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Calcium‐dependent inactivation and depletion of synaptic cleft calcium ions combine to regulate rod calcium currents under physiological conditions
Author(s) -
Rabl Katalin,
Thoreson Wallace B.
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02277.x
Subject(s) - calcium , biophysics , chemistry , calcium signaling , microbiology and biotechnology , biology , organic chemistry
L‐type Ca 2+ currents ( I Ca ) in rod photoreceptors exhibit Ca 2+ ‐dependent inactivation. Perforated‐patch whole‐cell recordings were obtained from isolated rods of the tiger salamander using 1.8 m m Ca 2+ in the bathing medium to determine the extent of Ca 2+ ‐dependent inactivation of I Ca with physiological [Ca 2+ ] and endogenous buffering. I Ca was measured with voltage ramps applied before and after 5‐s steps to −40, −30, −20, or −10 mV. Long depolarizing steps in isolated rods produced inactivation of I Ca ranging from 15% at −40 mV to > 80% at −10 mV. Because, in addition to Ca 2+ ‐dependent inactivation, depletion of synaptic cleft Ca 2+ accompanying activation of I Ca can reduce presynaptic I Ca at calycal synapses, we investigated whether a similar mechanism worked at the invaginating rod synapse. Rods from retinal slices with intact synapses were compared with isolated rods in which synaptic cleft depletion is absent. I Ca was more strongly depressed by depolarization of rods in retinal slices, with I Ca reduced by 47% following voltage steps to −40 mV. The depression of currents by depolarization was also greater for rods from retinal slices than isolated rods when Ca 2+ was replaced with Ba 2+ to reduce Ca 2+ ‐dependent inactivation. The stronger depolarization‐evoked inhibition of I Ca in retinal slices compared to isolated rods probably reflects depletion of synaptic cleft Ca 2+ arising from sustained Ca 2+ influx. Inactivation of I Ca exhibited slow onset and recovery. These findings suggest that Ca 2+ ‐dependent inactivation and depletion of synaptic cleft Ca 2+ may combine to regulate I Ca in response to light‐evoked changes in rod membrane potential.