• 1

    Sayegh AI, Reeve JR & Lampley ST, et al. Role for the enteric nervous system in the regulation of satiety via cholecystokinin-8. J Am Vet Med Assoc 2005;226:18091816.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2

    Janqueira LC, Carneiro J, Kelley RO. Basic histology. 9th ed.Stamford, Conn: Appleton and Lange, 1998.

  • 3

    Kamilaris TC, Johnson EO & Calogero AE, et al. Cholecystokinin-octapeptide stimulates hypothalamic-pituitaryadrenal function in rats: role of corticotropin-releasing hormone. Endocrinology 1992;130:17641774.

    • Search Google Scholar
    • Export Citation
  • 4

    Ruiz-Gayo M, Garrido MM, Fuentes JA. Inhibition of the hypothalamic-pituitary-adrenal axis in food-deprived rats by a CCK-A receptor antagonist. Br J Pharmacol 2000;129:839842.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5

    Gibbs J, Young RC, Smith GP. Cholecystokinin decreases food intake in rats. J Comp Physiol Psychol 1973;84:488495.

  • 6

    Nussdorfer GG, Spinazzi R, Mazzocchi G. Cholecystokinin and adrenal-cortex secretion. Vitam Horm 2005;71:433453.

  • 7

    Meister B, Broberger C & Villar MJ, et al. Cholecystokinin B receptor gene expression in hypothalamic neurosecretory neurons after experimental manipulations. Neuroendocrinology 1994;60:458469.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8

    Malendowicz LK, Spinazzi R & Majchrzak M, et al. Effects of prolonged cholecystokinin administration on rat pituitary-adrenocortical axis: role of the CCK receptor subtypes 1 and 2. Int J Mol Med 2003;12:903909.

    • Search Google Scholar
    • Export Citation
  • 9

    Rinaman L, Hoffman GE & Dohanics J, et al. Cholecystokinin activates catecholaminergic neurons in the caudal medulla that innervate the paraventricular nucleus of the hypothalamus in rats. J Comp Neurol 1995;360:246256.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10

    Verbalis JG, Stricker EM & Robinson AG, et al. Cholecystokinin activates c-fos expression in hypothalamic oxytocin and corticotropin-releasing hormone neurons. J Neuroendocrinol 1991;3:205213.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11

    Gulley S, Covasa M & Ritter RC, et al. Cholecystokinin 1 receptors mediate the increase in Fos-like immunoreactivity in the rat myenteric plexus following intestinal oleate infusion. Physiol Behav 2005;86:128135.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12

    Gulley S, Esdaile AR & Sullivan SN, et al. Chemical sympathectomy attenuates myenteric but not dorsal vagal complex Fos-like immunoreactivity induced by cholecystokinin-8 in the rat. Brain Res 2005;1064:119125.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13

    Gulley S, Sharma SK & Mansour MM, et al. Strain differences in myenteric neuron number and CCK1 receptor mRNA expression may account for differences in CCK induced c-Fos activation. Brain Res 2005;1058:109119.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14

    Gulley S, Sharma SK & Moran TH, et al. Cholecystokinin-8 increases Fos-like immunoreactivity in the brainstem and myenteric neurons of rats through CCK1 receptors. Peptides 2005;26:16171622.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15

    Raboin SJ, Gulley S & Henley SC, et al. Sympathectomy and demedullation increase myenteric Fos-like immunoreactivity by cholecystokinin-8 but only demedullation increases it in the dorsal vagal complex. Regul Pept 2006;134:141148.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16

    Sayegh AI, Covasa M, Ritter RC. Immunohistochemical phenotypes of enteric neurons activated by intestinal nutrients, in Proceedings. Soc Neurosci 30th Annu Meet 2000;1527.

    • Search Google Scholar
    • Export Citation
  • 17

    Sayegh AI, Covasa M, Ritter RC. Intestinal infusions of oleate and glucose activate distinct enteric neurons in the rat. Auton Neurosci 2004;115:5463.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18

    Sayegh AI, Ritter RC. CCK-A receptor activation induces fos expression in myenteric neurons of rat small intestine. Regul Pept 2000;88:7581.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19

    Sayegh AI, Ritter RC. Vagus nerve participates in CCK-induced Fos expression in hindbrain but not myenteric plexus. Brain Res 2000;878:155162.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20

    Sayegh AI, Ritter RC. Cholecystokinin activates specific enteric neurons in the rat small intestine. Peptides 2003;24:237244.

