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Acute modulation of P/Q-type (alpha1A) calcium channels by neuronal activity-dependent changes in intracellular Ca2+ concentration may contribute to short-term synaptic plasticity, potentially enriching the neurocomputational capabilities of the brain. An unconventional mechanism for such channel modulation has been proposed in which calmodulin (CaM) may(More)
L-type (CaV1.2) and P/Q-type (CaV2.1) calcium channels possess lobe-specific CaM regulation, where Ca2+ binding to one or the other lobe of CaM triggers regulation, even with inverted polarity of modulation between channels. Other major members of the CaV1-2 channel family, R-type (CaV2.3) and N-type (CaV2.2), have appeared to lack such CaM regulation. We(More)
Ca(V)1.3 channels comprise a vital subdivision of L-type Ca2+ channels: Ca(V)1.3 channels mediate neurotransmitter release from auditory inner hair cells (IHCs), pancreatic insulin secretion, and cardiac pacemaking. Fitting with these diverse roles, Ca(V)1.3 channels exhibit striking variability in their inactivation by intracellular Ca2+. IHCs show(More)
Among the most intriguing forms of Ca(2+) channel modulation is the regulation of L-type and P/Q-type channels by intracellular Ca(2+), acting via unconventional channel-calmodulin (CaM) interactions. In particular, overexpressing Ca(2+)-insensitive mutant CaM abolishes Ca(2+)-dependent modulation, hinting that Ca(2+)-free CaM may "preassociate" with these(More)
P-type (CaV2.1) Ca2+ channels are a central conduit of neuronal Ca2+ entry, so their Ca2+ feedback regulation promises widespread neurobiological impact. Heterologous expression of recombinant CaV2.1 channels demonstrates that the Ca2+ sensor calmodulin can trigger Ca2+-dependent facilitation (CDF) of channel opening. This facilitation occurs when local(More)
the activity-dependent I pCa facilitation may be mediated by NCS-1 at various synapses, thereby mediating activity-dependent synap-tic facilitation. The residual Ca 2ϩ hypothesis for the synaptic facilitation has been widely accepted, but its detailed mechanism is still unknown (31). One of the downstream effects of residual Ca 2ϩ is the facilitation of I(More)
legend: The top is an original receptive-field drawing taken from the notebooks of Hubel and Wiesel, December 11, 1962. It is the first documentation of a color-opponent neuron in macaque striate cortex. The neuron was suppressed by red in the receptive-field center, excited by red in the receptive-field surround, and excited by blue throughout. The bottom(More)
preassociation locus to be Ͻ10 Å (r) from the linker origin (Fig. 3E and fig. S3). This indication of strongly enriched local CaM seems robust, as fits based on measurements of free intracellular [CaM] in these cells (ϳ50 nM) (25–27) diverge from our data by orders of magnitude (Fig. 3E). Also, the suggestion of increased local [CaM] is insensitive to the(More)
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