Potentiation of GABAA receptor-mediated Cl- current by urotensin peptides in identified Aplysia neurons

✍ Scribed by Masashi Sawada; Mitsuyuki Ichinose

• Book ID: 101244517
• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 95 KB
• Volume: 56
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19990601)56:5<547::aid-jnr10>3.0.co;2-l

✦ Synopsis

␥-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the vertebrate and invertebrate central nervous systems, including those of molluscs. The effects of extracellularly applied urotensin peptides (urotensin I (UI) and urotensin II (UII)) on the GABA-induced Cl -current recorded from identified neurons (R9 and R12) of Aplysia kurodai were investigated using voltage-clamp and pressure ejection techniques. Focal application of 100 nM UI and UII potentiated the GABA-induced Cl -current without affecting the resting membrane conductance and holding current. The increase was completely reversible. The GABA-induced Cl -current also was potentiated by bath-applied UI and UII (5-10 nM). The potentiating effects of UI and UII on the GABA-induced Cl - current were concentration-dependent and completely reversible. These results suggest that neurotensin peptides may decrease neuronal excitability by potentiating the GABA A receptor-mediated Cl -current in the neurons of mammalian and invertebrate central nervous systems.