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E D Cohen

Publications and source records attributed to E D Cohen.

21 records · Page 2Linked to original sources

The role of NMDA and non-NMDA excitatory amino acid receptors in the functional organization of primate retinal ganglion cells.

The role of excitatory amino acid (EAA) receptors in primate retinal ganglion cell function was analyzed in a superfused retina-eyecup preparation using single-unit, extracellular recording techniques. The effects of bath applied L-2-amino-4-phosphonobutyrate (APB), N-methyl-D-aspartate (NMDA), and non-NMDA EAA receptor agonists and antagonists were examined on the light-evoked responses and resting firing rates of ganglion cells. APB (30-100 microM) reduced or blocked the light-evoked responses and resting firing rates of all ON-center ganglion cells; higher doses of APB (100 microM) were required to block the light-evoked responses of ON-transient cells. In contrast, an increase in resting firing rates was observed when L-APB was applied to some OFF-center ganglion cells. The EAA agonists kainate (KA) (10-20 microM) and NMDA (200-350 microM) increased the firing rate of virtually all ganglion cells examined. Quisqualate (10-20 microM) increased firing in most cells, but occasionally (4/13 cases) produced inhibition. The NMDA antagonist D-amino-phosphono-heptanoic acid (D-AP7) (200-250 microM) reduced the light-evoked responses of ganglion cells by an average of 12% from control levels, while resting firing rates declined 37%. In the presence of D-AP7, the basic receptive-field characteristics of cells were not significantly altered. In contrast, two non-NMDA receptor antagonists, NBQX (2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo-(F)-quinoxalinedione) and DNQX (6,7-dinitro-quinoxaline-2,3-dione), produced substantial reductions in the light-evoked responses (82%) and resting firing rates (87%) of all ganglion cell classes. A striking observation in some neurons was the recovery of a persistent transient light-evoked response in the presence of NBQX. This NBQX-insensitive, light-evoked response was always blocked by adding D-AP7. Thus, neurotransmission from bipolar to ganglion cells in primates is mediated predominantly by non-NMDA EAA receptors, with NMDA receptors forming a minor component of the light-evoked response.

Aminobutyrates↗

Voltage-gated calcium and sodium currents of starburst amacrine cells in the rabbit retina.

The voltage-gated calcium and sodium currents of starburst amacrine cells were examined in slices of the adult rabbit retina. ON-center starburst amacrine cells were targeted for whole-cell recording by prelabeling the retina with the nuclear dye 4'-6-diamidino-2-phenylindole hydrochloride (DAPI). Calcium currents were isolated using an external Ringer that contained tetrodotoxin to block sodium currents and barium to block potassium channels. When starburst amacrine cells were stepped to holding potentials positive to -50 mV, a series of voltage-dependent calcium currents were activated. The calcium current peaked at -10 mV. The calcium currents kinetics were mainly sustained in nature, showing only a small amount of slow inactivation. Nickel (100 microM), a T-type channel blocker, had no effect on the calcium current. Application of the L-type channel agonist BAY K8644 (1-2.5 microM) had small variable effects on the calcium current while the L-type channel antagonist nifedipine (10 microM) had no effect. However, addition of a reported N-type calcium channel antagonist, omega-conotoxin G6A (1 microM), blocked a large portion of the calcium current, as did a more nonselective antagonist, omega-conotoxin M7C (200 nM). Agatoxin 4A (500 nM) reduced a smaller sustained calcium current component, implying a P/Q-type calcium channel was present on these neurons. In addition to the calcium currents, a fast voltage-gated sodium current was observed in many starburst cells. This current could be blocked by tetrodotoxin (200-500 nM). The differing kinetics and durations of the sodium and calcium currents could play important roles in the regulation of synaptic release and in the coordination of spiking by starburst amacrine cell dendrites during retinal development and in the encoding of motion across the retinal surface.

Action Potentials↗