Cellular and subcellular distribution of substance P receptor immunoreactivity in the dorsal vagal complex of the rat and cat: A light and electron microscope study

Abstract

Immunoreactivity for the substance P receptor (NK1 receptor) has been investigated by light and electron microscopy in the dorsal vagal complexes of adult rats and cats. The general pattern of NK1 immunoreactivity was similar for both rat and cat. Numerous NK1-immunoreactive neurons were present in the area postrema, the nucleus of the solitary tract, and the dorsal motor nucleus of the vagus nerve. The density of labelled neurons differed between the subnuclei of the nucleus of the solitary tract. Overall, the efferent neurons of the dorsal motor nucleus of the vagus nerve highly expressed NK1 when compared to neurons in the nucleus of the solitary tract. The results are discussed with reference to the viscerotopic organisation of the dorsal vagal complex. Ultrastructural analysis demonstrated that NK1 immunoreactivity was present only at the membrane surface of somatic and dendritic profiles of neurons. No labelling was found in axon terminals, axons, or glial processes. NK1 immunoreactivity, as revealed by a preembedding immunogold technique in serial ultrathin sections, was preferentially located at nonsynaptic sites. A semiquantitative study suggested that the density of NK1 receptors is statistically higher at membrane sites free of any contact (synaptic or not) with axon terminals. The subcellular localisation of NK1 immunoreactivity was similar for neurons of both rat and cat. These results suggest that in the dorsal vagal complex, substance P might act on NK1 receptors through a process of volume transmission.

Circumventricular Organs

“…Binding sites/receptors for amylin (Sexton et al, 1994), canabinoid CB1 receptor, cholecystokinin CCK-1 receptor (Moran et al, 1986), angiotensin II AT 1 (Lenkei et al, 1997;Allen et al, 2000), atrial natriuretic peptide Saavedra et al, 1992), GLP-1 (Göke et al,1995), Ghrelin-GHRS receptor (Zigman et al, 2006); neuropeptide Y, Peptide YY and pancreatic polypeptide-Y1, Y2, Y4 and Y5 receptors (Martel et al, 1986;Kishi et al, 2005); purinergic P2X2 and P2X7 receptors (Kodama et al, 2007;Mangano et al, 2012), somatostatin (Patel et al, 1986), substance P NK-1 receptor (Baude and Shigemoto, 1998), vasoactive intestinal polypeptide (Shaffer and Moody, 1986), vasopressin (Phillips et al, 1988), and insulin (Werther et al, 1987) have been observed in the area postrema. Like the other sensory CVOs, the area postrema exhibits the CD14 lipopolysacharide receptor (Lacroix et al, 1998).…”

Subcellular vesicular aggregations of GABAB R1a and R1b receptors increase with age in neurons of the developing mouse brain

“…Since the antibody used in the EM study was directed against the intracellular C-terminal of the GABA B R1a/b receptor, such intracellular granular stainings could well be interpreted as GABA B receptor-containing vesicles. These vesicles might represent intracellular GABA B receptorcontaining transport vesicles, which are objects for targeted transport via an elaborate molecular machinery, as suggested by Baude and Shigemoto (1998). They interpreted a greater number of granular stainings as indicators of increased receptor turnover, the turnover time being estimated at about 4 h (Couve et al 1998).…”

“…also Boyes and Bolam 2003), while the diffusely distributed GABA B R1-IR gradually faded. During the first 4 post-natal days, GABA B R1a/b-IR was diffusely distributed in all regions; additional punctuate staining, possibly of intracellular granules as suggested by Baude and Shigemoto (1998), occurred in Fig. 1 The distribution of GABA B R1a/b-IR changes during early post-natal development in the forebrain of the mouse.…”

Functional interaction between nucleus tractus solitarius NK and 5-HT receptors in the inhibition of baroreflex in rats

“…5). The data of previous studies showing that (1) in some structures, NK 1 receptors are located on GABAergic interneurons [31,32], and (2) NTS contains high densities of both GABAergic interneurons [33] and NK 1 receptors [34,35], agree with this hypothesis. In addition, it is possible that, in a second independent pathway, responsible for the NK 1 receptor-independent inhibition of the cardiac carotid baroreflex bradycardia, GABAergic interneurons, directly activated by 5-HT 3 receptor-induced glutamate release during the defense reaction, would not be in relation with substance P interneurons and would inhibit cells receiving cardiac carotid sinus inputs (Fig.…”