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Article ; Online: Intergenerational Transmission of Stress in Humans.

Bowers, Mallory E / Yehuda, Rachel

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2016 Volume 41, Issue 1, Page(s) 232–244

Abstract: The hypothesis that offspring are affected by parental trauma or stress exposure, first noted anecdotally, is now supported empirically by data from Holocaust survivor offspring cohorts and other populations. These findings have been extended to less ... ...

Abstract	The hypothesis that offspring are affected by parental trauma or stress exposure, first noted anecdotally, is now supported empirically by data from Holocaust survivor offspring cohorts and other populations. These findings have been extended to less extreme forms of stress, where differential physical, behavioral, and cognitive outcomes are observed in affected offspring. Parental stress-mediated effects in offspring could be explained by genetics or social learning theory. Alternatively, biological variations stemming from stress exposure in parents could more directly have an impact on offspring, a concept we refer to here as 'intergenerational transmission', via changes to gametes and the gestational uterine environment. We further extend this definition to include the transmission of stress to offspring via early postnatal care, as animal studies demonstrate the importance of early maternal care of pups in affecting offsprings' long-term behavioral changes. Here, we review clinical observations in offspring, noting that offspring of stress- or trauma-exposed parents may be at greater risk for physical, behavioral, and cognitive problems, as well as psychopathology. Furthermore, we review findings concerning offspring biological correlates of parental stress, in particular, offspring neuroendocrine, epigenetic, and neuroanatomical changes, in an attempt to determine the extent of parental stress effects. Although understanding the etiology of effects in offspring is currently impeded by methodological constraints, and limitations in our knowledge, we summarize current information and conclude by presenting hypotheses that have been prompted by recent studies in the field.
MeSH term(s)	Animals ; Humans ; Hydrocortisone/blood ; Inheritance Patterns/genetics ; Parent-Child Relations ; Parenting/psychology ; Stress, Psychological/blood ; Stress, Psychological/genetics ; Stress, Psychological/psychology
Chemical Substances	Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2016-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2015.247
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Article ; Online: Short-Term Outcomes of Bimatoprost Sustained-Release Intracameral Implant in Glaucoma.

Wong, Michael K / Bowers, Mallory E / Ventimiglia, Jonas / Niknam, Rachel M / Moster, Marlene R / Pro, Michael J / Dale, Elizabeth / Kolomeyer, Natasha N / Lee, Daniel / Zheng, Cindy X

Journal of glaucoma

2023 Volume 32, Issue 9, Page(s) 738–743

Abstract: Prcis: This retrospective study found a statistically significant reduction in mean intraocular pressure (IOP) and the number of medications after intracameral Bimatoprost sustained release (SR) injection in patients with glaucoma. A history of ... ...

Abstract	Prcis: This retrospective study found a statistically significant reduction in mean intraocular pressure (IOP) and the number of medications after intracameral Bimatoprost sustained release (SR) injection in patients with glaucoma. A history of selective laser trabeculoplasty (SLT) did not impact treatment outcomes. Purpose: To determine outcomes of Bimatoprost SR on IOP and the number of topical IOP-lowering medications in patients with glaucoma. A secondary objective was to determine the outcomes of Bimatoprost SR in patients with a prior history of SLT. Methods: Retrospective case series. One hundred eighteen eyes from 84 patients that received Bimatoprost SR by 6 glaucoma specialists at Wills Eye Hospital from March 2020 to September 2021 were examined. The intervention was a single injection of intracameral Bimatoprost SR. The main outcome measures included IOP and the number of medications. Results: The most recent mean follow-up time for all eyes was 27.8 ± 18.6 weeks. The mean posttreatment IOP at the most recent follow-up of 16.6 ± 5.3 mm Hg was significantly lower than the mean under-therapy pretreatment IOP of 18.5 ± 5.7 mm Hg for all eyes ( P < 0.01). The mean posttreatment number of medications at the most recent follow-up of 1.3 ± 1.3 decreased compared with the number of pretreatment medications of 2.1 ± 1.4 for all eyes ( P < 0.01). Analysis of multilevel models controlling for demographic variables demonstrated a statistically significant reduction in IOP and number of medications posttreatment ( P < 0.01). A prior history of SLT (n = 54) had no impact on treatment for both IOP and the number of medications ( P > 0.1 for both). Conclusions: Intracameral Bimatoprost SR reduced IOP and decreased the number of medications. Prior history of SLT did not impact Bimatoprost SR treatment outcomes.
MeSH term(s)	Humans ; Bimatoprost ; Retrospective Studies ; Intraocular Pressure ; Delayed-Action Preparations ; Antihypertensive Agents/therapeutic use ; Glaucoma/drug therapy ; Glaucoma/surgery ; Trabeculectomy ; Treatment Outcome ; Laser Therapy
Chemical Substances	Bimatoprost (QXS94885MZ) ; Delayed-Action Preparations ; Antihypertensive Agents
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	913494-3
ISSN	1536-481X ; 1057-0829
ISSN (online)	1536-481X
ISSN	1057-0829
DOI	10.1097/IJG.0000000000002271
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Article ; Online: An Overview of Translationally Informed Treatments for Posttraumatic Stress Disorder: Animal Models of Pavlovian Fear Conditioning to Human Clinical Trials.

