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Differential distribution of endothelial nitric oxide synthase and neuronal nitric oxide synthase in rat nucleus tractus solitarii
Author(s) -
Lin LiHsien,
Taktakishvili Otar M.,
Talman William T.
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.a466
Subject(s) - enos , neun , nitric oxide , nitric oxide synthase , nucleus , chemistry , nitric oxide synthase type iii , glial fibrillary acidic protein , astrocyte , immunolabeling , medicine , microbiology and biotechnology , immunohistochemistry , endocrinology , biology , central nervous system
Studies have shown that nitric oxide (NO) may play an important role in the nucleus tractus solitarii (NTS) in modulating cardiovascular function. There are 3 isoforms of nitric oxide synthase (NOS) that synthesize NO. These are endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). While the distribution of nNOS in the NTS has been well documented, the distribution of eNOS in the NTS has not. We used double and triple fluorescent immunohistochemistry combined with confocal microscopy to compare and contrast the location of eNOS with that of nNOS. Immunoreactivity (IR) for eNOS, but not iNOS‐IR, was found in cells and processes in all NTS subnuclei. Although structures containing either eNOS‐IR or nNOS‐IR often were present in close proximity, they never colocalized. Almost all eNOS‐IR positive cells or processes, but no nNOS‐IR positive cells or processes, contained glial fibrillary acidic protein (GFAP, a glial marker)‐IR. All nNOS‐IR positive cells contained neuronal nuclear antigen (NeuN, a neuronal marker)‐IR, but none of the eNOS‐IR positive cells contained NeuN‐IR. We concluded that eNOS in the NTS is present only in astrocytes and endothelial cells, not in neurons. Our data suggest that while NO from nNOS may effect neurotransmission directly in the NTS, NO from eNOS in the NTS may modulate cardiovascular function through an interaction between astrocytes and neurons.