Rod photoreceptor signal and rod synapse: The influence of BK channels, gap junctions and calcium action potentials
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BK channels are found co-localized with Ca channels at the pre-synaptic terminals throughout the nervous system. I investigated the influence of this channel on neurotransmitter release in the salamander rod photoreceptors. Surprisingly, the BK channel facilitates transmitter release from rods. The two presynaptic channels form a positive coupled loop. Calcium influx activates the BK channel current, leading to potassium efflux that increases the calcium current. The rod's normal physiological voltage range is well matched to the dynamics of this positive loop. When the rod is further depolarized then the BK channel hyperpolarizing current overcomes its facilitatory effect, causing truncation of transmitter release. Thus the calcium channel-BK channel linkage performs two functions at the synapse: nonlinear potentiator and safety brake. Salamander rods are connected to each other with gap junctions. The gap junction transmission has high pass filter properties. Consistent with the high pass filter properties, the gap junction transmitted light response had a shorter time to peak and faster decline compared to the control light response. The gap junction transmission declined exponentially from the onset of the light response. However, gap junctions were not directly regulated by light. The gap junction transmitted light response follows the derivative of the control light response, which suggests that there is a capacitative component in the gap junction connections. This may also explain why gap junctions enhance the light response under full field stimulus conditions and the high pass filter properties of the rod network. The gap junctions are up regulated by D2-like dopamine receptors and down regulated by melatonin receptors and cAMP. Ca action potentials were observed during the rod light response under physiological conditions, during the recovery phase in response to strong light stimulus. The timing of the Ca action potentials depends on the light intensity proportionally. Therefore the Ca action potentials encode light intensities. The Ca action potentials are initiated by an overshoot created by both the biochemical process in the outer segment and anodal break excitation. They are also shaped by BK channels. They are probably responsible for the negative afterimage observed in psychophysical studies.