Bowers, Mallory E / Ressler, Kerry J

Biological psychiatry

2015 Volume 78, Issue 5, Page(s) E15–27

Abstract: Posttraumatic stress disorder manifests after exposure to a traumatic event and is characterized by avoidance/numbing, intrusive symptoms and flashbacks, mood and cognitive disruptions, and hyperarousal/reactivity symptoms. These symptoms reflect ... ...

Abstract	Posttraumatic stress disorder manifests after exposure to a traumatic event and is characterized by avoidance/numbing, intrusive symptoms and flashbacks, mood and cognitive disruptions, and hyperarousal/reactivity symptoms. These symptoms reflect dysregulation of the fear system likely caused by poor fear inhibition/extinction, increased generalization, and/or enhanced consolidation or acquisition of fear. These phenotypes can be modeled in animal subjects using Pavlovian fear conditioning, allowing investigation of the underlying neurobiology of normative and pathological fear. Preclinical studies reveal a number of neurotransmitter systems and circuits critical for aversive learning and memory that have informed the development of therapies used in human clinical trials. In this review, we discuss the evidence for a number of established and emerging pharmacotherapies and device-based treatments for posttraumatic stress disorder that have been developed via a bench to bedside translational model.
MeSH term(s)	Animals ; Clinical Trials as Topic ; Conditioning, Classical/physiology ; Disease Models, Animal ; Fear/psychology ; Humans ; Stress Disorders, Post-Traumatic/therapy ; Translational Medical Research
Language	English
Publishing date	2015-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2015.06.008
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Article ; Online: Sex-dependence of anxiety-like behavior in cannabinoid receptor 1 (Cnr1) knockout mice.

Bowers, Mallory E / Ressler, Kerry J

Behavioural brain research

2015 Volume 300, Page(s) 65–69

Abstract: Epidemiological data suggest women are at increased risk for developing anxiety and depression, although the mechanisms for this sex/gender difference remain incompletely understood. Pre-clinical studies have begun to investigate sex-dependent emotional ... ...

Abstract	Epidemiological data suggest women are at increased risk for developing anxiety and depression, although the mechanisms for this sex/gender difference remain incompletely understood. Pre-clinical studies have begun to investigate sex-dependent emotional learning and behavior in rodents, particularly as it relates to psychopathology; however, information about how gonadal hormones interact with the central nervous system is limited. We observe greater anxiety-like behavior in male mice with global knockout of the cannabinoid 1 receptor (Cnr1) compared to male, wild-type controls as measured by percent open arm entries on an elevated plus maze test. A similar increase in anxiety-like behavior, however, is not observed when comparing female Cnr1 knockouts to female wild-type subjects. Although, ovariectomy in female mice did not reverse this effect, both male and female adult mice with normative development were sensitive to Cnr1 antagonist-mediated increases in anxiety-like behavior. Together, these data support an interaction between sex, potentially mediated by gonadal hormones, and the endocannabinoid system at an early stage of development that is critical for establishing adult anxiety-like behavior.
MeSH term(s)	Animals ; Anxiety Disorders/physiopathology ; Cannabinoid Receptor Antagonists/pharmacology ; Exploratory Behavior/drug effects ; Exploratory Behavior/physiology ; Female ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Ovariectomy ; Piperidines/pharmacology ; Psychotropic Drugs/pharmacology ; Pyrazoles/pharmacology ; Receptor, Cannabinoid, CB1/antagonists & inhibitors ; Receptor, Cannabinoid, CB1/deficiency ; Receptor, Cannabinoid, CB1/genetics ; Rimonabant ; Sex Characteristics
Chemical Substances	CNR1 protein, mouse ; Cannabinoid Receptor Antagonists ; Piperidines ; Psychotropic Drugs ; Pyrazoles ; Receptor, Cannabinoid, CB1 ; Rimonabant (RML78EN3XE)
Language	English
Publishing date	2015-12-09
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2015.12.005
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Zs.A 1599: Show issues

