Functional GABA(B) receptors are expressed at the cone photoreceptor terminals in bullfrog retina.
GABA(B) receptors at the cone terminals in bullfrog retina were characterized by immunocytochemical and whole-cell patch clamp techniques in retinal slice preparations. Somata, axons and synaptic terminals (pedicles) of cones were both GABA(B) receptor (GABA(B)R) 1 and GABA(B)R2 immunoreactive. Physiologically, barium/calcium currents of cones to voltage steps were significantly reduced in size when GABA was puffed to cone terminals in the presence of picrotoxin that is supposed to block both GABA(A) and GABA(C) receptors. Similar reduction in barium currents was obtained with puff application of baclofen to cone terminals. These results suggest the presence of functional GABA(B) receptors at the bullfrog cone terminals. Suppression of barium currents of cones by baclofen was dose-dependent. Moreover, barium currents of cones were potentiated by background illumination, as compared with those recorded in the dark. 6,7-Dinitroquinoxaline-2,3-dione, an antagonist of non-NMDA receptors that hyperpolarizes horizontal cells and reduces GABA release from these cells, and saclofen, a GABA(B) receptor antagonist, both potentiated barium currents of cones in the dark, thereby mimicking the effects of background illumination. It is suggested that changes in calcium influx into the cone synaptic terminals due to activation of GABA(B) receptors may provide a negative feedback mechanism for regulating signal transmission between cones and second-order neurons in the retina by modifying the amount of glutamate released from the cones.
Liu
J
J
Institute of Neurobiology, Institutes of Brain Science, Fudan University, Shanghai 200433, China.
Zhao
J-W
JW
Du
J-L
JL
Yang
X-L
XL
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D001464:Barium / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D025461:Feedback, Physiological / Q000187:drug effects / Q000502:physiology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D007150:Immunohistochemistry; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism*; D011892:Rana catesbeiana; D018080:Receptors, GABA-B / Q000187:drug effects / Q000378:metabolism*; D012160:Retina / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D017949:Retinal Cone Photoreceptor Cells / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014785:Vision, Ocular / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000494:pharmacology
D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D018756:GABA Antagonists; C485504:Gabbr2 protein, mouse; D018080:Receptors, GABA-B; D001464:Barium; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D001418:Baclofen