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Aging Alters Sympathetic and Gene Expression Responses to Rostral Ventral Lateral Medulla (RVLM) Microinjection of Lipopolysaccharide (LPS)
Author(s) -
Craig R. A.,
Helwig B. G.,
Fels R. J.,
Kenney M. J.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a467-d
Subject(s) - rostral ventrolateral medulla , sympathetic nervous system , tlr4 , medicine , microinjection , endocrinology , immune system , receptor , lipopolysaccharide , biology , central nervous system , immunology , medulla oblongata , blood pressure
Bidirectional communication pathways exist between the nervous system and the immune system and alterations in immune system and sympathetic nerve discharge (SND) regulation occur with advancing age. The sympathetic nervous system is important for maintaining homeostasis under basal conditions and in response to acute and chronic stressors. However, it is not known how aging affects SND activation to an acute immune stressor. Preliminary data from our laboratory indicates age‐dependent attenuation of splenic SND responses to RVLM LPS microinjections in aged (24‐month old) rats compared with young (3‐months old) F344 rats, suggesting that aged rats exhibit altered brainstem‐mediated sympathetic responses to an acute immune stressor. The objective of the current study was to determine if aged F344 rats retain the molecular substrate responsible for conferring LPS responsiveness in the RVLM under basal conditions. Preliminary experiments using real‐time PCR with primers specific for the TLR4 receptor complex and associated signaling molecules suggest that aging does not affect the constitutive expression of TLR4 mRNA in the RVLM under basal conditions. Our preliminary data suggest that the attenuated sympathetic responses to RVLM LPS with age may be due to alterations in the expression of components of the TLR4 receptor complex and associated intracellular signaling molecules under conditions of an acute immune stressor. Supported by NIH HL‐65346 (MJK), HL‐69755 (MJK), and AHA Postdoctoral Grant 0520105Z (BGH).