Abstract
Transmitter release in neurons is thought to be mediated exclusively by high-voltage-activated (HVA) Ca(2+) channels. However, we now report that, in retinal bipolar cells, low-voltage-activated (LVA) Ca(2+) channels also mediate neurotransmitter release. Bipolar cells are specialized neurons that release neurotransmitter in response to graded depolarizations. Here we show that these cells express T-type Ca(2+) channel subunits and functional LVA Ca(2+) currents sensitive to mibefradil. Activation of these currents results in Ca(2+) influx into presynaptic terminals and exocytosis, which we detected as a capacitance increase in isolated terminals and the appearance of reciprocal currents in retinal slices. The involvement of T-type Ca(2+) channels in bipolar cell transmitter release may contribute to retinal information processing.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Calcium / metabolism
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Calcium Channel Blockers / pharmacology
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Calcium Channels, T-Type / genetics
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Calcium Channels, T-Type / metabolism*
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Chelating Agents / pharmacology
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Cobalt / pharmacology
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Egtazic Acid / analogs & derivatives*
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Egtazic Acid / pharmacology
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Electric Capacitance
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Exocytosis / physiology
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Mibefradil / pharmacology
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Neurotransmitter Agents / metabolism*
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Nimodipine / pharmacology
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Patch-Clamp Techniques
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Presynaptic Terminals / metabolism
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RNA, Messenger / analysis
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Rats
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Rats, Long-Evans
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Retina / cytology
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Retina / metabolism*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
Substances
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Calcium Channel Blockers
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Calcium Channels, T-Type
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Chelating Agents
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Neurotransmitter Agents
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RNA, Messenger
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Mibefradil
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Cobalt
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Egtazic Acid
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Nimodipine
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
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Calcium