Identification and localization of cell types that express endothelial and neuronal nitric oxide synthase in the rat nucleus tractus solitarii

Abstract

Numerous studies have suggested that nitric oxide (NO) in the nucleus tractus solitarii (NTS) participates in modulating cardiovascular function. Nitric oxide synthase (NOS), the enzyme responsible for synthesis of NO, exists in 3 isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). Although the distribution of nNOS in the NTS has been well documented, the distribution of eNOS in the NTS has not. Because recent studies have shown that eNOS may contribute to regulation of baroreceptor reflexes and arterial pressure, we examined the distribution of eNOS and the types of cells that express it in rat NTS by using multiple labels for immunofluorescent staining and confocal microscopy. Immunoreactivity (IR) for eNOS and nNOS was found in cells and processes in all NTS subnuclei, but eNOS-IR was more uniformly distributed than was nNOS-IR. Although structures containing either eNOS-IR or nNOS-IR were often present in close proximity, they never contained both isoforms. Almost all eNOS-IR positive structures, but no nNOS-IR positive structures, contained IR for the glial marker glial fibrillary acidic protein. Furthermore, while all nNOS-IR positive cells contained IR for the neuronal marker neuronal nuclear antigen (NeuN), none of the eNOS-IR positive cells contained NeuN-IR. We conclude that eNOS in the NTS is present only in astrocytes and endothelial cells, not in neurons. Our data complement previous physiological studies and suggest that although NO from nNOS may modulate neurotransmission directly in the NTS, NO from eNOS in the NTS may modulate cardiovascular function through an interaction between astrocytes and neurons.

Striatal NOS1 has dimorphic expression and activity under stress and nicotine sensitization

“…Regarding NOS3 expression, this isoform was only detected in the blood vessels of both the wild-type and KO animals, but not in neural cells, in agreement with previous findings (Seidel et al, 1997;Lin et al, 2007). Although some researchers have found NOS3 expression in neurons and astrocytes, this expression was a result of damage to the brain parenchyma (Seidel et al, 1997;Lin et al, 2007).…”

Cellular senescence, ageing and disease

“…A reduction in NO production by eNOS, for example, has been suggested to be a significant risk factor for cardiovascular disease (Cannon 1998). Also, eNOS activity has been shown to be present in astrocytes (Wienchen and Casagrande 1999;Lin et al 2007), but the impact of cellular senescence (if any) on eNOS activity on this cell type is currently lacking.…”

Nitric oxide inhibits excitatory vagal afferent input to nucleus tractus solitarius neurons in anaesthetized rats

“…Vagal afferents to the NTS also contain NOS, and vagal deafferentiation decreases NOS immunoreactivity in the NTS [9][10][11] . Our present study, by using ionophoresis drug application method, indicates that L-Arg and L-NAME are likely to act on the local NO pathways within the vicinity of the recording site, which was further confirmed by the effect of SNP on vagal afferent-evoked excitation.…”

“…Being an unstable molecule, NO is produced by nitric oxide synthase (NOS) under normal conditions in the brain. Evidence from histological studies shows that vagal afferents to the NTS containing NOS and vagal deafferentiation decrease the NOS immunoreactivity in the NTS [9][10][11] . NOS immunoreactivity has also been found in many nuclei of neurons within the medulla oblongata that sends projections to the NTS [12][13][14] , which suggests that NO generated in the NTS may modulate vagal afferent integration.…”