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Article ; Online: Interaction between the cholecystokinin and endogenous cannabinoid systems in cued fear expression and extinction retention.

Bowers, Mallory E / Ressler, Kerry J

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2014 Volume 40, Issue 3, Page(s) 688–700

Abstract: Post-traumatic stress disorder (PTSD) is thought to develop, in part, from improper inhibition of fear. Accordingly, one of the most effective treatment strategies for PTSD is exposure-based psychotherapy. Ideally, neuroscience would inform adjunct ... ...

Abstract	Post-traumatic stress disorder (PTSD) is thought to develop, in part, from improper inhibition of fear. Accordingly, one of the most effective treatment strategies for PTSD is exposure-based psychotherapy. Ideally, neuroscience would inform adjunct therapies that target the neurotransmitter systems involved in extinction processes. Separate studies have implicated the cholecystokinin (CCK) and endocannabinoid systems in fear; however, there is a high degree of anatomical colocalization between the cannabinoid 1 receptor (Cnr1) and CCK in the basolateral amygdala (BLA), a brain region critical for emotion regulation. Although most research has focused on GABA and GABAergic plasticity as the mechanism by which Cnr1 mediates fear inhibition, we hypothesize that a functional interaction between Cnr1 and CCKB receptor (CCKBR) is critical for fear extinction processes. In this study, systemic pharmacological manipulation of the cannabinoid system modulated cued fear expression in C57BL/6J mice after consolidation of auditory fear conditioning. Knockout of the CCKBR, however, had no effect on fear- or anxiety-like behaviors. Nonetheless, administration of a Cnr1 antagonist increased freezing behavior during a cued fear expression test in wild-type subjects, but had no effect on freezing behavior in CCKBR knockout littermates. In addition, we found that Cnr1-positive fibers form perisomatic clusters around CCKBR-positive cell bodies in the BLA. These CCKBR-positive cells comprise a molecularly heterogenous population of excitatory and inhibitory neurons. These findings provide novel evidence that Cnr1 contributes to cued fear expression via an interaction with the CCK system. Dysfunctional Cnr1-CCKBR interactions might contribute to the etiology of, or result from, fear-related psychiatric disease.
MeSH term(s)	Amidohydrolases/antagonists & inhibitors ; Animals ; Benzamides/pharmacology ; Cannabinoid Receptor Antagonists/pharmacology ; Carbamates/pharmacology ; Cholecystokinin/physiology ; Conditioning, Psychological/drug effects ; Conditioning, Psychological/physiology ; Cues ; Dose-Response Relationship, Drug ; Extinction, Psychological/drug effects ; Extinction, Psychological/physiology ; Fear/drug effects ; Fear/physiology ; Male ; Mice ; Mice, Knockout ; Piperidines/pharmacology ; Pyrazoles/pharmacology ; Receptor, Cannabinoid, CB1/antagonists & inhibitors ; Receptor, Cannabinoid, CB1/physiology ; Receptor, Cholecystokinin B/genetics ; Receptor, Cholecystokinin B/physiology ; Rimonabant
Chemical Substances	Benzamides ; Cannabinoid Receptor Antagonists ; Carbamates ; Piperidines ; Pyrazoles ; Receptor, Cannabinoid, CB1 ; Receptor, Cholecystokinin B ; cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester ; Cholecystokinin (9011-97-6) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-) ; Rimonabant (RML78EN3XE)
Language	English
Publishing date	2014-09-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2014.225
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Article ; Online: The role of the C2A domain of synaptotagmin 1 in asynchronous neurotransmitter release.