  • 21

    Sayegh AI, Ritter RC. Morphology and distribution of nitric oxide synthase-, neurokinin-1 receptor-, calretinin-, calbindin-, and neurofilament-M-immunoreactive neurons in the myenteric and submucosal plexuses of the rat small intestine. Anat Rec 2003;271A:209216.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22

    Schneider DA, Sayegh AI. Gastrointestinal neuroendocrinology. Vet Clin North Am Equine Pract 2002;18:205217.

  • 23

    Webb T, Gulley S & Esdaile AR, et al. Cholecystokinin-8 increases Fos-like immunoreactivity in myenteric neurons of the duodenum and jejunum more after intraperitoneal than after intravenous injection. Neurosci Lett 2005;389:157162.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24

    Webb T, Gulley S & Esdaile AR, et al. Effects of cholecystokinin-receptor antagonists on Fos-like immunoreactivity stimulated by sulfated cholecystokinin-8 in neurons of the myenteric plexus and hindbrain of rats. Am J Vet Res 2005;66:13081313.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25

    Paxinos G, Watson C. The rat brain in sterotaxic coordinates. San Diego: Academic Press Inc, 1997.

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Effect of adrenalectomy on cholecystokinin-8–induced Fos-like immunoreactivity in myenteric neurons and the dorsal vagal complex in rats

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  • 1 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 2 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 3 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 4 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 5 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 6 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.
  • | 7 Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088.

Abstract

Objective—To investigate the effect of adrenalectomy on cholecystokinin-8 (CCK-8)–induced Fos-like immunoreactivity (Fos-LI) in the myenteric neurons of the dorsal vagal complex (DVC) in rats.

Animals—16 male Sprague Dawley rats.

Procedures—Rats were allocated to 1 of 2 groups and underwent adrenalectomy or a sham adrenalectomy procedure. Rats were challenged with a supraphysiologic dose of CCK-8 (40 μg/kg) or physiologic saline (0.9% NaCl) solution (0.5 mL) administered IP; after 90 minutes, rats were euthanized, and Fos-LI was quantified in the DVC (at the levels of the area postrema, nucleus tractus solitarii, and dorsal motor nucleus of the vagus) and the myenteric neurons of the duodenum and jejunum by use of a diaminobenzidine reaction enhanced with nickel. The Fos-LI–positive cells were counted by use of an automated system and manually in the DVC and intestinal samples, respectively. Counts of Fos-LI in the different hindbrain levels and myenteric neurons were compared between the adrenalectomy- and shamtreated groups and between the CCK-8– and saline solution–treated groups.

Results—After adrenalectomy, CCK-8–induced Fos-LI was attenuated only in the myenteric neurons of the duodenum.

Conclusions and Clinical Relevance—Results indicate that the adrenal gland has a role in the activation of myenteric neurons by CCK-8 in rats.

Abstract

Objective—To investigate the effect of adrenalectomy on cholecystokinin-8 (CCK-8)–induced Fos-like immunoreactivity (Fos-LI) in the myenteric neurons of the dorsal vagal complex (DVC) in rats.

Animals—16 male Sprague Dawley rats.

Procedures—Rats were allocated to 1 of 2 groups and underwent adrenalectomy or a sham adrenalectomy procedure. Rats were challenged with a supraphysiologic dose of CCK-8 (40 μg/kg) or physiologic saline (0.9% NaCl) solution (0.5 mL) administered IP; after 90 minutes, rats were euthanized, and Fos-LI was quantified in the DVC (at the levels of the area postrema, nucleus tractus solitarii, and dorsal motor nucleus of the vagus) and the myenteric neurons of the duodenum and jejunum by use of a diaminobenzidine reaction enhanced with nickel. The Fos-LI–positive cells were counted by use of an automated system and manually in the DVC and intestinal samples, respectively. Counts of Fos-LI in the different hindbrain levels and myenteric neurons were compared between the adrenalectomy- and shamtreated groups and between the CCK-8– and saline solution–treated groups.

Results—After adrenalectomy, CCK-8–induced Fos-LI was attenuated only in the myenteric neurons of the duodenum.

Conclusions and Clinical Relevance—Results indicate that the adrenal gland has a role in the activation of myenteric neurons by CCK-8 in rats.

Contributor Notes

Supported by NIH Grant S06/GM08091-31, The Birmingham Racing Commission, Pfizer Student Fund Program, and the United Negro College Fund for the Henry C. McBay Research Fellowship.

Address correspondence to Dr. Sayegh.