Characterization of GABAB Receptors Involved in Inhibition of Motility Associated With Acetylcholine Release in the Dog Small Intestine: Possible Existence of a Heterodimer of GABAB1 and GABAB2 Subunits

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  • Kawakami Shunsuke
    Division of Surgery, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences Division of Pharmacology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Uezono Yasuhito
    Division of Pharmacology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Makimoto Noriaki
    Division of Surgery, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Enjoji Akihito
    Division of Surgery, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Kaibara Muneshige
    Division of Pharmacology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Kanematsu Takashi
    Division of Surgery, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences
  • Taniyama Kohtaro
    Division of Pharmacology, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences

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Abstract

Characterization of the γ-aminobutyric acid (GABA)B receptor involved in the motility of dog small intestine was analyzed by application of the microdialysis method to the small intestine of the whole body of the dog. The reverse transcription-polymerase chain reaction (RT-PCR) was used. Intraarterial administration of muscimol induced acceleration of motility associated with acetylcholine (ACh) release, these responses being antagonized by bicuculline. Intraarterial administration of baclofen induced inhibition of motility associated with ACh release, these responses being antagonized by CGP62349. GABA induced inhibition of motility associated with decrease in ACh release. CGP62349 alone induced acceleration of motility associated with increase in ACh release. RT-PCR revealed the presence of mRNAs for both subunits of GABAB receptor, GABAB1 and GABAB2, in the dog small intestine, although GABAB1 subunits were 6 isoforms of GABAB1 (GABAB1(a) – GABAB1(g)), except GABAB1(d). Thus, the GABAB receptor located at cholinergic neurons as a heterodimer with subunits of GABAB1 and GABAB2 in the dog small intestine operates predominantly relative to the GABAA receptor in physiological motility.<br>

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