Shields, Mallory C / Bowers, Matthew R / Kramer, Hannah L / Fulcer, McKenzie M / Perinet, Lara C / Metz, Marissa J / Reist, Noreen E

PloS one

2020 Volume 15, Issue 5, Page(s) e0232991

Abstract: ... to glutamate mutation, sytD-E). Analysis of both the original sytD-N mutation and our alternate sytD-E mutation ... is not increased in the sytD-E mutant. Thus, our work provides new mechanistic insight ...

Abstract	Following nerve stimulation, there are two distinct phases of Ca2+-dependent neurotransmitter release: a fast, synchronous release phase, and a prolonged, asynchronous release phase. Each of these phases is tightly regulated and mediated by distinct mechanisms. Synaptotagmin 1 is the major Ca2+ sensor that triggers fast, synchronous neurotransmitter release upon Ca2+ binding by its C2A and C2B domains. It has also been implicated in the inhibition of asynchronous neurotransmitter release, as blocking Ca2+ binding by the C2A domain of synaptotagmin 1 results in increased asynchronous release. However, the mutation used to block Ca2+ binding in the previous experiments (aspartate to asparagine mutations, sytD-N) had the unintended side effect of mimicking Ca2+ binding, raising the possibility that the increase in asynchronous release was directly caused by ostensibly constitutive Ca2+ binding. Thus, rather than modulating an asynchronous sensor, sytD-N may be mimicking one. To directly test the C2A inhibition hypothesis, we utilized an alternate C2A mutation that we designed to block Ca2+ binding without mimicking it (an aspartate to glutamate mutation, sytD-E). Analysis of both the original sytD-N mutation and our alternate sytD-E mutation at the Drosophila neuromuscular junction showed differential effects on asynchronous release, as well as on synchronous release and the frequency of spontaneous release. Importantly, we found that asynchronous release is not increased in the sytD-E mutant. Thus, our work provides new mechanistic insight into synaptotagmin 1 function during Ca2+-evoked synaptic transmission and demonstrates that Ca2+ binding by the C2A domain of synaptotagmin 1 does not inhibit asynchronous neurotransmitter release in vivo.
MeSH term(s)	Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Binding Sites/genetics ; Calcium/metabolism ; Drosophila Proteins/chemistry ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/metabolism ; Genes, Insect ; Mutagenesis, Site-Directed ; Neurotransmitter Agents/metabolism ; Protein Domains ; Synaptic Transmission ; Synaptic Vesicles/metabolism ; Synaptotagmin I/chemistry ; Synaptotagmin I/genetics ; Synaptotagmin I/metabolism
Chemical Substances	Drosophila Proteins ; Neurotransmitter Agents ; Synaptotagmin I ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0232991
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Article ; Online: The Class I HDAC inhibitor RGFP963 enhances consolidation of cued fear extinction.

Bowers, Mallory E / Xia, Bing / Carreiro, Samantha / Ressler, Kerry J

Learning & memory (Cold Spring Harbor, N.Y.)

2015 Volume 22, Issue 4, Page(s) 225–231

Abstract: Evidence indicates that broad, nonspecific histone deacetylase (HDAC) inhibition enhances learning and memory, however, the contribution of the various HDACs to specific forms of learning is incompletely understood. Here, we show that the Class I HDAC ... ...

