant agents with novel mechanisms have been largely unsuccessful since the 1950's until the discovery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that produces rapid and sustained antidepressant actions even in treatment-resistant patients. This finding has ushered in a new era for the development of novel rapid-acting antidepressants that act at the NMDA receptor complex, but without dissociative and psychotomimetic side effects of ketamine. Here, we review the current state of rapid-acting antidepressant drug development, including NMDA channel blockers, glycine site agents, and allosteric modulators, as well as ketamine stereoisomers and metabolites. In addition, we focus on the neurobiological mechanisms underlying the actions of these diverse agents and discuss evidence of convergent mechanisms including increased brain-derived neurotrophic factor signaling, increased synthesis of synaptic proteins, and most notably increased GluR1 and synaptic connectivity in the medial prefrontal cortex. These convergent mechanisms provide insight for potential additional novel targets for drug development (e.g., agents that increase synaptic protein synthesis and plasticity). Importantly, the convergent effects on synapse formation and plasticity also reverse the well-documented neuronal and synaptic deficits associated with stress and depression, and thereby target the underlying pathophysiology of major depressive disorder.
MeSH term(s)	Animals ; Antidepressive Agents/metabolism ; Antidepressive Agents/pharmacology ; Depression/drug therapy ; Depressive Disorder, Major/drug therapy ; Glutamic Acid/metabolism ; Humans ; Ketamine/pharmacology ; Neurobiology/methods ; Neurogenesis/drug effects ; Neurons/metabolism ; Receptors, AMPA/drug effects ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/drug effects ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction/drug effects ; Synapses/metabolism ; Synaptic Transmission/drug effects
Chemical Substances	Antidepressive Agents ; Receptors, AMPA ; Receptors, N-Methyl-D-Aspartate ; Glutamic Acid (3KX376GY7L) ; Ketamine (690G0D6V8H)
Language	English
Publishing date	2019-03-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-019-0400-x
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Article ; Online: Ketamine increases vmPFC activity: Effects of (R)- and (S)-stereoisomers and (2R,6R)-hydroxynorketamine metabolite.

Hare, Brendan D / Pothula, Santosh / DiLeone, Ralph J / Duman, Ronald S

Neuropharmacology

2020 Volume 166, Page(s) 107947

Abstract: Ketamine, an NMDA receptor antagonist and fast acting antidepressant, produces a rapid burst of glutamate in the ventral medial prefrontal cortex (mPFC). Preclinical studies have demonstrated that pyramidal cell activity in the vmPFC is necessary for the ...

Abstract	Ketamine, an NMDA receptor antagonist and fast acting antidepressant, produces a rapid burst of glutamate in the ventral medial prefrontal cortex (mPFC). Preclinical studies have demonstrated that pyramidal cell activity in the vmPFC is necessary for the rapid antidepressant response to ketamine in rodents. We sought to characterize the effects of ketamine and its stereoisomers (R and S), as well as a metabolite, (2R,6R)-hydroxynorketamine (HNK), on vmPFC activity using a genetically encoded calcium indicator (GCaMP6f). Ratiometric fiber photometry was utilized to monitor GCaMP6f fluorescence in pyramidal cells of mouse vmPFC prior to and immediately following administration of compounds. GCaMP6f signal was assessed to determine correspondance of activity between compounds. We observed dose dependent effects with (R,S)-ketamine (3-100 mg/kg), with the greatest effects on GCaMP6f activity at 30 mg/kg and lasting up to 20 min. (S)-ketamine (15 mg/kg), which has high affinity for the NMDA receptor channel produced similar effects to (R,S)-ketamine, but compounds with low NMDA receptor affinity, including (R)-ketamine (15 mg/kg) and (2R,6R)-HNK (30 mg/kg) had little or no effect on GCaMP6f activity. The initial response to administration of (R,S)-ketamine as well as (S)-ketamine is characterized by a brief period of robust GCaMP6f activation, consistent with increased activity of vmPFC pyramidal neurons. Because (2R,6R)-HNK and (R)-ketamine are reported to have antidepressant activity in rodent models the current results indicate that different initiating mechanisms lead to similar brain adaptive consequences that underlie the rapid antidepressant responses.
MeSH term(s)	Animals ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/chemistry ; Excitatory Amino Acid Antagonists/metabolism ; Excitatory Amino Acid Antagonists/pharmacology ; Ketamine/analogs & derivatives ; Ketamine/chemistry ; Ketamine/metabolism ; Ketamine/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Photometry/methods ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/metabolism ; Stereoisomerism
Chemical Substances	Excitatory Amino Acid Antagonists ; Ketamine (690G0D6V8H) ; 6-hydroxynorketamine (81395-70-2)
Language	English
Publishing date	2020-01-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2020.107947
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Article: Rapid Acting Antidepressants in Chronic Stress Models: Molecular and Cellular Mechanisms.

