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ARTICLE

T-Lymphocyte Activation Increases Hypothalamic and Amygdaloid Expression of CRH mRNA and Emotional Reactivity to Novelty

Alexander W. Kusnecov, Rumei Liang and Galina Shurin
Journal of Neuroscience 1 June 1999, 19 (11) 4533-4543; DOI: https://doi.org/10.1523/JNEUROSCI.19-11-04533.1999
Alexander W. Kusnecov
1Department of Psychology, Rutgers University, New Brunswick, New Jersey 08901, and Departments of
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Rumei Liang
2Pathology and
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Galina Shurin
3Surgery, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15238
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Abstract

Stimulation of T-cells with staphylococcal enterotoxin B (SEB) significantly elevates interleukin-2 (IL-2) and contemporaneous activation of the hypothalamic–pituitary–adrenal (HPA) axis andc-fos in the paraventricular nucleus (PVN) of BALB/cByJ mice. Such neural signaling may promote cognitive and emotional adaptation before or during infectious illness. Because corticotropin-releasing hormone (CRH) is an anxiogenic neuropeptide that may mediate the stressor-like effects of immunological stimuli, we measured neuronal CRH mRNA alterations in mice challenged with SEB. Increased CRH mRNA levels were observed in the PVN and central nucleus of the amygdala (ceA) 4–6 hr after SEB administration. This was associated with plasma ACTH increases, which could be abrogated by the systemic administration of anti-CRH antiserum. Additional experiments did not support a role for IL-2 or prostaglandin synthesis in activating the HPA axis. Behavioral experiments testing for conditioned taste aversion did not confirm that SEB challenge promotes malaise. However, consistent with the notion that central CRH alterations induced by SEB may affect emotionality (e.g., fear), SEB challenge augmented appetitive neophobia in a context-dependent manner, being marked in a novel and stressful environment. It is hypothesized that immunological stimuli generate a cascade of events that solicit integrative neural processes involved in emotional behavior. As such, these data support the contention that affective illness may be influenced by immunological processes and the production of cytokines and are consistent with other evidence demonstrating that autoimmune reactivity is associated with enhanced emotionality.

  • T-lymphocytes
  • corticotropin-releasing hormone
  • staphylococcal enterotoxin B
  • adrenocorticotropic hormone
  • psychoneuroimmunology
  • emotion
  • neophobia
  • interleukin-2
  • cytokines
  • prostaglandins
  • stress
  • amygdala
  • hypothalamus
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The Journal of Neuroscience: 19 (11)
Journal of Neuroscience
Vol. 19, Issue 11
1 Jun 1999
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T-Lymphocyte Activation Increases Hypothalamic and Amygdaloid Expression of CRH mRNA and Emotional Reactivity to Novelty
Alexander W. Kusnecov, Rumei Liang, Galina Shurin
Journal of Neuroscience 1 June 1999, 19 (11) 4533-4543; DOI: 10.1523/JNEUROSCI.19-11-04533.1999

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T-Lymphocyte Activation Increases Hypothalamic and Amygdaloid Expression of CRH mRNA and Emotional Reactivity to Novelty
Alexander W. Kusnecov, Rumei Liang, Galina Shurin
Journal of Neuroscience 1 June 1999, 19 (11) 4533-4543; DOI: 10.1523/JNEUROSCI.19-11-04533.1999
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  • Article
    • Abstract
    • MATERIALS AND METHODS
    • Drugs and reagents
    • Neuroendocrine and histochemical studies
    • Assays for ACTH and IL-2
    • Statistical analysis
    • RESULTS
    • DISCUSSION
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Keywords

  • T-lymphocytes
  • corticotropin-releasing hormone
  • staphylococcal enterotoxin B
  • adrenocorticotropic hormone
  • psychoneuroimmunology
  • emotion
  • neophobia
  • interleukin-2
  • cytokines
  • prostaglandins
  • stress
  • amygdala
  • hypothalamus

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