Abstract	Evidence indicates that broad, nonspecific histone deacetylase (HDAC) inhibition enhances learning and memory, however, the contribution of the various HDACs to specific forms of learning is incompletely understood. Here, we show that the Class I HDAC inhibitor, RGFP963, enhances consolidation of cued fear extinction. However, RGFP966, a strong inhibitor of HDAC3, does not significantly enhance consolidation of cued fear extinction. These data extend previous evidence that demonstrate the Class I HDACs play a role in the consolidation of long-term memory, suggesting that HDAC1 and/or HDAC2, but less likely HDAC3, may function as negative regulators of extinction retention. The development of specific HDAC inhibitors, such as RGFP963, will further illuminate the role of specific HDACs in various types of learning and memory. Moreover, HDAC inhibitors that enhance cued fear extinction may show translational promise for the treatment of fear-related disorders, including post-traumatic stress disorder (PTSD).
MeSH term(s)	Animals ; Brain/drug effects ; Brain/physiology ; Cues ; Extinction, Psychological/drug effects ; Extinction, Psychological/physiology ; Fear/drug effects ; Fear/physiology ; Freezing Reaction, Cataleptic/drug effects ; Freezing Reaction, Cataleptic/physiology ; Histone Deacetylase 1/antagonists & inhibitors ; Histone Deacetylase 1/metabolism ; Histone Deacetylase 2/antagonists & inhibitors ; Histone Deacetylase 2/metabolism ; Histone Deacetylase Inhibitors/pharmacokinetics ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Male ; Mice, Inbred C57BL ; Neuropsychological Tests
Chemical Substances	Histone Deacetylase Inhibitors ; Hdac1 protein, mouse (EC 3.5.1.98) ; Hdac2 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Histone Deacetylase 2 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98) ; histone deacetylase 3 (EC 3.5.1.98)
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1204777-6
ISSN	1549-5485 ; 1072-0502
ISSN (online)	1549-5485
ISSN	1072-0502
DOI	10.1101/lm.036699.114
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Article ; Online: Neuropeptide regulation of fear and anxiety: Implications of cholecystokinin, endogenous opioids, and neuropeptide Y.

Bowers, Mallory E / Choi, Dennis C / Ressler, Kerry J

Physiology & behavior

2012 Volume 107, Issue 5, Page(s) 699–710

Abstract: The neural circuitry of fear likely underlies anxiety and fear-related disorders such as specific and social phobia, panic disorder, and posttraumatic stress disorder. The primary pharmacological treatments currently utilized for these disorders include ... ...

Abstract	The neural circuitry of fear likely underlies anxiety and fear-related disorders such as specific and social phobia, panic disorder, and posttraumatic stress disorder. The primary pharmacological treatments currently utilized for these disorders include benzodiazepines, which act on the GABAergic receptor system, and antidepressants, which modulate the monamine systems. However, recent work on the regulation of fear neural circuitry suggests that specific neuropeptide modulation of this system is of critical importance. Recent reviews have examined the roles of the hypothalamic-pituitary-adrenal axis neuropeptides as well as the roles of neurotrophic factors in regulating fear. The present review, instead, will focus on three neuropeptide systems which have received less attention in recent years but which are clearly involved in regulating fear and its extinction. The endogenous opioid system, particularly activating the μ opioid receptors, has been demonstrated to regulate fear expression and extinction, possibly through functioning as an error signal within the ventrolateral periaqueductal gray to mark unreinforced conditioned stimuli. The cholecystokinin (CCK) system initially led to much excitement through its potential role in panic disorder. More recent work in the CCK neuropeptide pathway suggests that it may act in concordance with the endogenous cannabinoid system in the modulation of fear inhibition and extinction. Finally, older as well as very recent data suggests that neuropeptide Y (NPY) may play a very interesting role in counteracting stress effects, enhancing extinction, and enhancing resilience in fear and stress preclinical models. Future work in understanding the mechanisms of neuropeptide functioning, particularly within well-known behavioral circuits, are likely to provide fascinating new clues into the understanding of fear behavior as well as suggesting novel therapeutics for treating disorders of anxiety and fear dysregulation.
MeSH term(s)	Animals ; Anxiety/physiopathology ; Brain/physiology ; Cholecystokinin/physiology ; Fear/physiology ; Humans ; Neuropeptide Y/physiology ; Opioid Peptides/physiology
Chemical Substances	Neuropeptide Y ; Opioid Peptides ; Cholecystokinin (9011-97-6)
Language	English
Publishing date	2012-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2012.03.004
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Article ; Online: The role of the C2A domain of synaptotagmin 1 in asynchronous neurotransmitter release.

