Increased amygdalar metabotropic glutamate receptor 7 mRNA in a genetic mouse model of impaired fear extinction

O’Connor, Richard M.; McCafferty, Cian; Bravo, Javier A.; Singewald, Nicolas; Holmes, Andrew; Cryan, John F.

doi:10.1007/s00213-018-5031-4

Cited by 4 publications

(4 citation statements)

References 60 publications

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“…The exploitation of NMDARs may be further complicated not only by sex differences in the mechanisms underlying extinction, but also by the interaction between female reproductive history and the requirement for NMDARs in extinction reported by Tang and Graham (2019). Thus, a complex constellation of factors may contribute to individual differences in receptor expression, such as those described by O’Connor et al (2019) for metabotropic glutamate receptors, and consequent differences in fear extinction.…”

Section: New Mechanistic Insights Into the Psychopharmacology Of Extimentioning

confidence: 99%

Editorial: the psychopharmacology of extinction—from theory to therapy

Milton

Holmes

2019

Psychopharmacology

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Section: New Mechanistic Insights Into the Psychopharmacology Of Extimentioning

confidence: 99%

Editorial: the psychopharmacology of extinction—from theory to therapy

Milton

Holmes

2019

Psychopharmacology

Self Cite

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“…Individuals with ASD are at an additional risk for developing anxiety (Perihan et al, 2020). A growing body of studies has supported the notion that mGluR7 has a dominant role in anxiety role (Kotlinska et al, 2019;O'Connor et al, 2019). Data with AMN082 would suggest the use of mGluR7 receptor agonists for treating anxiety (Spooren et al, 2010;Cieślik et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of mGluR7 in the Prefrontal Cortex Attenuates Autistic Behaviors in Mice

Wang

Gao

Zhang

et al. 2021

Front. Cell. Neurosci.

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Autism spectrum disorder (ASD) is associated with a range of abnormalities pertaining to socialization, communication, repetitive behaviors, and restricted interests. Owing to its complexity, the etiology of ASD remains incompletely understood. The presynaptic G protein-coupled glutamate receptor metabotropic glutamate receptor 7 (mGluR7) is known to be essential for synaptic transmission and is also tightly linked with ASD incidence. Herein, we report that prefrontal cortex (PFC) mGluR7 protein levels were decreased in C57BL/6J mice exposed to valproic acid (VPA) and BTBR T+ Itpr3tf/J mice. The overexpression of mGluR7 in the PFC of these mice using a lentiviral vector was sufficient to reduce the severity of ASD-like behavioral patterns such that animals exhibited decreases in abnormal social interactions and communication, anxiety-like, and stereotyped/repetitive behaviors. Intriguingly, patch-clamp recordings revealed that the overexpression of mGluR7 suppressed neuronal excitability by inhibiting action potential discharge frequencies, together with enhanced action potential threshold and increased rheobase. These data offer a scientific basis for the additional study of mGluR7 as a promising therapeutic target in ASD and related neurodevelopmental disorders.

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“…Metabotropic glutamate receptors expressions are (mGlu) associated with fear extinction process. The increased expression of mGlu7 is associated with deficits in the fear extinction process in PTSD ( O’Connor et al, 2019 ). Another study reported that increased mGlu5 mRNA expression in the BLA, IL-PFC, and PL-PFC contributes to stress-resilient behavior after traumatic stress ( Shallcross et al, 2021 ).…”

Section: Molecular Mechanisms Affecting the Fear Circuitry In Ptsdmentioning

confidence: 99%

“…Increase the susceptibility of mice to PTSD-like behavior (Lebow et al, 2012) Increase expression of mGlu7 Deficits in fear extinction process (O'Connor et al, 2019) CPEB3 (cytoplasmic polyadenylation elementbinding protein 3)…”

Section: Genetic and Epigenetic Regulationmentioning

confidence: 99%

The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder

Iqbal,

Huang,

Xue

et al. 2023

Front. Neurosci.

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Post-traumatic stress disorder (PTSD) is a stress-associated complex and debilitating psychiatric disorder due to an imbalance of neurotransmitters in response to traumatic events or fear. PTSD is characterized by re-experiencing, avoidance behavior, hyperarousal, negative emotions, insomnia, personality changes, and memory problems following exposure to severe trauma. However, the biological mechanisms and symptomatology underlying this disorder are still largely unknown or poorly understood. Considerable evidence shows that PTSD results from a dysfunction in highly conserved brain systems involved in regulating stress, anxiety, fear, and reward circuitry. This review provides a contemporary update about PTSD, including new data from the clinical and preclinical literature on stress, PTSD, and fear memory consolidation and extinction processes. First, we present an overview of well-established laboratory models of PTSD and discuss their clinical translational value for finding various treatments for PTSD. We then highlight the research progress on the neural circuits of fear and extinction-related behavior, including the prefrontal cortex, hippocampus, and amygdala. We further describe different molecular mechanisms, including GABAergic, glutamatergic, cholinergic, and neurotropic signaling, responsible for the structural and functional changes during fear acquisition and fear extinction processes in PTSD.

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Increased amygdalar metabotropic glutamate receptor 7 mRNA in a genetic mouse model of impaired fear extinction

Cited by 4 publications

References 60 publications

Editorial: the psychopharmacology of extinction—from theory to therapy

Editorial: the psychopharmacology of extinction—from theory to therapy

Overexpression of mGluR7 in the Prefrontal Cortex Attenuates Autistic Behaviors in Mice

The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder

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