TY - JOUR
T1 - Switching between transient and sustained signalling at the rod bipolar-AII amacrine cell synapse of the mouse retina
AU - Snellman, Josefin
AU - Zenisek, David
AU - Nawy, Scott
PY - 2009
Y1 - 2009
N2 - At conventional synapses, invasion of an action potential into the presynaptic terminal produces a rapid Ca2+ influx and ultimately the release of synaptic vesicles. However, retinal rod bipolar cells (RBCs) generally do not produce action potentials, and the rate of depolarization of the axon terminal is instead governed by the rate of rise of the light response, which can be quite slow. Using paired whole-cell recordings, we measured the behaviour of the RBC-AII amacrine cell synapse while simulating light-induced depolarizations either by slowly ramping the RBC voltage or by depolarizing the RBC with the mGluR6 receptor antagonist (R,S)-α-cyclopropyl-4- phosphonophenylglycine (CPPG). Both voltage ramps and CPPG evoked slow activation of presynaptic Ca2+ currents and severely attenuated the early, transient component of the AII EPSC compared with voltage steps. We also found that the duration of the transient component was limited in time, and this limitation could not be explained by vesicle depletion, inhibitory feedback, or proton inhibition. Limiting the duration of the fast transient insures the availability of readily releasable vesicles to support a second, sustained component of release. The mGluR6 pathway modulator cGMP sped the rate of RBC depolarization in response to puffs of CPPG and consequently potentiated the transient component of the EPSC at the expense of the sustained component. We conclude that the rod bipolar cell is capable of both transient and sustained signalling, and modulation of the mGluR6 pathway by cGMP allows the RBC to switch between these two time courses of transmitter release.
AB - At conventional synapses, invasion of an action potential into the presynaptic terminal produces a rapid Ca2+ influx and ultimately the release of synaptic vesicles. However, retinal rod bipolar cells (RBCs) generally do not produce action potentials, and the rate of depolarization of the axon terminal is instead governed by the rate of rise of the light response, which can be quite slow. Using paired whole-cell recordings, we measured the behaviour of the RBC-AII amacrine cell synapse while simulating light-induced depolarizations either by slowly ramping the RBC voltage or by depolarizing the RBC with the mGluR6 receptor antagonist (R,S)-α-cyclopropyl-4- phosphonophenylglycine (CPPG). Both voltage ramps and CPPG evoked slow activation of presynaptic Ca2+ currents and severely attenuated the early, transient component of the AII EPSC compared with voltage steps. We also found that the duration of the transient component was limited in time, and this limitation could not be explained by vesicle depletion, inhibitory feedback, or proton inhibition. Limiting the duration of the fast transient insures the availability of readily releasable vesicles to support a second, sustained component of release. The mGluR6 pathway modulator cGMP sped the rate of RBC depolarization in response to puffs of CPPG and consequently potentiated the transient component of the EPSC at the expense of the sustained component. We conclude that the rod bipolar cell is capable of both transient and sustained signalling, and modulation of the mGluR6 pathway by cGMP allows the RBC to switch between these two time courses of transmitter release.
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U2 - 10.1113/jphysiol.2008.165241
DO - 10.1113/jphysiol.2008.165241
M3 - Article
C2 - 19332496
AN - SCOPUS:66549128896
SN - 0022-3751
VL - 587
SP - 2443
EP - 2455
JO - Journal of Physiology
JF - Journal of Physiology
IS - 11
ER -