ReviewFrontiers in systems neuroscience2022
Hyperexcitability: From Normal Fear to Pathological Anxiety and Trauma.
Review in Frontiers in systems neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Learning, sleep replay and consolidation of contextual fear memories: A neural network model.PLoS computational biology · 2026Article
- Burden of psychiatric disease inversely correlates with Alzheimer's age at onset.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Short-term risk of psychiatric adverse events following COVID-19 vaccination: nationwide self-controlled case series study.BJPsych open · 2025Article
- Differential modulation of freezing and 22-kHz USVs by shock intensity, tone-duration matching, and anxiety levels in rodent fear-conditioning paradigms.Learning & behavior · 2025Article
- Neurobiology of Chronic Pain, Posttraumatic Stress Disorder, and Mild Traumatic Brain Injury.Biology · 2025Review
- Stress-induced anxiety-related behavior in mice is driven by enhanced excitability of ventral tegmental area GABA neurons.Frontiers in behavioral neuroscience · 2024Article
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Authors and funding
2 authors.
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Abstract
Hyperexcitability in fear circuits is suggested to be important for development of pathological anxiety and trauma from adaptive mechanisms of fear. Hyperexcitability is proposed to be due to acquired sensitization in fear circuits that progressively becomes more severe over time causing changing symptoms in early and late pathology. We use the metaphor and mechanisms of kindling to examine gains and losses in function of one excitatory and one inhibitory neuropeptide, corticotrophin releasing factor and somatostatin, respectively, to explore this sensitization hypothesis. We suggest amygdala kindling induced hyperexcitability, hyper-inhibition and loss of inhibition provide clues to mechanisms for hyperexcitability and progressive changes in function initiated by stress and trauma.
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