Immunocytochemical localization of substance P neurokinin-1 receptors in rat gingival tissue

Abstract

The distributions of substance P (SP) and the neurokinin-1 receptor (NK1-R), the receptor preferentially activated by SP, were examined in rat gingiva by immunocytochemical methods with light and electron microscopy. SP-immunoreactive nerve fibers were located preferentially in the junctional epithelium (JE) but few in the other oral and oral sulcular epithelia. NK1-R immunoreactivity was found in the endothelial cells (capillaries and postcapillary venules underlying the JE). NK1-R-labeled and -unlabeled unmyelinated nerve fibers were located close to the blood vessels and partially or completely covered by a Schwann cell sheath. In the JE, labeled naked axons without Schwann cell sheaths were observed. Neutrophils and macrophages in the connective tissue underlying the JE and in the JE were also labeled with NK1-R. Furthermore, NK1-R was found in the JE cells. Basically, immunoreaction products for NK1-R were found throughout various cells (endothelial cells, neutrophils, and JE cells) at invaginations of the plasma membrane and in vesicular and granular structures that are probably endosomes and are found close to both the plasma membrane and the nucleus. This is a first report, demonstrating the presence of NK1-R in the gingival tissue in the normal nonstimulated condition. Furthermore, it is thought that SP may modulate the permeability of blood vessels beneath the JE, the production of antimicrobial agents in neutrophils, and the proliferation and endocytotic ability of JE cells through NK1-R.

Defective adipose tissue development associated with hepatomegaly in cathepsin E-deficient mice fed a high-fat diet

“…Immunohistochemistry was performed as described previously [13]. Briefly, 20-μm cryosections were treated with 0.3% Triton X-100 in PBS for 30 min, followed by 0.3% H2O2 in PBS for 60 min.…”

Biological Sealing and Defense Mechanisms in Peri-Implant Mucosa of Dental Implants

“…These receptors are also localized in neutrophils invading into the intercellular spaces between PIE cells (Figure 8c). Overall, the PIE shows a similar distribution of substance P-containing sensory nerve fibers and their neurokinin-1 receptors, compared to junctional epithelium Tanaka et al, 1996;Kido et al, 1999). …”

“…The sensory nerve fibers contain the neuropeptides, calcitonin gene-related peptide (Byers et al, 1987;Nagata et al, 1992Nagata et al, , 1994 and substance P (Nagata et al, , 1994Tanaka et al, 1996;Kido et al, 1999), and terminate close to endothelial cells, neutrophils, and junctional epithelial cells Tanaka et al, 1996). The peri-implant mucosa is also supplied with sensory nerves containing calcitonin generelated peptide (Fujii et al, 2003) and substance P (Yamaza et al, 2009) (Figure 7a).…”

“…Various mechanisms of peripheral host defense have been demonstrated in this epithelium (Schroeder & Listgarten, 1997) (Figure 9): (1) phagocytosis and anti-bacterial activity of neutrophils infiltrating into the junctional epithelium (Yamasaki et al, 1979, Tanaka et al, 1988, (2) outward flow of gingival sulcular fluid through the junctional epithelium (McDougall, 1970;Tanaka, 1984;Tanaka and Sakano, 1987), (3) fast turnover or apoptosis of junctional epithelial cells (Schroeder, 1986, Ekuni et al, 2005, (4) continuous epithelial attachment via the IBL throughout the enamel surface (Squier, 1991;Bartold, et al, 2000), (5) endocytotic capacity of junctional epithelial cells for external pathogens (Yamasaki et al, 1979;Tanaka 1984;Tanaka & Sakano, 1987;Ayasaka et al, 1989, Yamaza et al, 1997, and (6) neurotrophic modulation in the junctional epithelium (Kondo et al, 1995;Tanaka et al, 1996;Kido et al, 1999). Fig.…”

“…Substance P released from nerve terminals into the intercellular spaces between the nerve endings and neurokinin receptor-bearing cells may inhibit intraepithelial growth of peri-implant bacteria in the PIE. Thus substance Pneurokinin-1 receptor function could, at least partly, govern the local defense mechanisms in this transmucosal region around dental implants, as in the natural junctional epithelium (Kido et al, 1999;Brogden et al, 2005). Fig.…”