Role of interleukin-1 beta in impairment of contextual fear conditioning caused by social isolation

Isolating rats immediately after conditioning impairs contextual but not auditory-cue fear conditioning. The reported experiments examine the involvement of brain interleukin-1β (IL-1β) in the impairment in contextual fear conditioning caused by social isolation. As measured by the conditioned freez...

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Veröffentlicht in:Behavioural brain research 1999-12, Vol.106 (1), p.109-118
Hauptverfasser: Pugh, C.Rachal, Nguyen, Kien T, Gonyea, Jennifer L, Fleshner, Monika, Watkins, Linda R, Maier, Steven F, Rudy, Jerry W
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container_issue 1
container_start_page 109
container_title Behavioural brain research
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creator Pugh, C.Rachal
Nguyen, Kien T
Gonyea, Jennifer L
Fleshner, Monika
Watkins, Linda R
Maier, Steven F
Rudy, Jerry W
description Isolating rats immediately after conditioning impairs contextual but not auditory-cue fear conditioning. The reported experiments examine the involvement of brain interleukin-1β (IL-1β) in the impairment in contextual fear conditioning caused by social isolation. As measured by the conditioned freezing response, 5 h of social isolation after conditioning, impaired contextual but not auditory-cue fear conditioning in adult male Sprague–Dawley rats. Social isolation for 1 or 3 h after conditioning also increased IL-1β protein in the hippocampus and cerebral cortex. No differences in IL-1β protein levels were found in the pituitary or the hypothalamus. Intracerebroventricular (ICV) IL-1 receptor antagonist (IL-1ra) given after conditioning prevented the impairment in contextual fear conditioning caused by isolation. ICV IL-1ra had no effect on auditory-cue fear conditioning in these same animals, nor did it affect the level of contextual fear conditioning displayed by home cage controls. Like isolation, ICV IL-1β (10 or 20 ng) after conditioning also impaired contextual but not auditory-cue fear conditioning. These results suggest that increased levels of brain IL-1β play a role in producing the impairment in contextual fear conditioning produced by social isolation. These findings also add to the generality of the idea that stressors induce IL-1β activity in the brain and that IL-1β may play physiological roles in the uninjured brain.
doi_str_mv 10.1016/S0166-4328(99)00098-4
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The reported experiments examine the involvement of brain interleukin-1β (IL-1β) in the impairment in contextual fear conditioning caused by social isolation. As measured by the conditioned freezing response, 5 h of social isolation after conditioning, impaired contextual but not auditory-cue fear conditioning in adult male Sprague–Dawley rats. Social isolation for 1 or 3 h after conditioning also increased IL-1β protein in the hippocampus and cerebral cortex. No differences in IL-1β protein levels were found in the pituitary or the hypothalamus. Intracerebroventricular (ICV) IL-1 receptor antagonist (IL-1ra) given after conditioning prevented the impairment in contextual fear conditioning caused by isolation. ICV IL-1ra had no effect on auditory-cue fear conditioning in these same animals, nor did it affect the level of contextual fear conditioning displayed by home cage controls. 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The reported experiments examine the involvement of brain interleukin-1β (IL-1β) in the impairment in contextual fear conditioning caused by social isolation. As measured by the conditioned freezing response, 5 h of social isolation after conditioning, impaired contextual but not auditory-cue fear conditioning in adult male Sprague–Dawley rats. Social isolation for 1 or 3 h after conditioning also increased IL-1β protein in the hippocampus and cerebral cortex. No differences in IL-1β protein levels were found in the pituitary or the hypothalamus. Intracerebroventricular (ICV) IL-1 receptor antagonist (IL-1ra) given after conditioning prevented the impairment in contextual fear conditioning caused by isolation. ICV IL-1ra had no effect on auditory-cue fear conditioning in these same animals, nor did it affect the level of contextual fear conditioning displayed by home cage controls. 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Like isolation, ICV IL-1β (10 or 20 ng) after conditioning also impaired contextual but not auditory-cue fear conditioning. These results suggest that increased levels of brain IL-1β play a role in producing the impairment in contextual fear conditioning produced by social isolation. These findings also add to the generality of the idea that stressors induce IL-1β activity in the brain and that IL-1β may play physiological roles in the uninjured brain.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>10595426</pmid><doi>10.1016/S0166-4328(99)00098-4</doi><tpages>10</tpages></addata></record>
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source MEDLINE; Access via ScienceDirect (Elsevier)
subjects Acoustic Stimulation
Animals
Behavioral psychophysiology
Biological and medical sciences
Brain
Brain Chemistry - physiology
Conditioning (Psychology) - physiology
Cues
Dose-Response Relationship, Drug
Fear - physiology
Fear - psychology
Fundamental and applied biological sciences. Psychology
Hippocampus
Humans
Immunology and behavior
interleukin 1^b
interleukin 1b
Interleukin-1 - administration & dosage
Interleukin-1 - metabolism
Interleukin-1 - pharmacology
Intracerebroventricular
Learning
Long-Term Potentiation - physiology
Male
Microinjections
Proinflammatory cytokines
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Rat
Rats
Rats, Sprague-Dawley
Recombinant Proteins - administration & dosage
Recombinant Proteins - pharmacology
Social Isolation - psychology
Space life sciences
Stress
title Role of interleukin-1 beta in impairment of contextual fear conditioning caused by social isolation
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