Hare, Brendan D / Ghosal, Sriparna / Duman, Ronald S

Chronic stress (Thousand Oaks, Calif.)

2017 Volume 1

Abstract: Stress-associated disorders, including depression and anxiety, impact nearly 20% of individuals in the United States. The social, health, and economic burden imposed by stress-associated disorders requires in depth research efforts to identify suitable ... ...

Abstract	Stress-associated disorders, including depression and anxiety, impact nearly 20% of individuals in the United States. The social, health, and economic burden imposed by stress-associated disorders requires in depth research efforts to identify suitable treatment strategies. Traditional medications (e.g., selective serotonin reuptake inhibitors, monoamine oxidase inhibitors) have significant limitations, notably a time lag for therapeutic response that is compounded by low rates of efficacy. Excitement over ketamine, a rapid acting antidepressant effective in treatment resistant patients, is tempered by transient dissociative and psychotomimetic effects, as well as abuse potential. Rodent stress models are commonly used to produce behavioral abnormalities that resemble those observed in stress-associated disorders. Stress models also produce molecular and cellular morphological changes in stress sensitive brain regions, including the prefrontal cortex and hippocampus that resemble alterations observed in depression. Rapid acting antidepressants such as ketamine can rescue stress-associated morphological and behavioral changes in rodent models. Here, we review the literature supporting a role for rapid acting antidepressants in opposing the effects of stress, and summarize research efforts seeking to elucidate the molecular, cellular, and circuit level targets of these agents.
Language	English
Publishing date	2017-04-10
Publishing country	United States
Document type	Journal Article
ISSN	2470-5470
ISSN	2470-5470
DOI	10.1177/2470547017697317
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Article ; Online: Influence of Chronic Electroconvulsive Seizures on Plasticity-Associated Gene Expression and Perineuronal Nets Within the Hippocampi of Young Adult and Middle-Aged Sprague-Dawley Rats.

Jaggar, Minal / Ghosh, Shreya / Janakiraman, Balaganesh / Chatterjee, Ashmita / Maheshwari, Megha / Dewan, Vani / Hare, Brendan / Deb, Sukrita / Figueiredo, Dwight / Duman, Ronald S / Vaidya, Vidita A

The international journal of neuropsychopharmacology

2023 Volume 26, Issue 4, Page(s) 294–306

Abstract: Background: Electroconvulsive seizure therapy is often used in both treatment-resistant and geriatric depression. However, preclinical studies identifying targets of chronic electroconvulsive seizure (ECS) are predominantly focused on animal models in ... ...

Abstract	Background: Electroconvulsive seizure therapy is often used in both treatment-resistant and geriatric depression. However, preclinical studies identifying targets of chronic electroconvulsive seizure (ECS) are predominantly focused on animal models in young adulthood. Given that putative transcriptional, neurogenic, and neuroplastic mechanisms implicated in the behavioral effects of chronic ECS themselves exhibit age-dependent modulation, it remains unknown whether the molecular and cellular targets of chronic ECS vary with age. Methods: We subjected young adult (2-3 months) and middle-aged (12-13 months), male Sprague Dawley rats to sham or chronic ECS and assessed for despair-like behavior, hippocampal gene expression, hippocampal neurogenesis, and neuroplastic changes in the extracellular matrix, reelin, and perineuronal net numbers. Results: Chronic ECS reduced despair-like behavior at both ages, accompanied by overlapping and unique changes in activity-dependent and trophic factor gene expression. Although chronic ECS had a similar impact on quiescent neural progenitor numbers at both ages, the eventual increase in hippocampal progenitor proliferation was substantially higher in young adulthood. We noted a decline in reelin⁺ cell numbers following chronic ECS only in young adulthood. In contrast, an age-invariant, robust dissolution of perineuronal net numbers that encapsulate parvalbumin⁺ neurons in the hippocampus were observed following chronic ECS. Conclusion: Our findings indicate that age is a key variable in determining the nature of chronic ECS-evoked molecular and cellular changes in the hippocampus. This raises the intriguing possibility that chronic ECS may recruit distinct, as well as overlapping, mechanisms to drive antidepressant-like behavioral changes in an age-dependent manner.
MeSH term(s)	Rats ; Animals ; Male ; Rats, Sprague-Dawley ; Electroshock ; Hippocampus ; Electroconvulsive Therapy ; Seizures/metabolism ; Gene Expression
Language	English
Publishing date	2023-02-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1440129-0
ISSN	1469-5111 ; 1461-1457
ISSN (online)	1469-5111
ISSN	1461-1457
DOI	10.1093/ijnp/pyad008
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