CRF Mediates Stress-Induced Pathophysiological High-Frequency Oscillations in Traumatic Brain Injury

Autor: Paul S. Jung, Michelle Everest, Julio Martinez-Trujillo, Francisco Bautista Cruz, Michael O. Poulter, Chakravarthi Narla
Rok vydání: 2019
Předmět:
Male
Corticotropin-Releasing Hormone
Traumatic brain injury
Medical Physiology
Inhibitory postsynaptic potential
Receptors
Corticotropin-Releasing Hormone
Amygdala
Rats
Sprague-Dawley
03 medical and health sciences
Epilepsy
stress
0302 clinical medicine
Brain Injuries
Traumatic
Limbic System
Animals
Medicine
rat
030304 developmental biology
0303 health sciences
business.industry
General Neuroscience
traumatic brain injury
Antagonist
3.1
General Medicine
New Research
medicine.disease
Pharmacy and Pharmaceutical Sciences
voltage sensitive dye imaging ripples
Rats
nervous system diseases
Disease Models
Animal
medicine.anatomical_structure
nervous system
Excitatory postsynaptic potential
GABAergic
epilepsy
Disorders of the Nervous System
Kindling model
business
Neuroscience
Stress
Psychological
030217 neurology & neurosurgery
Zdroj: Physiology and Pharmacology Publications
eNeuro
Popis: It is not known why there is increased risk to have seizures with increased anxiety and stress after traumatic brain injury (TBI). Stressors cause the release of corticotropin-releasing factor (CRF) both from the hypothalamic pituitary adrenal (HPA) axis and from CNS neurons located in the central amygdala and GABAergic interneurons. We have previously shown that CRF signaling is plastic, becoming excitatory instead of inhibitory after the kindling model of epilepsy. Here, using Sprague Dawley rats we have found that CRF signaling increased excitability after TBI. Following TBI, CRF type 1 receptor (CRFR1)-mediated activity caused abnormally large electrical responses in the amygdala, including fast ripples, which are considered to be epileptogenic. After TBI, we also found the ripple (120–250 Hz) and fast ripple activity (>250 Hz) was cross-frequency coupled with θ (3–8 Hz) oscillations. CRFR1antagonists reduced the incidence of phase coupling between ripples and fast ripples. Our observations indicate that pathophysiological signaling of the CRFR1increases the incidence of epileptiform activity after TBI. The use for CRFR1antagonist may be useful to reduce the severity and frequency of TBI associated epileptic seizures.
Databáze: OpenAIRE
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