title: Membrane conductances involved in amplification of small signals by sodium channels in photoreceptors of drone honey bee.
abstract: 1. Voltage signals of about 1 mV evoked in photoreceptors of the drone honey bee by shallow modulation of a background illumination of an intensity useful for behaviour are thought to be amplified by voltage-dependent Na+ channels. To elucidate the roles of the various membrane conductances in this amplification we have studied the effects of the Na+ channel blocker tetrodotoxin (TTX) and various putative K+ channel blockers on the membrane potential, Vm. 2. Superfusion of a slice of retina with 0.5-10 mM-4-aminopyridine (4-AP) depolarized the membrane and, in fifty of sixty-three cells induced repetitive action potentials. Ionophoretic injection of tetraethylammonium produced similar effects. 3. In order to measure the depolarization caused by 4-AP, action potentials were prevented by application of TTX: 4-AP was applied when the membrane was depolarized to different levels by light. 4-AP induced an additional depolarization at all membrane potentials tested (-64 to -27 mV). We conclude that there are 4-AP-sensitive K+ channels that are open at constant voltage over this range. 4. 4-AP slowed down the recovery phase of the action potential induced by a light flash by a factor that ranged from 0.51 to 0.16. This reduction could be accounted for by the reduction in a voltage-independent K+ conductance estimated from the steady-state depolarization. 5. After the voltage-gated Na+ channels had been blocked by TTX, exposure to 4-AP further changed the amplitude of the response to a small (approximately 10%) decremental light stimulus. The change was an increase when the background illumination brought Vm to potentials more negative than about -40 mV; it was a decrease when Vm > -40 mV. The data could be fitted by a circuit representation of the membrane with a light-activated conductance and a K+ conductance (EK = -66 mV) that was partly blocked by 4-AP. The voltage range studied was from -52 to -27 mV; neither conductance in the model was voltage dependent. 6. The responses to small changes in light intensity in the absence of TTX were mimicked by a model. We conclude that a voltage-dependent Na+ conductance described by the Hodgkin-Huxley equations can amplify small voltage changes in a cell membrane that is also capable of generating action potentials; the magnitude of the K+ conductance is critical for optimization of signals while avoiding membrane instability.
authors.affiliation: INSERM U176, Bordeaux, France.
authors.forename: A M
authors.initials: AM
authors.lastname: Vallet
authors.forename: J A
authors.initials: JA
authors.lastname: Coles
authors.forename: J C
authors.initials: JC
authors.lastname: Eilbeck
authors.forename: A C
authors.initials: AC
authors.lastname: Scott
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001516:Bees; D008027:Light; D008433:Mathematics; D008564:Membrane Potentials / Q000187:drug effects; D008954:Models, Biological; D010783:Photometry; D010786:Photoreceptor Cells / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D015222:Sodium Channels; D013779:Tetrodotoxin; D015761:4-Aminopyridine