Cardiovascular roles of tachykinin peptides in the nucleus tractus solitarii of rats

Nagashima, Akira; Takáno, Yukio; Tateishi, Kensuke; Matsuoka, Yoshikazu; Hamaoka, Toshiyuki; Kamiya, Hiro-o

doi:10.1016/0006-8993(89)90848-2

Cited by 55 publications

(27 citation statements)

References 25 publications

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“…The present study revealed intense expression of NKR-HS and NKR-LI in many regions of the hypothalamus, nucleus of the solitary tract, and dorsal motor nucleus of the vagus nerve, suggesting the involvement of NKR in autonomic functions. It has been reported that intracerebroventricular injection of NHz-senktide, a synthetic peptide highly selective for NKR (Wormser et al, 1986;Laufer et al, 19881, potentially inhibits salt appetite (Massi et al, 1988) and that microinjection of senktide into the nucleus of the solitary tract causes long-lasting hypertension and tachycardia (Nagashima et al, 1989). It is also likely that intracerebroventricular injection of NK increases the blood pressure mainly via release of vasopressin from the hypothalamus through NKR (Polidori et al, 1989;Takano et al, 1990).…”

Section: Discussionmentioning

confidence: 98%

Localization of the neuromedin K receptor (NK3) in the central nervous system of the rat

et al. 1996

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The distribution of the neuromedin K receptor (NK3; NKR) in the central nervous system was investigated in the adult rat by using in situ hybridization and immunohistochemical techniques. The rabbit anti-NKR antibody was raised against a bacterial fusion protein containing a C-terminal portion of NKR and affinity purified with a Sepharose 4B column conjugated to the fusion protein. Immunoblot analysis was performed to test the reactivity and specificity of the antibody. Crude membrane was prepared from cDNA-transfected Chinese hamster ovary (CHO) cells expressing each of the rat NKR, substance P receptor (NK1; SPR), and substance K receptor (NK2; SKR) and from the hypothalamus, cerebral cortex, and cerebellum. Immunoreactive bands were observed specifically in the NKR-CHO cells, hypothalamus, and cerebral cortex but not in the SPR- or SKR-CHO cells, nor in the cerebellum. Molecular weights of the immunoreactive bands ranged from 73 to 89 kDa and from 59 to 83 kDa in the NKR-CHO cells and tissues, respectively. The distribution of NKR-like immunoreactivity coincided with that of NKR mRNA. The expression of NKR was indicated on neuronal cell bodies and dendrites. NKR was found to be expressed intensely or moderately in neurons in the glomerular and granule cell layers of the main olfactory bulb; glomerular and mitral cell layers of the accessory olfactory bulb; layers IV and V of the cerebral neocortex; medial septal nucleus; nucleus of the diagonal band; bed nucleus of the stria terminalis; globus pallidus; ventral pallidum; paraventricular nucleus; supraoptic nucleus; zona incerta; dorsal, lateral, and posterior hypothalamic areas; amygdaloid nuclei; medial habenular nucleus; ventral tegmental area; midbrain periaqueductal gray; interpeduncular nuclei; substantia nigra pars compacta; linear, median, dorsal, and pontine raphe nuclei; posteromedial tegmental nucleus; sphenoid nucleus; nucleus of the solitary tract; intermediate and rostroventrolateral reticular nuclei; and lamina II of the caudal spinal trigeminal nucleus and spinal dorsal horn. These findings are discussed in relation to the physiological functions associated with neuromedin K.

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Section: Discussionmentioning

confidence: 98%

Localization of the neuromedin K receptor (NK3) in the central nervous system of the rat

et al. 1996

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“…First, centrally administered senktide may activate NTS neurons, and this activation contributes to the pressor response. Microinjections of senktide into the NTS produce a dose-dependent hypertension (Nagashima et al, 1989). Therefore, activation of the NTS may contribute to the neural component of the pressor response caused by senktide.…”

Section: Cardiovascular Regulationmentioning

confidence: 99%

“…Activation of NK 3 receptors affects neural transmission in several sensory systems, cardiovascular function (e.g., blood pressure and heart rate), pituitary secretion, and fluid and electrolyte balance (Papir-Kircheli et al, 1987;Massi et al, 1988bMassi et al, , 1991aNagashima et al, 1989;Polidori et al, 1989;Takano et al, 1993;Smith and Flynn, 1994;Couture et al, 1995;Eguchi et al, 1996). Given the importance of NK 3 receptors and their ligand in many regulatory functions, it is not surprising that investigators have sought to identify particular sites that mediate the actions of NK 3 agonists.…”

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confidence: 98%

Distribution of fos-like immunoreactivity within the rat brain following intraventricular injection of the selective NK3 receptor agonist senktide

