Inhibition of salt appetite in the rat following injection of tachykinins into the medial amygdala

Massi, Maurizio; Gentili, Luigi; Perfumi, Marina; de, G.; Schulkin, Jay

doi:10.1016/0006-8993(90)91082-r

Cited by 32 publications

(15 citation statements)

References 41 publications

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“…Some progress has been made in identifying the brain system that mediates the action of NK 3 agonists on salt intake. For example, injections of NK 3 receptor agonists into a limited number of brain regions, such as the medial amygdala and BNST, inhibit salt intake (Massi et al, 1990;Pompei et al, 1991). This finding is in keeping with the presence of NK 3 receptors in these two nuclei and results linking the medial amygdala and BNST to the regulation of salt intake (Gentil et al, 1968;Nachman and Ashe, 1974;Nitabach et al, 1989;Galaverna et al, 1992;Reilly et al, 1994;ZardettoSmith et al, 1994).…”

Section: Salt Intakementioning

confidence: 61%

“…This finding is in keeping with the presence of NK 3 receptors in these two nuclei and results linking the medial amygdala and BNST to the regulation of salt intake (Gentil et al, 1968;Nachman and Ashe, 1974;Nitabach et al, 1989;Galaverna et al, 1992;Reilly et al, 1994;ZardettoSmith et al, 1994). We report a high number of FLIpositive cells after senktide injection in the same regions of the amygdala where injections of NK 3 receptor agonists suppress salt intake (Massi et al, 1990).…”

Section: Salt Intakementioning

confidence: 98%

“…Intraventricular injections of NK 3 agonists are very potent in inhibiting need-free and sodium deficiency-induced salt intake by rats (Massi et al, 1990;Ciccocippo et al, 1994;Smith and Flynn, 1994). Some progress has been made in identifying the brain system that mediates the action of NK 3 agonists on salt intake.…”

Section: Salt Intakementioning

confidence: 98%

“…Much of what we know about the sites that mediate the biological actions of NK 3 agonists is based on mapping strategies that utilize either local injections (Massi et al, 1988a(Massi et al, , 1990Liminga et al, 1991;Stoessl et al, 1991) or electrophysiology (Keegan et al, 1992;Norris et al, 1993;Boden and Woodruff, 1994;Seabrook et al, 1995;Maubach and Jones, 1997;Nalivaiko et al, 1997) to target individual sites one at a time. The limitation that these techniques share is that they are not well suited to provide an encompassing picture of the synaptically linked, multineuronal pathways that underlie a functional system.…”

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confidence: 99%

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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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Section: Salt Intakementioning

confidence: 61%

Section: Salt Intakementioning

confidence: 98%

Section: Salt Intakementioning

confidence: 98%

mentioning

confidence: 99%

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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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“…In contrast, the presence of NK2 receptors in the rat brain remains controversial (Mantyh et al, 1989;Quirion et al, 1991;Takeda & Krause 1991;Mussap et al, 1993) (Buck et al, 1986;Bergstrom et al, 1987;Buck & Krstenansky, 1987;Foster & Tridgett, 1988;Burcher et al, 1989;Geraghty et al, 1992). High-affinity NK2 binding sites were found using the radioligand [1251]-NPy in the rat CNS (Dam et al, 1990c;Takeda & Krause, 1991 (Massi et al, 1990;, other investigators (Badgery-Parker et al, 1993) have reported weak specific binding for a new NK2 radioligand ['251]-[Lys5,Tyr (12)7,MeLeu9,Nle'0]-NKA (4-10) in adult rat brain, suggesting a low level of central NK2 receptors. Consistent with the relative abundance of y-PPT mRNA in rat brain (Krause et al, 1987;Marchand et al, 1993) and ['251]-NPy in the rat CNS (Dam et al, 1990c) in comparison with NK2-like binding sites, distinct NPy-preferring receptors may exist.…”

Section: Discussionmentioning

confidence: 99%

Intracerebroventricular responses to neuropeptide γ in the conscious rat: characterization of its receptor with selective antagonists

Picard

Couture

1996

British J Pharmacology

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Substance P and neurokinin A variations throughout the rat estrous cycle; comparison with ovariectomized and male rats: II. Trigeminal nucleus and cervical spinal cord

Duval

Lenoir

Moussaoui³

et al. 1996

J. Neurosci. Res.

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Substance P and neurokinin A were assayed in the trigeminal nucleus and cervical spinal cord of 4‐day cycling female, ovariectomized, and male rats. During the estrous cycle, levels were largely stable in the trigeminal nucleus. In ovariectomized rats, the levels differed from those on any day of the estrous cycle suggesting a weak effect of ovarian steroids. In males, the variations in the substance P and neurokinin A contents in the trigeminal nucleus were not similar to those in either cyclic or ovariectomized rats. The levels fluctuated substantially in the cervical spinal cord. During the first 3 days of the estrous cycle, the substance P and neurokinin A contents fell concomitant with the 17β‐estradiol surge, suggesting a downregulation of substance P and neurokinin A contents by 17β‐estradiol. Furthermore, on estrus, progesterone seemed to inhibit the accumulation of both neurokinins. Testosterone may stimulate accumulation of substance P and neurokinin A in the cervical spinal cord, with a marked circadian rhythm. These results are in favor of the neurokinin content of the spinal cord being regulated by the gonadal steroids. In the trigeminal nucleus, only testosterone has an effect. © 1996 Wiley‐Liss, Inc.

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Inhibition of salt appetite in the rat following injection of tachykinins into the medial amygdala

Cited by 32 publications

References 41 publications

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

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

Intracerebroventricular responses to neuropeptide γ in the conscious rat: characterization of its receptor with selective antagonists

Substance P and neurokinin A variations throughout the rat estrous cycle; comparison with ovariectomized and male rats: II. Trigeminal nucleus and cervical spinal cord

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