Glutamate receptors within the nucleus of solitary tract contribute to pancreatic secretion stimulated by intraduodenal hypertonic saline.
It is well known that central transmission of vago-vagal reflex within the nucleus of solitary tract (NST) plays an important role in the regulation of gastrointestinal functions. The present study was designed to assess the role of NST glutamate receptor mechanism in pancreatic secretion evoked by intraduodenal hypertonic saline (HS) in anesthetized rats. Intraduodenal infusion of HS significantly (P<0.01) stimulated pancreatic protein output (from 2.60+/-0.09 to 4.18+/-0.24 mg/15 min). Bilaterally microinjected L-glutamate (5 nmol) into the medial nucleus of solitary tract (mNST) produced a significant increase of pancreatic protein secretion (from 2.65+/-0.12 to 4.80+/-0.34 mg/15 min, P<0.01). Bilateral injection of glutamate receptor antagonist kynurenic acid (KYN, 5 nmol) into the mNST completely abolished the increase of pancreatic protein output stimulated by intraduodenal HS (from 4.28+/-0.21 to 2.83+/-0.19 mg/15 min). Either NMDA receptor antagonist dl-2-amino-5-phosphonopentanoic acid (AP5, 1.5 nmol) or AMPA/Kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 1.5 nmol) injected into the mNST markedly attenuated (P<0.05) the pancreatic protein secretion stimulated by intraduodenal HS. In conclusion, these findings showed that blockade of the NST glutamate receptors, including NMDA and AMPA/Kainate receptors antagonized pancreatic secretion evoked by intraduodenal osmolality factor, and suggested that glutamate receptor mechanism within the NST contributed to the central regulation of pancreatic secretion.
Liao
Zhuan
Z
Department of Gastroenterology, Changhai Hospital, Second Military Medical University, 174 Chang-Hai Road, Shanghai 200433, PR China. zhuanliao@hotmail.com
Li
Zhao-Shen
ZS
Lu
Yan
Y
Wang
Wei-Zhong
WZ
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D004386:Duodenum / Q000294:innervation / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D007736:Kynurenic Acid / Q000494:pharmacology; D008297:Male; D008845:Microinjections; D009952:Ornithine / Q000031:analogs & derivatives / Q000494:pharmacology; D009994:Osmolar Concentration; D010179:Pancreas / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017470:Receptors, Glutamate / Q000502:physiology*; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D017470:Receptors, Glutamate; D012462:Saline Solution, Hypertonic; C004976:delta-N-hydroxyornithine; D018698:Glutamic Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D009952:Ornithine; D007736:Kynurenic Acid