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Transformation of signals by interneurones in the barnacle's visual pathway
Author(s) -
Oertel Donata,
Stuart Ann E.
Publication year - 1981
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1981.sp013577
Subject(s) - depolarization , membrane potential , hyperpolarization (physics) , resting potential , biophysics , horseradish peroxidase , reversal potential , intracellular , electrophysiology , chemistry , biology , anatomy , neuroscience , patch clamp , microbiology and biotechnology , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy , enzyme
1. The photoreceptors of the median eye of the giant barnacle drive decrementally‐conducting neurones in the supraoesophageal ganglion termed ‘inverting cells’ (I‐cells) which in turn drive impulse‐producing neurones termed ‘amplifying cells’ (A‐cells). Using intracellular recording techniques we have studied the role of I‐cells in visual processing. 2. Horseradish peroxidase injections show that I‐cells are interneurones whose processes are confined to the regions of the photoreceptor terminals on both sides of the bilaterally symmetrical ganglion. 3. In the dark, I‐cell membrane potentials (‐45 mV) are considerably less negative than those of other ganglion cells (‐60 to ‐70 mV). At the onset of a maintained light, I‐cells undergo a transient peak hyperpolarization which declines to a steady‐state response. Both response components are graded with light intensity. 4. The reversal potential of the peak of the I‐cell light response depends on the external K + concentration more strongly than does the dark resting potential (3‐30 m m ‐K + ). This evidence indicates that the hyperpolarization results from an increase in the cell's permeability to K + ions. 5. At the offset of light an I‐cell undergoes a transient depolarization that overshoots the dark membrane potential. Dimming of a background light can also cause the I‐cell membrane potential to overshoot its dark resting value. This overshoot is associated with a large depolarizing synaptic potential in A‐cells. 6. An overshoot of the dark resting potential can also be elicited by the break of a hyperpolarizing pulse of current injected into an I‐cell. The amplitude of this overshoot increases with pulse duration over a time course of seconds. 7. In the presence of external tetraethylammonium ion (TEA) and tetrodotoxin, (TTX), the break of a hyperpolarizing pulse or the onset of a depolarizing pulse can evoke in an I‐cell an action potential whose rate of rise and amplitude depend on the external Ca concentration. This action potential can be maintained by replacement of external Ca with Ba, or blocked by addition of 15 m m ‐Co to the saline. These observation's indicate that depolarizing potential changes in this cell activate a voltage‐sensitive Ca conductance. 8. When hyperpolarizing current pulses are injected into an I‐cell, the voltage during the pulse sags back slowly towards the dark resting potential. Thus, during hyperpolarization with light or current an I‐cell's membrane properties change over a time course of seconds. 9. The onset of a depolarizing pulse or the offset of a hyperpolarizing pulse of current injected into an I‐cell leads to a transient depolarization of a simultaneously impaled A‐cell. Synaptic transmission occurs when the I‐cell is depolarized to the vicinity of the dark resting potential. The amplitude of the response in an A‐cell depends on the rate of change of the I‐cell voltage.