This Article Full Text Full Text (PDF) All Versions of this Article: 145/8/3652    most recent Author Manuscript (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Peters, J. H. Articles by Simasko, S. M. Search for Related Content PubMed PubMed Citation Articles by Peters, J. H. Articles by Simasko, S. M.

Cooperative Activation of Cultured Vagal Afferent Neurons by Leptin and Cholecystokinin

Program in Neuroscience, Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164

Address all correspondence and requests for reprints to: James H. Peters, Program in Neuroscience, Department of Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164-6520. E-mail: petersj{at}vetmed.wsu.edu.

To test the hypothesis that leptin can directly activate vagal afferent neurons, we used fluorescence imaging to detect acute changes in cytosolic calcium after leptin application to primary cultures of vagal afferent neurons dissociated from adult rat nodose ganglia. We found that approximately 40% of vagal afferent neurons exposed to leptin (40 ng/ml) responded with rapid and reversible increases in cytosolic calcium. These responses were dependent upon extracellular calcium. As previously reported, about 35% of vagal afferents increase cytosolic calcium in response to the gut-peptide cholecystokinin (CCK). A majority (74%) of neurons that responded to CCK also exhibited increases in cytosolic calcium in response to leptin. In addition, synergistic increases in cytosolic calcium were observed when leptin and CCK were applied in combination. These results demonstrate that leptin acts directly on vagal afferent neurons to trigger acute influxes of extracellular calcium. Our results also suggest cooperation between leptin and CCK in the activation of some vagal afferent neurons. Acute activation of vagal afferents by leptin alone and in combination with CCK may contribute to modulation of visceral reflexes and control of food intake.

This article has been cited by other articles:

				J. H. Peters, S. M. Simasko, and R. C. Ritter Leptin Analog Antagonizes Leptin Effects on Food Intake and Body Weight but Mimics Leptin-Induced Vagal Afferent Activation Endocrinology, June 1, 2007; 148(6): 2878 - 2885. [Abstract] [Full Text] [PDF]

				M. Covasa CCK- and leptin-induced vagal afferent activation: a model for organ-specific endocrine modulation of visceral sensory information Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2006; 290(6): R1542 - R1543. [Full Text] [PDF]

				J. Sanchez, P. Oliver, O. Miralles, E. Ceresi, C. Pico, and A. Palou Leptin Orally Supplied to Neonate Rats Is Directly Uptaken by the Immature Stomach and May Regulate Short-Term Feeding Endocrinology, June 1, 2005; 146(6): 2575 - 2582. [Abstract] [Full Text] [PDF]