Author:
Rosen Jeffrey B.,Schulkin Jay
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.
Funder
National Institute of General Medical Sciences
Health Resources and Services Administration
Subject
Cellular and Molecular Neuroscience,Cognitive Neuroscience,Developmental Neuroscience,Neuroscience (miscellaneous)
Reference301 articles.
1. The kindling model of epilepsy;Abel;Animal Models of Neurological Disease, II Neuromethods,1992
2. Anticipatory threat responding: associations with anxiety, development, and brain structure.;Abend;Biol. Psychiat.,2020
3. Threat imminence reveals links among unfolding of anticipatory physiological response, cortical-subcortical intrinsic functional connectivity, and anxiety.;Abend;Neurobiol. Stress,2022
4. Transmitter systems involved in neural plasticity underlying increased anxiety and defense—implications for understanding anxiety following traumatic stress.;Adamec;Neurosci. Biobehav. Rev.,1997
5. Neuroplasticity in specific limbic system circuits may mediate specific kindling induced changes in animal affect—implications for understanding anxiety associated with epilepsy.;Adamec;Neurosci. Biobehav. Rev.,2000
Cited by
4 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献