Mallory C Shields / Matthew R Bowers / Hannah L Kramer / McKenzie M Fulcer / Lara C Perinet / Marissa J Metz / Noreen E Reist

PLoS ONE, Vol 15, Iss 5, p e

2020 Volume 0232991

Abstract	Following nerve stimulation, there are two distinct phases of Ca2+-dependent neurotransmitter release: a fast, synchronous release phase, and a prolonged, asynchronous release phase. Each of these phases is tightly regulated and mediated by distinct mechanisms. Synaptotagmin 1 is the major Ca2+ sensor that triggers fast, synchronous neurotransmitter release upon Ca2+ binding by its C2A and C2B domains. It has also been implicated in the inhibition of asynchronous neurotransmitter release, as blocking Ca2+ binding by the C2A domain of synaptotagmin 1 results in increased asynchronous release. However, the mutation used to block Ca2+ binding in the previous experiments (aspartate to asparagine mutations, sytD-N) had the unintended side effect of mimicking Ca2+ binding, raising the possibility that the increase in asynchronous release was directly caused by ostensibly constitutive Ca2+ binding. Thus, rather than modulating an asynchronous sensor, sytD-N may be mimicking one. To directly test the C2A inhibition hypothesis, we utilized an alternate C2A mutation that we designed to block Ca2+ binding without mimicking it (an aspartate to glutamate mutation, sytD-E). Analysis of both the original sytD-N mutation and our alternate sytD-E mutation at the Drosophila neuromuscular junction showed differential effects on asynchronous release, as well as on synchronous release and the frequency of spontaneous release. Importantly, we found that asynchronous release is not increased in the sytD-E mutant. Thus, our work provides new mechanistic insight into synaptotagmin 1 function during Ca2+-evoked synaptic transmission and demonstrates that Ca2+ binding by the C2A domain of synaptotagmin 1 does not inhibit asynchronous neurotransmitter release in vivo.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Neuropeptide regulation of fear and anxiety: Implications of cholecystokinin, endogenous opioids, and neuropeptide Y

Bowers, Mallory E / Choi, Dennis C / Ressler, Kerry J

Physiology & behavior. 2012 Dec. 5, v. 107, no. 5

2012

Abstract	The neural circuitry of fear likely underlies anxiety and fear-related disorders such as specific and social phobia, panic disorder, and posttraumatic stress disorder. The primary pharmacological treatments currently utilized for these disorders include benzodiazepines, which act on the GABAergic receptor system, and antidepressants, which modulate the monamine systems. However, recent work on the regulation of fear neural circuitry suggests that specific neuropeptide modulation of this system is of critical importance. Recent reviews have examined the roles of the hypothalamic-pituitary-adrenal axis neuropeptides as well as the roles of neurotrophic factors in regulating fear. The present review, instead, will focus on three neuropeptide systems which have received less attention in recent years but which are clearly involved in regulating fear and its extinction. The endogenous opioid system, particularly activating the μ opioid receptors, has been demonstrated to regulate fear expression and extinction, possibly through functioning as an error signal within the ventrolateral periaqueductal gray to mark unreinforced conditioned stimuli. The cholecystokinin (CCK) system initially led to much excitement through its potential role in panic disorder. More recent work in the CCK neuropeptide pathway suggests that it may act in concordance with the endogenous cannabinoid system in the modulation of fear inhibition and extinction. Finally, older as well as very recent data suggests that neuropeptide Y (NPY) may play a very interesting role in counteracting stress effects, enhancing extinction, and enhancing resilience in fear and stress preclinical models. Future work in understanding the mechanisms of neuropeptide functioning, particularly within well-known behavioral circuits, are likely to provide fascinating new clues into the understanding of fear behavior as well as suggesting novel therapeutics for treating disorders of anxiety and fear dysregulation.
Keywords	antidepressants ; anxiety ; benzodiazepines ; cannabinoids ; cholecystokinin ; extinction ; fearfulness ; models ; narcotics ; neuropeptide Y ; neurotrophins ; receptors ; therapeutics
Language	English
Dates of publication	2012-1205
Size	p. 699-710.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2012.03.004
Database	NAL-Catalogue (AGRICOLA)

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Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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Order via subito

Inter-library loan at ZB MED

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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Full text online

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Inter-library loan at ZB MED

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In stock of ZB MED Bonn / Germany

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Inter-library loan at ZB MED