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• W1968651154 endingPage "836" @default.
• W1968651154 startingPage "825" @default.
• W1968651154 abstract "In Brief Accumulating evidence suggests an important contribution of reactive oxygen species (ROS) to pain and neuropsychiatric disorders, but their role in pain-related plasticity in the brain is largely unknown. Neuroplasticity in the central nucleus of the amygdala (CeA) correlates positively with pain behaviors in different models. Little is known, however, about mechanisms of visceral pain–related amygdala changes. The electrophysiological and behavioral studies reported here addressed the role of ROS in the CeA in a visceral pain model induced by intracolonic zymosan. Vocalizations to colorectal distension and anxiety-like behavior increased after intracolonic zymosan and were inhibited by intra-CeA application of a ROS scavenger (tempol, a superoxide dismutase mimetic). Tempol also induced a place preference in zymosan-treated rats but not in controls. Single-unit recordings of CeA neurons in anesthetized rats showed increases of background activity and responses to visceral stimuli after intracolonic zymosan. Intra-CeA application of tempol inhibited the increased activity but had no effect under normal conditions. Whole-cell patch-clamp recordings of CeA neurons in brain slices from zymosan-treated rats showed that tempol decreased neuronal excitability and excitatory synaptic transmission of presumed nociceptive inputs from the brainstem (parabrachial area) through a combination of presynaptic and postsynaptic actions. Tempol had no effect in brain slices from sham controls. The results suggest that ROS contribute to visceral pain–related hyperactivity of amygdala neurons and amygdala-dependent behaviors through a mechanism that involves increased excitatory transmission and excitability of CeA neurons. Electrophysiological and behavioral data identify reactive oxygen species in the amygdala, the brain's emotional center, as a visceral pain mechanism." @default.
• W1968651154 created "2016-06-24" @default.
• W1968651154 creator A5010444377 @default.
• W1968651154 creator A5054742181 @default.
• W1968651154 creator A5086674481 @default.
• W1968651154 date "2015-05-01" @default.
• W1968651154 modified "2023-10-14" @default.
• W1968651154 title "Reactive oxygen species mediate visceral pain–related amygdala plasticity and behaviors" @default.
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• W1968651154 doi "https://doi.org/10.1097/j.pain.0000000000000120" @default.
• W1968651154 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4402250" @default.
• W1968651154 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25734993" @default.
• W1968651154 hasPublicationYear "2015" @default.
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