ArticleTranslational psychiatry2012
In vivo knockdown of GAD67 in the amygdala disrupts fear extinction and the anxiolytic-like effect of diazepam in mice.
Article in Translational psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
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- Clusterin Regulates the Mechanisms of Neuroinflammation and Neuronal Circuit Impairment in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Effects of TrkB-related induced metaplasticity within the BLA on anxiety, extinction learning, and plasticity in BLA-modulated brain regions.Behavioral and brain functions : BBF · 2025Article
- Impaired oxytocin signalling in the central amygdala in rats with chronic heart failure.The Journal of physiology · 2024Article
- Chronic Nasal Administration of Kisspeptin-54 Regulates Mood-Related Disorders Via Amygdaloid GABA in Hemi-Parkinsonian RatsBalkan medical journal · 2024Article
- Article
- Understanding the mechanism of action and clinical effects of neuroactive steroids and GABAergic compounds in major depressive disorder.Translational psychiatry · 2023Review
- Subgenual and Hippocampal Pathways in Amygdala Are Set to Balance Affect and Context Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Memory retrieval, reconsolidation, and extinction: Exploring the boundary conditions of post-conditioning cue exposure.Frontiers in synaptic neuroscience · 2023Review
- Beyond the γ-aminobutyric acid hypothesis of schizophrenia.Frontiers in cellular neuroscience · 2023Review
- GABAergic circuits of the basolateral amygdala and generation of anxiety after traumatic brain injury.Amino acids · 2022Review
- Alpha-synuclein pathology, microgliosis, and parvalbumin neuron loss in the amygdala associated with enhanced fear in the Thy1-aSyn model of Parkinson's disease.Neurobiology of disease · 2021Article
- Genetic deletion of the 67-kDa isoform of glutamate decarboxylase alters conditioned fear behavior in rats.FEBS open bio · 2021Article
- Behavioral Consequences of a Combination ofFrontiers in pharmacology · 2021Article
- Animal models of PTSD: a challenge to be met.Molecular psychiatry · 2019Review
- Conditioned stimulus presentations alter anxiety level in fear-conditioned mice.Molecular brain · 2019Article
- Limited prefrontal cortical regulation over the basolateral amygdala in adolescent rats.Scientific reports · 2018Article
- Age-Related Susceptibility to Epileptogenesis and Neuronal Loss in Male Fischer Rats Exposed to Soman and Treated With Medical Countermeasures.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
In mammals, γ-aminobutyric acid (GABA) transmission in the amygdala is particularly important for controlling levels of fear and anxiety. Most GABA synthesis in the brain is catalyzed in inhibitory neurons from L-glutamic acid by the enzyme glutamic acid decarboxylase 67 (GAD67). In the current study, we sought to examine the acquisition and extinction of conditioned fear in mice with knocked down expression of the GABA synthesizing enzyme GAD67 in the amygdala using a lentiviral-based (LV) RNA interference strategy to locally induce loss-of-function. In vitro experiments revealed that our LV-siRNA-GAD67 construct diminished the expression of GAD67 as determined with western blot and fluorescent immunocytochemical analyses. In vivo experiments, in which male C57BL/6J mice received bilateral amygdala microinjections, revealed that LV-siRNA-GAD67 injections produce significant inhibition of endogenous GAD67 when compared with control injections. In contrast, no significant changes in GAD65 expression were detected in the amygdala, validating the specificity of LV knockdown. Behavioral experiments showed that LV knockdown of GAD67 results in a deficit in the extinction, but not the acquisition or retention, of fear as measured by conditioned freezing. GAD67 knockdown did not affect baseline locomotion or basal measures of anxiety as measured in open field apparatus. However, diminished GAD67 in the amygdala blunted the anxiolytic-like effect of diazepam (1.5 mg kg(-1)) as measured in the elevated plus maze. Together, these studies suggest that of GABAergic transmission in amygdala mediates the inhibition of conditioned fear and the anxiolytic-like effect of diazepam in adult mice.
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