The rst interesting property of the e ye discovered by LaCourse (1981) and described by LaCourse and Northrop (1983) was that it is an entirely OFF system. That is, the eye produced spikes on its optic nerve bers only at OFF of general illumination. The number of spikes and their instantaneous frequency depends on the intensity, wavelength, and duration of the light exposure before the light is turned off. LaCourse found that there was an optimum light level (other factors held constant) to elicit a maximum number of spikes at OFF. The peak response occurred for a white (tungsten) light stimulus of 2 ^W/cm2; it fell to zero for intensities less than about 2 nW/cm2, and above about 1 mW/cm2. LaCourse also examined the wavelength action spectrum of the OFF response using nearly monochromatic light from a single-grating monochromator adjusted for constant intensity. Response was strongest between 460 to 550 nm wavelengths; there were two peaks in the action spectrum, however: one at 490 nm (blue) and the other at 520 nm (green).
LaCourse also found that an intensity-dependent latency to the OFF response existed. At threshold intensity, the latency was very large, about 2 s; it steadily decreased to about 100 ^ at the maximum response intensity, and again slowly increased as the intensity was increased past that for the peak response.
LaCourse did not do intracellular recording from the Mytilus PRCs. He did measure the extracellular "ERG" voltage for the eye, however, using a glass micro-electrode lled with sea water. The reference electrode was placed far from the eye in the gills. The microelectrode was advanced from the eyecup into the middle of the PRCs and thence to the area on the optic nerve. A ash of light produced a positive ERG potential, suggesting that the light caused the intracellular potential (Vm) of the PRCs to go negative, hyperpolarizing them. At OFF, when spikes occurred on the optic nerve bers, the ERG went ne gative, suggesting that Vm went positive, depolarizing the cells and leading to spikes.
A putative scenario describing the Mytilus' PRC/optic nerve behavior can be borrowed from what is known about vertebrate rods and cones. In their case, light (photons) is captured by a photoreceptor pigment (a rhodopsin). An enzyme cascade occurs in which rhodopsin . activated rhodopsin (metarhodopsin II) . a GTP-binding protein (transducin) . an enzyme hydrolyzing cGMP (cGMP-phos-phodiesterase) . closure of membrane-bound, cGMP-gated cation channels. When the channels close, the normal (dark) rate of cation inward leakage (e.g., Na+) is exceeded by the rate of outward cation pumping, so Vm goes negative, hyperpolar-izing the cell (Kolb et al., 1996). In the dark, the membrane cation channels gradually open, allowing Vm to again go positive, depolarizing the rod. A similar series of events may occur in Mytilus eyes. That the these eyes only re at OFF is reasonable because this is when Vm rebounds positively toward what might be the normal ring threshold for these PRCs.
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