Current source density analysis of retinal field potentials. II. Pharmacological analysis of the b-wave and M-wave

Abstract

1. The actions of two pharmacological agents, barium ions (Ba2+) and picrotoxin (PTX), were examined on components of the electroretinogram (ERG) in frog retina. Depth profiles of light-evoked field potentials were recorded, and current source densities (CSDs) were computed from these. 2. Ba2+ abolished the M-wave, slow PIII, and the c-wave, but only decreased b-wave amplitude down to approximately 65% of control amplitude. 3. Ba2+ abolished a slow current sink in the inner plexiform layer (IPL) and the source at the inner limiting membrane (ILM). This IPL sink/ILM source appears to generate the M-wave. 4. Ba2+ decreased the current sink at the outer plexiform layer (OPL) to approximately 70% of control amplitude, and it increased an IPL source. This Ba(2+)-resistant OPL sink/IPL source appears to generate a significant portion of the b-wave. The Ba(2+)-sensitive portion of the b-wave might be generated by Müller cells. 5. PTX enhanced retinal field potentials, particularly the M-wave in the proximal retina. This enhanced M-wave was shown to originate from an enhanced IPL sink/ILM source. 6. Our results suggest that the M-wave originates from Müller cells, through the spatial buffering of the light-evoked increase in [K+]o of the proximal retina. A portion of the b-wave may also originate from Müller cells, but a stronger direct contribution from depolarizing bipolar cells is suggested.

Genetic Inactivation of an Inwardly Rectifying Potassium Channel (Kir4.1 Subunit) in Mice: Phenotypic Impact in Retina

“…The origin of another ERG component, the b-wave, has provoked controversy over the past 50 years (Newman, 2000). The b-wave was initially believed to be generated by retinal neurons (Tomita and Funaishi, 1952), then attributed to a K ϩ current generated by Müller cells (Miller and Dowling, 1970;Newman, 1980;, and, most recently, to retinal neurons once again (Xu and Karwoski, 1994). Our results strongly support a neuronal origin of the response.…”

Regulation of Rod Phototransduction Machinery by Ciliary Neurotrophic Factor

“…2 D) (Naarendorp et al, 2001) and reflects the activity of secondorder rod bipolar cells (Newman and Odette, 1984;Stockton and Slaughter, 1989;Xu and Karwoski, 1994;Robson and Frishman, 1995). This region of the b-wave intensity-response curve can be modeled using the Naka-Rushton equation, as an indicator of rod-initiated retinal function (Fulton and Rushton, 1978;Arden et al, 1983).…”

Primate Retinal Signaling Pathways: Suppressingon-Pathway Activity in Monkey With Glutamate Analogues Mimics Human CSNB1-NYXGenetic Night Blindness

“…Although the function of nyctalopin remains unknown, electrophysiology studies of CSNB1 using noninvasive electroretinogram (ERG) recordings indicate that the defect lies postsynaptic to the rod photoreceptors, as the rod-driven a-wave remains normal but the dark-adapted ERG b-wave is absent (Miyake et al 1986). The a-wave originates from hyperpolarization of the rod photoreceptors on exposure to light stimuli (Baylor et al 1984;Granit 1947;Penn and Hagins 1972), whereas the b-wave reflects activity of postsynaptic bipolar cells directly or indirectly (Gurevich and Slaughter 1993;Robson and Frishman 1995;Xu and Karwoski 1994). The rod pathology has only depolarizing bipolar cells (DBC) (Dacheux and Raviola 1986;Wassle and Boycott 1991).…”