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Potentiation of GABA A receptor‐mediated Cl ‐ current by urotensin peptides in identified Aplysia neurons
Author(s) -
Sawada Masashi,
Ichinose Mitsuyuki
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990601)56:5<547::aid-jnr10>3.0.co;2-l
Subject(s) - urotensin ii , aplysia , gabaa receptor , long term potentiation , neurotransmitter , inhibitory postsynaptic potential , receptor , reversal potential , biology , voltage clamp , medicine , gamma aminobutyric acid , chemistry , neuroscience , biophysics , endocrinology , central nervous system , patch clamp , membrane potential , biochemistry
γ‐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. J. Neurosci. Res. 56:547–552, 1999. © 1999 Wiley‐Liss, Inc.