Smith

Flynn

2000

J. Comp. Neurol.

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Neurokinin B (NKB) is one member of an evolutionarily conserved family of neuropeptides, the tachykinins. Preferential binding of NKB to endogenous NK(3) receptors affects a variety of biological and physiological processes, including endocrine secretions, sensory transmission, and fluid and electrolyte homeostasis. In light of its widespread biological actions, immunohistochemical detection of the c-Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] substance P [6-11]), senktide. Quantitative analysis revealed that treatment with isotonic saline or 200 ng senktide resulted in the differential expression of Fos-like immunoreactivity (FLI) throughout the brain. Senktide induced the highest number of FLI neurons in the lateral septum, bed nucleus of the stria terminalis, amygdala, paraventricular nucleus of the hypothalamus, median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus, periaqueductal gray, and medial nucleus of the solitary tract compared to isotonic saline controls. Additional regions that contained elevated FLI following icv injection of senktide, relative to saline injection, included the cerebral cortex, lateral hypothalamic nucleus, suprachiasmatic nucleus, ventral tegmental area, substantia nigra, inferior colliculus, locus coeruleus, zona incerta, and arcuate nucleus. Our data indicate that activation of NK(3) receptors induces the expression of FLI within circumscribed regions of the rat brain. This pattern of neuronal activation overlaps with nuclei known to regulate homeostatic processes, such as endocrine secretion, cardiovascular function, salt intake, and nociception.

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“…We focused on these regions because of the involvement of hypothalamic tachykinins in the control of anterior pituitary function (Kerdelhué et al, 1978;Vijayan and McCann, 1979;Eckstein et al, 1980;Dees et al, 1985;Ohtsuka et al, 1987;Arisawa et al, 1990;Picanco-Diniz et al, 1990;Kalra et al, 1991;Debeljuk et al, 1992;Shamgochian and Leeman, 1992), cardiovascular regulation (Hall et al, 1989;Nagashima et al, 1989;Itoi et al, 1994) and sexual behavior (Dornan and Malsbury, 1989;Kalra et al, 1991;Olster and Blaustein, 1992a,b;Swann and Macchione, 1992;Swann and Newman, 1992;Akesson, 1993). Previous immunohistochemical studies of the distribution of tachykinins in the human hypothalamus utilized antibodies that do not distinguish between SP and NKB (Constantinidis et al, 1983;Bouras et al, 1986;Mai et al, 1986).…”

mentioning

confidence: 99%

Localization of neurons expressing substance P and neurokinin B gene transcripts in the human hypothalamus and basal forebrain

et al. 1997

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In situ hybridization histochemistry was used to map the distribution of neurons expressing the substance P (SP) or neurokinin B (NKB) genes in the human hypothalamus and basal forebrain. Hypothalami from five adult males were frozen in isopentane at -30 degrees C and serially sectioned at 20 jm thickness. Every 20th section was hybridized with [35S]-labeled, 48-base synthetic cDNA probes that were complementary to either SP or NKB mRNAs. Slides were dipped into nuclear emulsion for visualization of mRNAs at the single-cell level. The location of labeled neurons (greater than x 5 background) was mapped by using an image-combining computer microscope system. A distinct and complementary distribution pattern of SP and NKB neurons was observed in the human hypothalamus and basal forebrain. NKB was the predominant tachykinin in the rostral hypothalamus, whereas SP mRNA predominated in the posterior hypothalamus. Numerous NKB neurons were identified in the magnocellular basal forebrain, the bed nucleus of stria terminalis, and the anterior hypothalamic area. Scattered NKB neurons were present in the infundibular and paraventricular nuclei, paraolfactory gyrus, posterior hypothalamic area, lateral division of the medial mammillary nucleus, and amygdala. Numerous neurons expressing SP mRNAs were identified in the premammillary, supramammillary, and medial mammillary nuclei; the posterior hypothalamic area; and the corpus striatum. Scattered SP neurons were also observed in the preoptic area; the infundibular, intermediate, dorsomedial, and ventromedial nuclei; the infundibular stalk; the amygdala; the bed nucleus of stria terminalis; and the paraolfactory gyrus. These studies provide the first description of the location of neurons that express tachykinin gene transcripts in the human hypothalamus.

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Cardiovascular roles of tachykinin peptides in the nucleus tractus solitarii of rats

Cited by 55 publications

References 25 publications

Localization of the neuromedin K receptor (NK3) in the central nervous system of the rat

Localization of the neuromedin K receptor (NK3) in the central nervous system of the rat

Distribution of fos-like immunoreactivity within the rat brain following intraventricular injection of the selective NK3 receptor agonist senktide

Localization of neurons expressing substance P and neurokinin B gene transcripts in the human hypothalamus and basal forebrain

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