| Modeling Results |
Current in response to 50 msec light stimulus:
Simulations (above) show that the ligand of the fast transient light-induced sodium current is IP3, not calcium. The simulated IP3-gated sodium current (right) resembles the early transient component of the measured light-induced current (left). The simulated calcium-gated sodium current (middle) has a delay longer than measured, and an inactivation phase which is too fast.
Calcium in response to 2 sec light stimulus:
![]() | Sources of calcium in the soma include influx through voltage dependent channels (smaller, early calcium elevation) and release of calcium from intracellular stores (larger, late calcium elevation). Diffusion from the rhabdomere does not contribute. |
Response to GABA stimulation
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The turbulence US causes hair cells to release GABA onto the terminal branches of the type B photoreceptor. The response to GABA stimulation consists of an IPSP followed several seconds later by a small depolarization lasting for several seconds. The cause of the late depolarization has not been determined, but observations are consistent with a G protein- dependent closure of potassium leak channels.

The late depolarization and input resistance elevation can be accounted for by a closure of calcium-sensitive leak potassium currents. The top traces show membrane potential in the soma and terminal branches before, during and after GABA stimulation. Hyperpolarizing current pulses are used to measure input resistance. Both a late depolarization and an increase in input resistance are apparent and last until approximately 8 or 9 seconds after the beginning of the GABA stimulation. The bottom traces show conductance of the potassium leak channels in the synaptic branch, non-synaptic branch, and each of the four isopotential axon compartments.